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Peter Passmore - One of the best experts on this subject based on the ideXlab platform.
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Aspirin and other non‐steroidal anti‐inflammatory drugs for the Prevention of Dementia
The Cochrane database of systematic reviews, 2020Co-Authors: Fionnuala Jordan, Bernadette Mcguinness, Peter Passmore, Terry J Quinn, John P. Kelly, Catrin Tudur Smith, Kathy Murphy, Declan DevaneAbstract:BACKGROUND Dementia is a worldwide concern. Its global prevalence is increasing. At present, there is no medication licensed to prevent or delay the onset of Dementia. Inflammation has been suggested as a key factor in Dementia pathogenesis. Therefore, medications with anti-inflammatory properties could be beneficial for Dementia Prevention. OBJECTIVES To evaluate the effectiveness and adverse effects of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) for the primary or secondary Prevention of Dementia. SEARCH METHODS We searched ALOIS, the specialised register of the Cochrane Dementia and Cognitive Improvement Group up to 9 January 2020. ALOIS contains records of clinical trials identified from monthly searches of several major healthcare databases, trial registries and grey literature sources. We ran additional searches across MEDLINE (OvidSP), Embase (OvidSP) and six other databases to ensure that the searches were as comprehensive and up-to-date as possible. We also reviewed citations of reference lists of included studies. SELECTION CRITERIA We searched for randomised controlled trials (RCTs) and controlled clinical trials (CCTs) comparing aspirin or other NSAIDs with placebo for the primary or secondary Prevention of Dementia. We included trials with cognitively healthy participants (primary Prevention) or participants with mild cognitive impairment (MCI) or cognitive complaints (secondary Prevention). DATA COLLECTION AND ANALYSIS We used standard methodological procedures according to the Cochrane Handbook for Systematic Reviews of Interventions. We rated the strength of evidence for each outcome using the GRADE approach. MAIN RESULTS We included four RCTs with 23,187 participants. Because of the diversity of these trials, we did not combine data to give summary estimates, but presented a narrative description of the evidence. We identified one trial (19,114 participants) comparing low-dose aspirin (100 mg once daily) to placebo. Participants were aged 70 years or older with no history of Dementia, cardiovascular disease or physical disability. Interim analysis indicated no significant treatment effect and the trial was terminated slightly early after a median of 4.7 years' follow-up. There was no evidence of a difference in incidence of Dementia between aspirin and placebo groups (risk ratio (RR) 0.98, 95% CI 0.83 to 1.15; high-certainty evidence). Participants allocated aspirin had higher rates of major bleeding (RR 1.37, 95% CI 1.17 to 1.60, high-certainty evidence) and slightly higher mortality (RR 1.14, 95% CI 1.01 to 1.28; high-certainty evidence). There was no evidence of a difference in activities of daily living between groups (RR 0.84, 95% CI 0.70 to 1.02; high-certainty evidence). We identified three trials comparing non-aspirin NSAIDs to placebo. All three trials were terminated early due to adverse events associated with NSAIDs reported in other trials. One trial (2528 participants) investigated the cyclo-oxygenase-2 (COX-2) inhibitor celecoxib (200 mg twice daily) and the non-selective NSAID naproxen (220 mg twice daily) for preventing Dementia in cognitively healthy older adults with a family history of Alzheimer's disease (AD). Median follow-up was 734 days. Combining both NSAID treatment arms, there was no evidence of a difference in the incidence of AD between participants allocated NSAIDs and those allocated placebo (RR 1.91, 95% CI 0.89 to 4.10; moderate-certainty evidence). There was also no evidence of a difference in rates of myocardial infarction (RR 1.21, 95% CI 0.61 to 2.40), stroke (RR 1.82, 95% CI 0.76 to 4.37) or mortality (RR 1.37, 95% CI 0.78 to 2.43) between treatment groups (all moderate-certainty evidence). One trial (88 participants) assessed the effectiveness of celecoxib (200 mg or 400 mg daily) in delaying cognitive decline in participants aged 40 to 81 years with mild age-related memory loss but normal memory performance scores. Mean duration of follow-up was 17.6 months in the celecoxib group and 18.1 months in the placebo group. There was no evidence of a difference between groups in test scores in any of six cognitive domains. Participants allocated celecoxib experienced more gastrointestinal adverse events than those allocated placebo (RR 2.66, 95% CI 1.05 to 6.75; low-certainty evidence). One trial (1457 participants) assessed the effectiveness of the COX-2 inhibitor rofecoxib (25 mg once daily) in delaying or preventing a diagnosis of AD in participants with MCI. Median duration of study participation was 115 weeks in the rofecoxib group and 130 weeks in the placebo group. There was a higher incidence of AD in the rofecoxib than the placebo group (RR 1.32, 95% CI 1.01 to 1.72; moderate-certainty evidence). There was no evidence of a difference between groups in cardiovascular adverse events (RR 1.07, 95% CI 0.68 to 1.66; moderate-certainty evidence) or mortality (RR 1.62, 95% CI 0.85 to 3.05; moderate-certainty evidence). Participants allocated rofecoxib had more upper gastrointestinal adverse events (RR 3.53, 95% CI 1.17 to 10.68; moderate-certainty evidence). Reported annual mean difference scores showed no evidence of a difference between groups in activities of daily living (year 1: no data available; year 2: 0.0, 95% CI -0.1 to 0.2; year 3: 0.1, 95% CI -0.1 to 0.3; year 4: 0.1, 95% CI -0.1 to 0.4; moderate-certainty evidence). AUTHORS' CONCLUSIONS There is no evidence to support the use of low-dose aspirin or other NSAIDs of any class (celecoxib, rofecoxib or naproxen) for the Prevention of Dementia, but there was evidence of harm. Although there were limitations in the available evidence, it seems unlikely that there is any need for further trials of low-dose aspirin for Dementia Prevention. If future studies of NSAIDs for Dementia Prevention are planned, they will need to be cognisant of the safety concerns arising from the existing studies.
