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Nicole Mahy - One of the best experts on this subject based on the ideXlab platform.
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canine Cognitive Deficit correlates with diffuse plaque maturation and s100β astrocytosis but not with insulin cerebrospinal fluid level
Acta Neuropathologica, 2006Co-Authors: Marco Pugliese, Maria Concetta Geloso, Josep Lluís Carrasco, Joan Mascort, Fabrizio Michetti, Nicole MahyAbstract:Like humans, canines develop with aging β-amyloid (Aβ) plaques and a progressive Cognitive Deficit on tasks similar to those used in diagnosis and follow-up of Alzheimer’s disease. Owing to that, dogs are quite unique to investigate the early events taking place in the diffuse Aβ plaque maturation and its relationship with Cognitive Deficit. The aim of the present investigation was to study the link between the diffuse Aβ plaque maturation and the astro- and microglial reactivity. The involvement of insulin and beta-subunit of S100 protein (S100β) overexpression in the process was also investigated. Aβ plaques were measured and counted in prefrontal cortex of 16 pet dogs of different breeds, weight and sex, classified as control and with a light or severe Cognitive Deficit. A correlation between canine graded Cognitive Deficit, diffuse plaque maturation, and S100β (−) astrocytosis, but not with cerebrospinal fluid insulin level, was found that may reflect the very early events of Aβ deposition in Alzheimer’s disease.
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canine Cognitive Deficit correlates with diffuse plaque maturation and s100beta astrocytosis but not with insulin cerebrospinal fluid level
Acta Neuropathologica, 2006Co-Authors: Marco Pugliese, Maria Concetta Geloso, Josep Lluís Carrasco, Joan Mascort, Fabrizio Michetti, Nicole MahyAbstract:Like humans, canines develop with aging β-amyloid (Aβ) plaques and a progressive Cognitive Deficit on tasks similar to those used in diagnosis and follow-up of Alzheimer’s disease. Owing to that, dogs are quite unique to investigate the early events taking place in the diffuse Aβ plaque maturation and its relationship with Cognitive Deficit. The aim of the present investigation was to study the link between the diffuse Aβ plaque maturation and the astro- and microglial reactivity. The involvement of insulin and beta-subunit of S100 protein (S100β) overexpression in the process was also investigated. Aβ plaques were measured and counted in prefrontal cortex of 16 pet dogs of different breeds, weight and sex, classified as control and with a light or severe Cognitive Deficit. A correlation between canine graded Cognitive Deficit, diffuse plaque maturation, and S100β (−) astrocytosis, but not with cerebrospinal fluid insulin level, was found that may reflect the very early events of Aβ deposition in Alzheimer’s disease.
Olesya Ajnakina - One of the best experts on this subject based on the ideXlab platform.
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schizophrenia polygenic risk predicts general Cognitive Deficit but not Cognitive decline in healthy older adults
Translational Psychiatry, 2020Co-Authors: Adrianna P Kepinska, James H Maccabe, Dorina Cadar, Andrew Steptoe, Robin M Murray, Olesya AjnakinaAbstract:There has been a long argument over whether schizophrenia is a neurodegenerative disorder associated with progressive Cognitive impairment. Given high heritability of schizophrenia, ascertaning if genetic susceptibility to schizophrenia is also associated with Cognitive decline in healthy people would support the view that schizophrenia leads to an accelerated Cognitive decline. Using the population representative sample of 6817 adults aged >50 years from the English Longitudinal Study of Ageing, we investigated associations between the biennial rate of decline in Cognitive ability and the schizophrenia polygenic score (SZ-PGS) during the 10-year follow-up period. SZ-PGS was calculated based on summary statistics from the Schizophrenia Working Group of the Psychiatric Genomics Consortium. Cognition was measured sequentially across four time points using verbal memory and semantic fluency tests. The average baseline verbal memory was 10.4 (SD = 3.4) and semantic fluency was 20.7 (SD = 6.3). One standard deviation (1-SD) increase in SZ-PGS was associated with lower baseline semantic fluency (β = -0.25, 95%CI = -0.40 to -0.10, p = 0.002); this association was significant in men (β = -0.36, 95%CI = -0.59 to -0.12, p = 0.003) and in those who were aged 60-69 years old (β = -0.32, 95%CI = -0.58 to -0.05, p = 0.019). Similarly, 1-SD increase in SZ-PGS was associated with lower verbal memory score at baseline in men only (β = -0.12, 95%CI = -0.23 to -0.01, p = 0.040). However, SZ-PGS was not associated with a greater rate of decline in these Cognitive domains during the 10-year follow-up. Our findings highlight that while genetic susceptibility to schizophrenia conveys developmental Cognitive Deficit, it is not associated with an ongoing Cognitive decline, at least in later life. These results do not support the neo-Kraepelinian notion of schizophrenia as a genetically determined progressively deteriorating brain disease.
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p06 schizophrenia polygenic risk predicts general Cognitive Deficit but not further Cognitive decline in healthy older adults
Journal of Epidemiology and Community Health, 2020Co-Authors: Adrianna P Kepinska, James H Maccabe, Dorina Cadar, Andrew Steptoe, Olesya Ajnakina, Robin M MurrayAbstract:Background There has been a long argument over whether or not schizophrenia is a neurodegenerative disorder associated with progressive brain changes and increasing Cognitive impairment. Building on the fact that schizophrenia is highly heritable and overlaps genetically with general Cognitive ability, we investigated whether common genetic variants associated with schizophrenia additively confer a stable Deficit in Cognitive ability, a greater risk of Cognitive decline over time, or both, over the 8-year follow-up, independently from the effects of the apolipoprotein E gene (APOE-e4), in phenotypically well-defined sample of healthy older adults. Methods We used data from the English Longitudinal Study of Ageing study which encompassed 6817 population-representative English adults who were followed-up for 8 years. Cognitive function was measured with well-established tests of memory (tests of immediate and delayed word recall combined into a single measure of correctly recalled words) and executive function (a test of verbal fluency where participants name as many animals as possible in a minute). Polygenic score for schizophrenia (SZ-PGS) was calculated based on the results from Psychiatric Genomics Consortium. Linear mixed effect models with maximum likelihood estimation were used to estimate baseline status and rate of change in cognition associated with SZ-PGS. Results The sample baseline mean age was 64.3 years old (standard deviation (SD)=9.3, range=50–101); 25.3% (N=1724) of participants were carriers of APOE-e4 and 46.2% (N=3159) were men. The average baseline memory score was 10.4 (SD=3.4) and executive function score was 20.7 (SD=6.3). One standard deviation increase in SZ-PGS was associated with a lower baseline executive function score (-0.23, 95%CI-0.38 – -0.08) but not memory. SZ-PGS was not associated with rates of change in these Cognitive domains during the 8-year follow-up period. However, APOE-e4, tobacco smoking and lower wealth were associated with a decrease in the rate of memory and executive function during follow-up. Discussion Common genetic variants associated with schizophrenia additively confer a stable Deficit in Cognitive ability but not Cognitive ageing. The fact that we observed Cognitive decline in our sample over the 8-year follow-up, associated with of APOE-e4, tobacco smoking and lower wealth demonstrates that our study had the capacity to show Cognitive decline. Therefore, we may conclude that while genetic susceptibility to schizophrenia conveys developmental Cognitive Deficit, it does not result in an ongoing Cognitive decline, at least in later life. This, in turn, disproves the Kraepelinan notion of schizophrenia as a genetically determined progressively deteriorating brain disease.
Marco Pugliese - One of the best experts on this subject based on the ideXlab platform.