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aspirin and other non steroidal anti inflammatory drugs for the Prevention of Dementia
Cochrane Database of Systematic Reviews, 2020Co-Authors: Fionnuala Jordan, Bernadette Mcguinness, Peter Passmore, Terry J Quinn, John P. Kelly, Catrin Tudur Smith, Kathy Murphy, Declan DevaneAbstract:BACKGROUND Dementia is a worldwide concern. Its global prevalence is increasing. At present, there is no medication licensed to prevent or delay the onset of Dementia. Inflammation has been suggested as a key factor in Dementia pathogenesis. Therefore, medications with anti-inflammatory properties could be beneficial for Dementia Prevention. OBJECTIVES To evaluate the effectiveness and adverse effects of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) for the primary or secondary Prevention of Dementia. SEARCH METHODS We searched ALOIS, the specialised register of the Cochrane Dementia and Cognitive Improvement Group up to 9 January 2020. ALOIS contains records of clinical trials identified from monthly searches of several major healthcare databases, trial registries and grey literature sources. We ran additional searches across MEDLINE (OvidSP), Embase (OvidSP) and six other databases to ensure that the searches were as comprehensive and up-to-date as possible. We also reviewed citations of reference lists of included studies. SELECTION CRITERIA We searched for randomised controlled trials (RCTs) and controlled clinical trials (CCTs) comparing aspirin or other NSAIDs with placebo for the primary or secondary Prevention of Dementia. We included trials with cognitively healthy participants (primary Prevention) or participants with mild cognitive impairment (MCI) or cognitive complaints (secondary Prevention). DATA COLLECTION AND ANALYSIS We used standard methodological procedures according to the Cochrane Handbook for Systematic Reviews of Interventions. We rated the strength of evidence for each outcome using the GRADE approach. MAIN RESULTS We included four RCTs with 23,187 participants. Because of the diversity of these trials, we did not combine data to give summary estimates, but presented a narrative description of the evidence. We identified one trial (19,114 participants) comparing low-dose aspirin (100 mg once daily) to placebo. Participants were aged 70 years or older with no history of Dementia, cardiovascular disease or physical disability. Interim analysis indicated no significant treatment effect and the trial was terminated slightly early after a median of 4.7 years' follow-up. There was no evidence of a difference in incidence of Dementia between aspirin and placebo groups (risk ratio (RR) 0.98, 95% CI 0.83 to 1.15; high-certainty evidence). Participants allocated aspirin had higher rates of major bleeding (RR 1.37, 95% CI 1.17 to 1.60, high-certainty evidence) and slightly higher mortality (RR 1.14, 95% CI 1.01 to 1.28; high-certainty evidence). There was no evidence of a difference in activities of daily living between groups (RR 0.84, 95% CI 0.70 to 1.02; high-certainty evidence). We identified three trials comparing non-aspirin NSAIDs to placebo. All three trials were terminated early due to adverse events associated with NSAIDs reported in other trials. One trial (2528 participants) investigated the cyclo-oxygenase-2 (COX-2) inhibitor celecoxib (200 mg twice daily) and the non-selective NSAID naproxen (220 mg twice daily) for preventing Dementia in cognitively healthy older adults with a family history of Alzheimer's disease (AD). Median follow-up was 734 days. Combining both NSAID treatment arms, there was no evidence of a difference in the incidence of AD between participants allocated NSAIDs and those allocated placebo (RR 1.91, 95% CI 0.89 to 4.10; moderate-certainty evidence). There was also no evidence of a difference in rates of myocardial infarction (RR 1.21, 95% CI 0.61 to 2.40), stroke (RR 1.82, 95% CI 0.76 to 4.37) or mortality (RR 1.37, 95% CI 0.78 to 2.43) between treatment groups (all moderate-certainty evidence). One trial (88 participants) assessed the effectiveness of celecoxib (200 mg or 400 mg daily) in delaying cognitive decline in participants aged 40 to 81 years with mild age-related memory loss but normal memory performance scores. Mean duration of follow-up was 17.6 months in the celecoxib group and 18.1 months in the placebo group. There was no evidence of a difference between groups in test scores in any of six cognitive domains. Participants allocated celecoxib experienced more gastrointestinal adverse events than those allocated placebo (RR 2.66, 95% CI 1.05 to 6.75; low-certainty evidence). One trial (1457 participants) assessed the effectiveness of the COX-2 inhibitor rofecoxib (25 mg once daily) in delaying or preventing a diagnosis of AD in participants with MCI. Median duration of study participation was 115 weeks in the rofecoxib group and 130 weeks in the placebo group. There was a higher incidence of AD in the rofecoxib than the placebo group (RR 1.32, 95% CI 1.01 to 1.72; moderate-certainty evidence). There was no evidence of a difference between groups in cardiovascular adverse events (RR 1.07, 95% CI 0.68 to 1.66; moderate-certainty evidence) or mortality (RR 1.62, 95% CI 0.85 to 3.05; moderate-certainty evidence). Participants allocated rofecoxib had more upper gastrointestinal adverse events (RR 3.53, 95% CI 1.17 to 10.68; moderate-certainty evidence). Reported annual mean difference scores showed no evidence of a difference between groups in activities of daily living (year 1: no data available; year 2: 0.0, 95% CI -0.1 to 0.2; year 3: 0.1, 95% CI -0.1 to 0.3; year 4: 0.1, 95% CI -0.1 to 0.4; moderate-certainty evidence). AUTHORS' CONCLUSIONS There is no evidence to support the use of low-dose aspirin or other NSAIDs of any class (celecoxib, rofecoxib or naproxen) for the Prevention of Dementia, but there was evidence of harm. Although there were limitations in the available evidence, it seems unlikely that there is any need for further trials of low-dose aspirin for Dementia Prevention. If future studies of NSAIDs for Dementia Prevention are planned, they will need to be cognisant of the safety concerns arising from the existing studies.
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statins for the Prevention of Dementia
Cochrane Database of Systematic Reviews, 2016Co-Authors: Bernadette Mcguinness, David Craig, Roger Bullock, Peter PassmoreAbstract:Background This is an update of a Cochrane review first published in 2001 and then updated in 2009. Vascular risk factors including high cholesterol levels increase the risk of Dementia due to Alzheimer's disease and of vascular Dementia. Some observational studies have suggested an association between statin use and lowered incidence of Dementia. Objectives To evaluate the efficacy and safety of statins for the Prevention of Dementia in people at risk of Dementia due to their age and to determine whether the efficacy and safety of statins for this purpose depends on cholesterol level, apolipoprotein E (ApoE) genotype or cognitive level. Search methods We searched ALOIS (the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group), The Cochrane Library, MEDLINE, EMBASE, PsycINFO, CINAHL, LILACS, ClinicalTrials.gov and the World Health Organization (WHO) Portal on 11 November 2015. Selection criteria We included double-blind, randomised, placebo-controlled trials in which statins were administered for at least 12 months to people at risk of Dementia. Data collection and analysis We used standard methodological procedures expected by Cochrane. Main results We included two trials with 26,340 participants aged 40 to 82 years of whom 11,610 were aged 70 or older. All participants had a history of, or risk factors for, vascular disease. The studies used different statins (simvastatin and pravastatin). Mean follow-up was 3.2 years in one study and five years in one study. The risk of bias was low. Only one study reported on the incidence of Dementia (20,536 participants, 31 cases in each group; odds ratio (OR) 1.00, 95% confidence interval (CI) 0.61 to 1.65, moderate quality evidence, downgraded due to imprecision). Both studies assessed cognitive function, but at different times using different scales, so we judged the results unsuitable for a meta-analysis. There were no differences between statin and placebo groups on five different cognitive tests (high quality evidence). Rates of treatment discontinuation due to non-fatal adverse events were less than 5% in both studies and there was no difference between statin and placebo groups in the risk of withdrawal due to adverse events (26,340 participants, 2 studies, OR 0.94, 95% CI 0.83 to 1.05). Authors' conclusions There is good evidence that statins given in late life to people at risk of vascular disease do not prevent cognitive decline or Dementia. Biologically, it seems feasible that statins could prevent Dementia due to their role in cholesterol reduction and initial evidence from observational studies was very promising. However, indication bias may have been a factor in these studies and the evidence from subsequent RCTs has been negative. There were limitations in the included studies involving the cognitive assessments used and the inclusion of participants at moderate to high vascular risk only.
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The Cochrane Library - Statins for the Prevention of Dementia
The Cochrane database of systematic reviews, 2016Co-Authors: Bernadette Mcguinness, David Craig, Roger Bullock, Peter PassmoreAbstract:Background This is an update of a Cochrane review first published in 2001 and then updated in 2009. Vascular risk factors including high cholesterol levels increase the risk of Dementia due to Alzheimer's disease and of vascular Dementia. Some observational studies have suggested an association between statin use and lowered incidence of Dementia. Objectives To evaluate the efficacy and safety of statins for the Prevention of Dementia in people at risk of Dementia due to their age and to determine whether the efficacy and safety of statins for this purpose depends on cholesterol level, apolipoprotein E (ApoE) genotype or cognitive level. Search methods We searched ALOIS (the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group), The Cochrane Library, MEDLINE, EMBASE, PsycINFO, CINAHL, LILACS, ClinicalTrials.gov and the World Health Organization (WHO) Portal on 11 November 2015. Selection criteria We included double-blind, randomised, placebo-controlled trials in which statins were administered for at least 12 months to people at risk of Dementia. Data collection and analysis We used standard methodological procedures expected by Cochrane. Main results We included two trials with 26,340 participants aged 40 to 82 years of whom 11,610 were aged 70 or older. All participants had a history of, or risk factors for, vascular disease. The studies used different statins (simvastatin and pravastatin). Mean follow-up was 3.2 years in one study and five years in one study. The risk of bias was low. Only one study reported on the incidence of Dementia (20,536 participants, 31 cases in each group; odds ratio (OR) 1.00, 95% confidence interval (CI) 0.61 to 1.65, moderate quality evidence, downgraded due to imprecision). Both studies assessed cognitive function, but at different times using different scales, so we judged the results unsuitable for a meta-analysis. There were no differences between statin and placebo groups on five different cognitive tests (high quality evidence). Rates of treatment discontinuation due to non-fatal adverse events were less than 5% in both studies and there was no difference between statin and placebo groups in the risk of withdrawal due to adverse events (26,340 participants, 2 studies, OR 0.94, 95% CI 0.83 to 1.05). Authors' conclusions There is good evidence that statins given in late life to people at risk of vascular disease do not prevent cognitive decline or Dementia. Biologically, it seems feasible that statins could prevent Dementia due to their role in cholesterol reduction and initial evidence from observational studies was very promising. However, indication bias may have been a factor in these studies and the evidence from subsequent RCTs has been negative. There were limitations in the included studies involving the cognitive assessments used and the inclusion of participants at moderate to high vascular risk only.
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Statins for the Prevention of Dementia.
The Cochrane database of systematic reviews, 2009Co-Authors: Bernadette Mcguinness, David Craig, Roger Bullock, Peter PassmoreAbstract:This is an update of a Cochrane review first published in 2001. At that stage there was insufficient evidence to recommend statins for the Prevention of Alzheimer's disease (AD). The scope of this review has been expanded to include all forms of Dementia. To assess the effects of statins in the Prevention of Dementia. The Specialized Register of the Cochrane Dementia and Cognitive Improvement Group, The Cochrane Library, MEDLINE, EMBASE, PsycINFO, CINAHL and LILACS were searched on 10 October 2007 using the terms statin*, lovastatin*, pravastatin*, simvastatin*, fluvastatin*, atorvastatin* and rosuvastatin*. The CDCIG Register contains records from many healthcare databases, SIGLE, LILACS as well as many trials databases and is updated regularly. Double-blind randomized placebo-controlled trials of statins in people at risk of AD and Dementia. Two independent reviewers extracted and assessed data independently and agreement was reached after discussion. Adverse effects were noted. Two trials were identified with 26,340 participants; HPS 2002 and PROSPER 2002. Age range was 40-82 years across the two studies, PROSPER 2002 included 5804 patients aged 70-82 years and HPS included 20,536 patients with 5806 at least 70 years old at study entry. Mean total cholesterol 5.9 mmol/l, LDL cholesterol 3.4 mmol/l at study entry with mean reduction in LDL cholesterol of 1.0 mmol/l in simvastatin treated patients compared to placebo in HPS 2002. Mean total cholesterol 5.7 mmol/l, LDL cholesterol 3.8 mmol/l at study entry with mean reduction in LDL cholesterol of 1.02 mmol/l in pravastatin treated patients compared to placebo in PROSPER 2002. Mean follow-up 3.2 years in PROSPER, 5 years in HPS 2002. Cognition was measured at different times and with different scales so could not be combined in a meta-analysis. There was no difference in incidence of Dementia in HPS 2002 (31 cases in simvastatin group, 31 cases in placebo group) nor in performance on the modified Telephone Interview for Cognitive Status at final follow-up (23.7% simvastatin group cognitively impaired vs 24.2% in placebo group). There was no difference in cognition between groups either in relation to age at study entry or previous history of cerebrovascular disease. Cognitive function declined at the same rate in both treatment groups in PROSPER 2002, there was no significant difference between pravastatin treated and placebo groups in performance on letter digit codes, picture word learning test, Stroop and Mini Mental State Examination. There was no evidence that statins were detrimental to cognition. There is good evidence from RCTs that statins given in late life to individuals at risk of vascular disease have no effect in preventing AD or Dementia. Biologically it seems feasible that statins could prevent Dementia due to their role in cholesterol reduction and initial evidence from observational studies was very promising. Indication bias may have been a factor in these studies however and the evidence from subsequent RCTs has been negative.
Bernadette Mcguinness - One of the best experts on this subject based on the ideXlab platform.
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Aspirin and other non‐steroidal anti‐inflammatory drugs for the Prevention of Dementia
The Cochrane database of systematic reviews, 2020Co-Authors: Fionnuala Jordan, Bernadette Mcguinness, Peter Passmore, Terry J Quinn, John P. Kelly, Catrin Tudur Smith, Kathy Murphy, Declan DevaneAbstract:BACKGROUND Dementia is a worldwide concern. Its global prevalence is increasing. At present, there is no medication licensed to prevent or delay the onset of Dementia. Inflammation has been suggested as a key factor in Dementia pathogenesis. Therefore, medications with anti-inflammatory properties could be beneficial for Dementia Prevention. OBJECTIVES To evaluate the effectiveness and adverse effects of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) for the primary or secondary Prevention of Dementia. SEARCH METHODS We searched ALOIS, the specialised register of the Cochrane Dementia and Cognitive Improvement Group up to 9 January 2020. ALOIS contains records of clinical trials identified from monthly searches of several major healthcare databases, trial registries and grey literature sources. We ran additional searches across MEDLINE (OvidSP), Embase (OvidSP) and six other databases to ensure that the searches were as comprehensive and up-to-date as possible. We also reviewed citations of reference lists of included studies. SELECTION CRITERIA We searched for randomised controlled trials (RCTs) and controlled clinical trials (CCTs) comparing aspirin or other NSAIDs with placebo for the primary or secondary Prevention of Dementia. We included trials with cognitively healthy participants (primary Prevention) or participants with mild cognitive impairment (MCI) or cognitive complaints (secondary Prevention). DATA COLLECTION AND ANALYSIS We used standard methodological procedures according to the Cochrane Handbook for Systematic Reviews of Interventions. We rated the strength of evidence for each outcome using the GRADE approach. MAIN RESULTS We included four RCTs with 23,187 participants. Because of the diversity of these trials, we did not combine data to give summary estimates, but presented a narrative description of the evidence. We identified one trial (19,114 participants) comparing low-dose aspirin (100 mg once daily) to placebo. Participants were aged 70 years or older with no history of Dementia, cardiovascular disease or physical disability. Interim analysis indicated no significant treatment effect and the trial was terminated slightly early after a median of 4.7 years' follow-up. There was no evidence of a difference in incidence of Dementia between aspirin and placebo groups (risk ratio (RR) 0.98, 95% CI 0.83 to 1.15; high-certainty evidence). Participants allocated aspirin had higher rates of major bleeding (RR 1.37, 95% CI 1.17 to 1.60, high-certainty evidence) and slightly higher mortality (RR 1.14, 95% CI 1.01 to 1.28; high-certainty evidence). There was no evidence of a difference in activities of daily living between groups (RR 0.84, 95% CI 0.70 to 1.02; high-certainty evidence). We identified three trials comparing non-aspirin NSAIDs to placebo. All three trials were terminated early due to adverse events associated with NSAIDs reported in other trials. One trial (2528 participants) investigated the cyclo-oxygenase-2 (COX-2) inhibitor celecoxib (200 mg twice daily) and the non-selective NSAID naproxen (220 mg twice daily) for preventing Dementia in cognitively healthy older adults with a family history of Alzheimer's disease (AD). Median follow-up was 734 days. Combining both NSAID treatment arms, there was no evidence of a difference in the incidence of AD between participants allocated NSAIDs and those allocated placebo (RR 1.91, 95% CI 0.89 to 4.10; moderate-certainty evidence). There was also no evidence of a difference in rates of myocardial infarction (RR 1.21, 95% CI 0.61 to 2.40), stroke (RR 1.82, 95% CI 0.76 to 4.37) or mortality (RR 1.37, 95% CI 0.78 to 2.43) between treatment groups (all moderate-certainty evidence). One trial (88 participants) assessed the effectiveness of celecoxib (200 mg or 400 mg daily) in delaying cognitive decline in participants aged 40 to 81 years with mild age-related memory loss but normal memory performance scores. Mean duration of follow-up was 17.6 months in the celecoxib group and 18.1 months in the placebo group. There was no evidence of a difference between groups in test scores in any of six cognitive domains. Participants allocated celecoxib experienced more gastrointestinal adverse events than those allocated placebo (RR 2.66, 95% CI 1.05 to 6.75; low-certainty evidence). One trial (1457 participants) assessed the effectiveness of the COX-2 inhibitor rofecoxib (25 mg once daily) in delaying or preventing a diagnosis of AD in participants with MCI. Median duration of study participation was 115 weeks in the rofecoxib group and 130 weeks in the placebo group. There was a higher incidence of AD in the rofecoxib than the placebo group (RR 1.32, 95% CI 1.01 to 1.72; moderate-certainty evidence). There was no evidence of a difference between groups in cardiovascular adverse events (RR 1.07, 95% CI 0.68 to 1.66; moderate-certainty evidence) or mortality (RR 1.62, 95% CI 0.85 to 3.05; moderate-certainty evidence). Participants allocated rofecoxib had more upper gastrointestinal adverse events (RR 3.53, 95% CI 1.17 to 10.68; moderate-certainty evidence). Reported annual mean difference scores showed no evidence of a difference between groups in activities of daily living (year 1: no data available; year 2: 0.0, 95% CI -0.1 to 0.2; year 3: 0.1, 95% CI -0.1 to 0.3; year 4: 0.1, 95% CI -0.1 to 0.4; moderate-certainty evidence). AUTHORS' CONCLUSIONS There is no evidence to support the use of low-dose aspirin or other NSAIDs of any class (celecoxib, rofecoxib or naproxen) for the Prevention of Dementia, but there was evidence of harm. Although there were limitations in the available evidence, it seems unlikely that there is any need for further trials of low-dose aspirin for Dementia Prevention. If future studies of NSAIDs for Dementia Prevention are planned, they will need to be cognisant of the safety concerns arising from the existing studies.
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aspirin and other non steroidal anti inflammatory drugs for the Prevention of Dementia
Cochrane Database of Systematic Reviews, 2020Co-Authors: Fionnuala Jordan, Bernadette Mcguinness, Peter Passmore, Terry J Quinn, John P. Kelly, Catrin Tudur Smith, Kathy Murphy, Declan DevaneAbstract:BACKGROUND Dementia is a worldwide concern. Its global prevalence is increasing. At present, there is no medication licensed to prevent or delay the onset of Dementia. Inflammation has been suggested as a key factor in Dementia pathogenesis. Therefore, medications with anti-inflammatory properties could be beneficial for Dementia Prevention. OBJECTIVES To evaluate the effectiveness and adverse effects of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) for the primary or secondary Prevention of Dementia. SEARCH METHODS We searched ALOIS, the specialised register of the Cochrane Dementia and Cognitive Improvement Group up to 9 January 2020. ALOIS contains records of clinical trials identified from monthly searches of several major healthcare databases, trial registries and grey literature sources. We ran additional searches across MEDLINE (OvidSP), Embase (OvidSP) and six other databases to ensure that the searches were as comprehensive and up-to-date as possible. We also reviewed citations of reference lists of included studies. SELECTION CRITERIA We searched for randomised controlled trials (RCTs) and controlled clinical trials (CCTs) comparing aspirin or other NSAIDs with placebo for the primary or secondary Prevention of Dementia. We included trials with cognitively healthy participants (primary Prevention) or participants with mild cognitive impairment (MCI) or cognitive complaints (secondary Prevention). DATA COLLECTION AND ANALYSIS We used standard methodological procedures according to the Cochrane Handbook for Systematic Reviews of Interventions. We rated the strength of evidence for each outcome using the GRADE approach. MAIN RESULTS We included four RCTs with 23,187 participants. Because of the diversity of these trials, we did not combine data to give summary estimates, but presented a narrative description of the evidence. We identified one trial (19,114 participants) comparing low-dose aspirin (100 mg once daily) to placebo. Participants were aged 70 years or older with no history of Dementia, cardiovascular disease or physical disability. Interim analysis indicated no significant treatment effect and the trial was terminated slightly early after a median of 4.7 years' follow-up. There was no evidence of a difference in incidence of Dementia between aspirin and placebo groups (risk ratio (RR) 0.98, 95% CI 0.83 to 1.15; high-certainty evidence). Participants allocated aspirin had higher rates of major bleeding (RR 1.37, 95% CI 1.17 to 1.60, high-certainty evidence) and slightly higher mortality (RR 1.14, 95% CI 1.01 to 1.28; high-certainty evidence). There was no evidence of a difference in activities of daily living between groups (RR 0.84, 95% CI 0.70 to 1.02; high-certainty evidence). We identified three trials comparing non-aspirin NSAIDs to placebo. All three trials were terminated early due to adverse events associated with NSAIDs reported in other trials. One trial (2528 participants) investigated the cyclo-oxygenase-2 (COX-2) inhibitor celecoxib (200 mg twice daily) and the non-selective NSAID naproxen (220 mg twice daily) for preventing Dementia in cognitively healthy older adults with a family history of Alzheimer's disease (AD). Median follow-up was 734 days. Combining both NSAID treatment arms, there was no evidence of a difference in the incidence of AD between participants allocated NSAIDs and those allocated placebo (RR 1.91, 95% CI 0.89 to 4.10; moderate-certainty evidence). There was also no evidence of a difference in rates of myocardial infarction (RR 1.21, 95% CI 0.61 to 2.40), stroke (RR 1.82, 95% CI 0.76 to 4.37) or mortality (RR 1.37, 95% CI 0.78 to 2.43) between treatment groups (all moderate-certainty evidence). One trial (88 participants) assessed the effectiveness of celecoxib (200 mg or 400 mg daily) in delaying cognitive decline in participants aged 40 to 81 years with mild age-related memory loss but normal memory performance scores. Mean duration of follow-up was 17.6 months in the celecoxib group and 18.1 months in the placebo group. There was no evidence of a difference between groups in test scores in any of six cognitive domains. Participants allocated celecoxib experienced more gastrointestinal adverse events than those allocated placebo (RR 2.66, 95% CI 1.05 to 6.75; low-certainty evidence). One trial (1457 participants) assessed the effectiveness of the COX-2 inhibitor rofecoxib (25 mg once daily) in delaying or preventing a diagnosis of AD in participants with MCI. Median duration of study participation was 115 weeks in the rofecoxib group and 130 weeks in the placebo group. There was a higher incidence of AD in the rofecoxib than the placebo group (RR 1.32, 95% CI 1.01 to 1.72; moderate-certainty evidence). There was no evidence of a difference between groups in cardiovascular adverse events (RR 1.07, 95% CI 0.68 to 1.66; moderate-certainty evidence) or mortality (RR 1.62, 95% CI 0.85 to 3.05; moderate-certainty evidence). Participants allocated rofecoxib had more upper gastrointestinal adverse events (RR 3.53, 95% CI 1.17 to 10.68; moderate-certainty evidence). Reported annual mean difference scores showed no evidence of a difference between groups in activities of daily living (year 1: no data available; year 2: 0.0, 95% CI -0.1 to 0.2; year 3: 0.1, 95% CI -0.1 to 0.3; year 4: 0.1, 95% CI -0.1 to 0.4; moderate-certainty evidence). AUTHORS' CONCLUSIONS There is no evidence to support the use of low-dose aspirin or other NSAIDs of any class (celecoxib, rofecoxib or naproxen) for the Prevention of Dementia, but there was evidence of harm. Although there were limitations in the available evidence, it seems unlikely that there is any need for further trials of low-dose aspirin for Dementia Prevention. If future studies of NSAIDs for Dementia Prevention are planned, they will need to be cognisant of the safety concerns arising from the existing studies.
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statins for the Prevention of Dementia
Cochrane Database of Systematic Reviews, 2016Co-Authors: Bernadette Mcguinness, David Craig, Roger Bullock, Peter PassmoreAbstract:Background This is an update of a Cochrane review first published in 2001 and then updated in 2009. Vascular risk factors including high cholesterol levels increase the risk of Dementia due to Alzheimer's disease and of vascular Dementia. Some observational studies have suggested an association between statin use and lowered incidence of Dementia. Objectives To evaluate the efficacy and safety of statins for the Prevention of Dementia in people at risk of Dementia due to their age and to determine whether the efficacy and safety of statins for this purpose depends on cholesterol level, apolipoprotein E (ApoE) genotype or cognitive level. Search methods We searched ALOIS (the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group), The Cochrane Library, MEDLINE, EMBASE, PsycINFO, CINAHL, LILACS, ClinicalTrials.gov and the World Health Organization (WHO) Portal on 11 November 2015. Selection criteria We included double-blind, randomised, placebo-controlled trials in which statins were administered for at least 12 months to people at risk of Dementia. Data collection and analysis We used standard methodological procedures expected by Cochrane. Main results We included two trials with 26,340 participants aged 40 to 82 years of whom 11,610 were aged 70 or older. All participants had a history of, or risk factors for, vascular disease. The studies used different statins (simvastatin and pravastatin). Mean follow-up was 3.2 years in one study and five years in one study. The risk of bias was low. Only one study reported on the incidence of Dementia (20,536 participants, 31 cases in each group; odds ratio (OR) 1.00, 95% confidence interval (CI) 0.61 to 1.65, moderate quality evidence, downgraded due to imprecision). Both studies assessed cognitive function, but at different times using different scales, so we judged the results unsuitable for a meta-analysis. There were no differences between statin and placebo groups on five different cognitive tests (high quality evidence). Rates of treatment discontinuation due to non-fatal adverse events were less than 5% in both studies and there was no difference between statin and placebo groups in the risk of withdrawal due to adverse events (26,340 participants, 2 studies, OR 0.94, 95% CI 0.83 to 1.05). Authors' conclusions There is good evidence that statins given in late life to people at risk of vascular disease do not prevent cognitive decline or Dementia. Biologically, it seems feasible that statins could prevent Dementia due to their role in cholesterol reduction and initial evidence from observational studies was very promising. However, indication bias may have been a factor in these studies and the evidence from subsequent RCTs has been negative. There were limitations in the included studies involving the cognitive assessments used and the inclusion of participants at moderate to high vascular risk only.
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The Cochrane Library - Statins for the Prevention of Dementia
The Cochrane database of systematic reviews, 2016Co-Authors: Bernadette Mcguinness, David Craig, Roger Bullock, Peter PassmoreAbstract:Background This is an update of a Cochrane review first published in 2001 and then updated in 2009. Vascular risk factors including high cholesterol levels increase the risk of Dementia due to Alzheimer's disease and of vascular Dementia. Some observational studies have suggested an association between statin use and lowered incidence of Dementia. Objectives To evaluate the efficacy and safety of statins for the Prevention of Dementia in people at risk of Dementia due to their age and to determine whether the efficacy and safety of statins for this purpose depends on cholesterol level, apolipoprotein E (ApoE) genotype or cognitive level. Search methods We searched ALOIS (the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group), The Cochrane Library, MEDLINE, EMBASE, PsycINFO, CINAHL, LILACS, ClinicalTrials.gov and the World Health Organization (WHO) Portal on 11 November 2015. Selection criteria We included double-blind, randomised, placebo-controlled trials in which statins were administered for at least 12 months to people at risk of Dementia. Data collection and analysis We used standard methodological procedures expected by Cochrane. Main results We included two trials with 26,340 participants aged 40 to 82 years of whom 11,610 were aged 70 or older. All participants had a history of, or risk factors for, vascular disease. The studies used different statins (simvastatin and pravastatin). Mean follow-up was 3.2 years in one study and five years in one study. The risk of bias was low. Only one study reported on the incidence of Dementia (20,536 participants, 31 cases in each group; odds ratio (OR) 1.00, 95% confidence interval (CI) 0.61 to 1.65, moderate quality evidence, downgraded due to imprecision). Both studies assessed cognitive function, but at different times using different scales, so we judged the results unsuitable for a meta-analysis. There were no differences between statin and placebo groups on five different cognitive tests (high quality evidence). Rates of treatment discontinuation due to non-fatal adverse events were less than 5% in both studies and there was no difference between statin and placebo groups in the risk of withdrawal due to adverse events (26,340 participants, 2 studies, OR 0.94, 95% CI 0.83 to 1.05). Authors' conclusions There is good evidence that statins given in late life to people at risk of vascular disease do not prevent cognitive decline or Dementia. Biologically, it seems feasible that statins could prevent Dementia due to their role in cholesterol reduction and initial evidence from observational studies was very promising. However, indication bias may have been a factor in these studies and the evidence from subsequent RCTs has been negative. There were limitations in the included studies involving the cognitive assessments used and the inclusion of participants at moderate to high vascular risk only.
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Statins for the Prevention of Dementia.
The Cochrane database of systematic reviews, 2009Co-Authors: Bernadette Mcguinness, David Craig, Roger Bullock, Peter PassmoreAbstract:This is an update of a Cochrane review first published in 2001. At that stage there was insufficient evidence to recommend statins for the Prevention of Alzheimer's disease (AD). The scope of this review has been expanded to include all forms of Dementia. To assess the effects of statins in the Prevention of Dementia. The Specialized Register of the Cochrane Dementia and Cognitive Improvement Group, The Cochrane Library, MEDLINE, EMBASE, PsycINFO, CINAHL and LILACS were searched on 10 October 2007 using the terms statin*, lovastatin*, pravastatin*, simvastatin*, fluvastatin*, atorvastatin* and rosuvastatin*. The CDCIG Register contains records from many healthcare databases, SIGLE, LILACS as well as many trials databases and is updated regularly. Double-blind randomized placebo-controlled trials of statins in people at risk of AD and Dementia. Two independent reviewers extracted and assessed data independently and agreement was reached after discussion. Adverse effects were noted. Two trials were identified with 26,340 participants; HPS 2002 and PROSPER 2002. Age range was 40-82 years across the two studies, PROSPER 2002 included 5804 patients aged 70-82 years and HPS included 20,536 patients with 5806 at least 70 years old at study entry. Mean total cholesterol 5.9 mmol/l, LDL cholesterol 3.4 mmol/l at study entry with mean reduction in LDL cholesterol of 1.0 mmol/l in simvastatin treated patients compared to placebo in HPS 2002. Mean total cholesterol 5.7 mmol/l, LDL cholesterol 3.8 mmol/l at study entry with mean reduction in LDL cholesterol of 1.02 mmol/l in pravastatin treated patients compared to placebo in PROSPER 2002. Mean follow-up 3.2 years in PROSPER, 5 years in HPS 2002. Cognition was measured at different times and with different scales so could not be combined in a meta-analysis. There was no difference in incidence of Dementia in HPS 2002 (31 cases in simvastatin group, 31 cases in placebo group) nor in performance on the modified Telephone Interview for Cognitive Status at final follow-up (23.7% simvastatin group cognitively impaired vs 24.2% in placebo group). There was no difference in cognition between groups either in relation to age at study entry or previous history of cerebrovascular disease. Cognitive function declined at the same rate in both treatment groups in PROSPER 2002, there was no significant difference between pravastatin treated and placebo groups in performance on letter digit codes, picture word learning test, Stroop and Mini Mental State Examination. There was no evidence that statins were detrimental to cognition. There is good evidence from RCTs that statins given in late life to individuals at risk of vascular disease have no effect in preventing AD or Dementia. Biologically it seems feasible that statins could prevent Dementia due to their role in cholesterol reduction and initial evidence from observational studies was very promising. Indication bias may have been a factor in these studies however and the evidence from subsequent RCTs has been negative.
Edo Richard - One of the best experts on this subject based on the ideXlab platform.
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Multi-domain interventions for the Prevention of Dementia and cognitive decline
Cochrane Database of Systematic Reviews, 2020Co-Authors: Melanie Hafdi, Marieke P. Hoevenaar-blom, Edo RichardAbstract:This is a protocol for a Cochrane Review (Intervention). The objectives are as follows:. To assess the effects of multi-domain interventions for the Prevention of cognitive decline and Dementia (a) in unselected populations and (b) in populations with or without cognitive impairment who are at increased risk of cognitive decline and Dementia.
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A Population Perspective on Prevention of Dementia.
Journal of clinical medicine, 2019Co-Authors: Esmé Eggink, Eric P. Moll Van Charante, Willem A. Van Gool, Edo RichardAbstract:The global number of people living with Dementia is expected to increase to 130 million in 2050. Based on extensive evidence from observational studies, it is estimated that about 30% of Dementia cases may be attributable to potentially modifiable risk factors. This suggests that interventions targeting these factors could perhaps delay or prevent the onset of Dementia. Since the vast majority of people with Dementia live in low- and middle-income countries, such interventions should preferably be easy and affordable to implement across a wide range of health care systems. However, to date, results from Dementia Prevention trials do not provide convincing evidence that treatment of these risk factors reduces the risk of Dementia. The current paper aims to give an overview of available evidence for the potential for Dementia Prevention. In particular, we discuss methodological issues that might complicate the development of effective Prevention interventions and explore the opportunities and challenges for future Dementia Prevention research. Currently, several ongoing and planned trials are testing the effect of multi-domain interventions on Dementia risk in high-risk populations. It is desirable that future Dementia strategies also target the wider population, through interventions on the individual, community, and population level, in order to constrain the growing prevalence of Dementia worldwide.
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Effect of Long-Term Vascular Care on Progression of Cerebrovascular Lesions: Magnetic Resonance Imaging Substudy of the PreDIVA Trial (Prevention of Dementia by Intensive Vascular Care)
Stroke, 2017Co-Authors: Jan Willem Van Dalen, Eric P. Moll Van Charante, Willem A. Van Gool, Matthan W. A. Caan, Philip Scheltens, Charles B.l.m. Majoie, Aart J. Nederveen, Edo RichardAbstract:Background and Purpose— This study aimed to evaluate the effect of a nurse-led multidomain cardiovascular intervention on white matter hyperintensity (WMH) progression and incident lacunar infarcts in community-dwelling elderly with hypertension. Methods— The preDIVA trial (Prevention of Dementia by Intensive Vascular Care) was an open-label, cluster-randomized controlled trial in community-dwelling individuals aged 70 to 78 years. General practices were assigned by computer-generated randomization to 6-year nurse-led, multidomain intensive vascular care or standard care. of 3526 preDIVA participants, 195 nondemented participants with a systolic blood pressure ≥140 mm Hg were consecutively recruited to undergo magnetic resonance imaging at 2 to 3 and 5 to 6 years after baseline. WMH volumes were measured automatically, lacunar infarcts assessed visually, blinded to treatment allocation. Results— One hundred and twenty-six participants were available for longitudinal analysis (64 intervention and 62 control). Annual WMH volume increase in milliliter was similar for intervention (mean=0.73, SD=0.84) and control (mean=0.70, SD=0.59) participants (adjusted mean difference, −0.08 mL; 95% confidence interval, −0.30 to 0.15; P =0.50). Analyses suggested greater intervention effects with increasing baseline WMH volumes ( P for interaction=0.03). New lacunar infarcts developed in 6 (9%) intervention and 2 (3%) control participants (odds ratio, 2.2; 95% confidence interval, 0.4–12.1; P =0.36). Conclusions— Nurse-led vascular care in hypertensive community-dwelling older persons did not diminish WMH accumulation over 3 years. However, our results do suggest this type of intervention could be effective in persons with high WMH volumes. There was no effect on lacunar infarcts incidence but numbers were low. Clinical Trial Information— URL: http://www.isrctn.com/ISRCTN29711771. Unique identifier: ISRCTN29711771.
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Determinants of Dropout and Nonadherence in a Dementia Prevention Randomized Controlled Trial: The Prevention of Dementia by Intensive Vascular Care Trial
Journal of the American Geriatrics Society, 2017Co-Authors: Cathrien Beishuizen, Nicola Coley, Eric P. Moll Van Charante, Willem A. Van Gool, Edo Richard, Sandrine AndrieuAbstract:Objectives To explore and compare sociodemographic, clinical, and neuropsychiatric determinants of dropout and nonadherence in older people participating in an open-label cluster-randomized controlled trial—the Prevention of Dementia by Intensive Vascular care (preDIVA) trial—over 6 years. Design Secondary analysis. Setting One hundred sixteen general practices in the Netherlands. Participants Community-dwelling individuals aged 70 to 78 (N = 2,994). Intervention Nurse-led multidomain intervention targeting cardiovascular risk factors to prevent Dementia. Measurements The associations between participant baseline sociodemographic (age, sex, education), clinical (medical history, disability, cardiovascular risk), neuropsychiatric (depressive symptoms (Geriatric Depression Scale-15), and cognitive (Mini-Mental State Examination)) characteristics and dropout from the trial and nonadherence to the trial intervention were explored using multilevel logistic regression models. Results Older age, poorer cognitive function, more symptoms of depression, and greater disability were the most important determinants of dropout of older people. The presence of cardiovascular risk factors was not associated with dropout but was associated with nonadherence. Being overweight was a risk factor for nonadherence, whereas people with high blood pressure or a low level of physical exercise adhered better to the intervention. The association between poorer cognitive function and symptoms of depression and dropout was stronger in the control group than in the intervention group, and vice versa for increased disability. Conclusion In a large Dementia Prevention trial with 6-year follow-up, dropout was associated with older age, poorer cognitive function, symptoms of depression, and disability at baseline. These findings can help to guide the design of future Dementia Prevention trials in older adults. The associations found between cardiovascular risk factors and nonadherence need to be confirmed in other older populations receiving cardiovascular Prevention interventions.
Lewis H Kuller - One of the best experts on this subject based on the ideXlab platform.
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the ginkgo evaluation of memory gem study design and baseline data of a randomized trial of ginkgo biloba extract in Prevention of Dementia
Contemporary Clinical Trials, 2006Co-Authors: Steven T Dekosky, Annette L Fitzpatrick, Diane G Ives, Judith Saxton, Jeff D Williamson, Oscar L Lopez, Gregory L Burke, Linda P Fried, Lewis H Kuller, John A RobbinsAbstract:The epidemic of late life Dementia, prominence of use of alternative medications and supplements, and initiation of efforts to determine how to prevent Dementia have led to efforts to conduct studies aimed at Prevention of Dementia. The GEM (Ginkgo Evaluation of Memory) study was initially designed as a 5-year, randomized double-blind, placebo-controlled trial of Ginkgo biloba, administered in a dose of 120 mg twice per day as EGb761, in the Prevention of Dementia (and especially Alzheimer's disease) in normal elderly or those with mild cognitive impairment. The study anticipates 8.5 years of participant follow-up. Initial power calculations based on estimates of incidence rates of Dementia in the target population (age 75+) led to a 3000-person study, which was successfully recruited at four clinical sites around the United States from September 2000 to June 2002. Primary outcome is incidence of all-cause Dementia; secondary outcomes include rate of cognitive and functional decline, the incidence of cardiovascular and cerebrovascular events, and mortality. Following screening to exclude participants with incident Dementia at baseline, an extensive neuropsychological assessment was performed and participants were randomly assigned to treatment groups. All participants are required to have a proxy who agreed to provide an independent assessment of the functional and cognitive abilities of the participant. Assessments are repeated every 6 months. Significant decline at any visit, defined by specific changes in cognitive screening scores, leads to a repeat detailed neuropsychological battery, neurological and medical evaluation and MRI scan of the brain. The final diagnosis of Dementia is achieved by a consensus panel of experts. Side effects and adverse events are tracked by computer at the central data coordinating center and unblinded data are reviewed by an independent safety monitoring board. Studies such as these are necessary for this and a variety of other potential protective agents to evaluate their effectiveness in preventing or slowing the emergence of Dementia in the elderly population.
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Potential Prevention of Alzheimer disease and Dementia
Alzheimer Disease & Associated Disorders, 1996Co-Authors: Lewis H KullerAbstract:The Prevention of Dementia is of critical importance. The increasing population of high-risk older individuals will result in an increasing prevalence of Dementia. Primary Prevention of Dementia and Alzheimer disease can take either a public health or high-risk preventive medicine approach. At the present time, there is little evidence to support a specific primary public health approach such as a specific nutrient. The possible association of vascular disease with Dementia may offer the best preventive high-risk approach. The identification of individuals with clinical and subclinical vascular disease is possible. There is a very high prevalence of subclinical cerebral infarction in older individuals. Specific treatments can prevent clinical disease such as stroke and coronary heart disease. Whether therapies will prevent some Dementia can be determined.
Françoise Forette - One of the best experts on this subject based on the ideXlab platform.
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Treatment of hypertension and Prevention of Dementia
Alzheimer's & dementia : the journal of the Alzheimer's Association, 2005Co-Authors: Olivier Hanon, Françoise ForetteAbstract:Abstract Because of the aging population, the frequency of Dementia will dramatically increase in the coming years. Prevention of cognitive disorders and Dementia has become a major public health challenge. High blood pressure is a major risk factor for cerebrovascular diseases and is also correlated closely with cognitive decline and Dementia. Several epidemiologic studies have found that cognitive functions are often inversely proportional to blood pressure values measured 15 or 20 years previously. Moreover, the use of antihypertensive drugs has been shown to help prevent cognitive decline, opening the way to the Prevention of Dementia (vascular or Alzheimer’s type). These results indicate that incidence of Dementia should constitute a major outcome of future trials comparing different classes of antihypertensive drugs.
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Prevention of Dementia: lessons from SYST-EUR and PROGRESS.
Journal of the Neurological Sciences, 2004Co-Authors: Olivier Hanon, Françoise ForetteAbstract:Hypertension is one of the principal risk factors for cerebrovascular diseases, closely correlated also with cognitive decline and Dementia. Data from recent therapeutic trials (SYST-EUR, PROGRESS) open the way toward the Prevention of Dementia (vascular or Alzheimer's type) by antihypertensive treatments. The results of these two studies suggest different mechanisms of action of antihypertensive drugs in the Prevention of cognitive decline. The use of angiotensin converting enzyme (ACE) inhibitors, with or without diuretics, resulted in decrease incidence of stroke-related Dementia, but Dementia without stroke was not reduced. With the dihydropyridine calcium antagonists, a reduction in both Alzheimer's type and vascular Dementia was demonstrated.
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Prevention of Dementia and cerebroprotection with antihypertensive drugs.
Current hypertension reports, 2004Co-Authors: Olivier Hanon, Marie Laure Seux, Hermine Lenoir, Anne-sophie Rigaud, Françoise ForetteAbstract:High blood pressure is a major risk factor for stroke and is also closely correlated with cognitive decline and Dementia. Indeed, most longitudinal studies showed that cognitive functioning is often inversely proportional to blood pressure values measured 15 or 20 years previously. Because of the aging of the population, the frequency of stroke and Dementia will dramatically increase in the coming years. Therefore, the Prevention of cerebrovascular and cognitive disorders represents a major challenge. Antihypertensive drugs have shown clinical benefits in both primary and secondary Prevention of strokes. Consensus is generally that blood-pressure lowering represents the major determinant of the benefit conferred by the antihypertensive treatment for stroke Prevention; however, recent studies have suggested some differences between classes of antihypertensive drugs. The results of therapeutic trials (Systolic Hypertension in Europe [Syst-Eur], Perindopril Protection Against Recurrent Stroke Study [PROGRESS]) open the way to the Prevention of Dementia (vascular or Alzheimer’s type) by antihypertensive treatments. These two studies suggest different mechanisms for the Prevention of cognitive decline using antihypertensive drugs. In this context, reduced incidence of Dementia should be the primary outcome of future trials comparing different classes of antihypertensive drugs.