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canine Cognitive Deficit correlates with diffuse plaque maturation and s100β astrocytosis but not with insulin cerebrospinal fluid level
Acta Neuropathologica, 2006Co-Authors: Marco Pugliese, Maria Concetta Geloso, Josep Lluís Carrasco, Joan Mascort, Fabrizio Michetti, Nicole MahyAbstract:Like humans, canines develop with aging β-amyloid (Aβ) plaques and a progressive Cognitive Deficit on tasks similar to those used in diagnosis and follow-up of Alzheimer’s disease. Owing to that, dogs are quite unique to investigate the early events taking place in the diffuse Aβ plaque maturation and its relationship with Cognitive Deficit. The aim of the present investigation was to study the link between the diffuse Aβ plaque maturation and the astro- and microglial reactivity. The involvement of insulin and beta-subunit of S100 protein (S100β) overexpression in the process was also investigated. Aβ plaques were measured and counted in prefrontal cortex of 16 pet dogs of different breeds, weight and sex, classified as control and with a light or severe Cognitive Deficit. A correlation between canine graded Cognitive Deficit, diffuse plaque maturation, and S100β (−) astrocytosis, but not with cerebrospinal fluid insulin level, was found that may reflect the very early events of Aβ deposition in Alzheimer’s disease.
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canine Cognitive Deficit correlates with diffuse plaque maturation and s100beta astrocytosis but not with insulin cerebrospinal fluid level
Acta Neuropathologica, 2006Co-Authors: Marco Pugliese, Maria Concetta Geloso, Josep Lluís Carrasco, Joan Mascort, Fabrizio Michetti, Nicole MahyAbstract:Like humans, canines develop with aging β-amyloid (Aβ) plaques and a progressive Cognitive Deficit on tasks similar to those used in diagnosis and follow-up of Alzheimer’s disease. Owing to that, dogs are quite unique to investigate the early events taking place in the diffuse Aβ plaque maturation and its relationship with Cognitive Deficit. The aim of the present investigation was to study the link between the diffuse Aβ plaque maturation and the astro- and microglial reactivity. The involvement of insulin and beta-subunit of S100 protein (S100β) overexpression in the process was also investigated. Aβ plaques were measured and counted in prefrontal cortex of 16 pet dogs of different breeds, weight and sex, classified as control and with a light or severe Cognitive Deficit. A correlation between canine graded Cognitive Deficit, diffuse plaque maturation, and S100β (−) astrocytosis, but not with cerebrospinal fluid insulin level, was found that may reflect the very early events of Aβ deposition in Alzheimer’s disease.
Maria Cristina Morgantikossmann - One of the best experts on this subject based on the ideXlab platform.
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erythropoietin improves motor and Cognitive Deficit axonal pathology and neuroinflammation in a combined model of diffuse traumatic brain injury and hypoxia in association with upregulation of the erythropoietin receptor
Journal of Neuroinflammation, 2013Co-Authors: Sarah C Hellewell, Edwin Bingbing Yan, Duwage Dasuni Sathsara Alwis, Nicole Bye, Maria Cristina MorgantikossmannAbstract:Diffuse axonal injury is a common consequence of traumatic brain injury (TBI) and often co-occurs with hypoxia, resulting in poor neurological outcome for which there is no current therapy. Here, we investigate the ability of the multifunctional compound erythropoietin (EPO) to provide neuroprotection when administered to rats after diffuse TBI alone or with post-traumatic hypoxia. Sprague–Dawley rats were subjected to diffuse traumatic axonal injury (TAI) followed by 30 minutes of hypoxic (Hx, 12% O2) or normoxic ventilation, and were administered recombinant human EPO-α (5000 IU/kg) or saline at 1 and 24 hours post-injury. The parameters examined included: 1) behavioural and Cognitive Deficit using the Rotarod, open field and novel object recognition tests; 2) axonal pathology (NF-200); 3) callosal degradation (hematoxylin and eosin stain); 3) dendritic loss (MAP2); 4) expression and localisation of the EPO receptor (EpoR); 5) activation/infiltration of microglia/macrophages (CD68) and production of IL-1β. EPO significantly improved sensorimotor and Cognitive recovery when administered to TAI rats with hypoxia (TAI + Hx). A single dose of EPO at 1 hour reduced axonal damage in the white matter of TAI + Hx rats at 1 day by 60% compared to vehicle. MAP2 was decreased in the lateral septal nucleus of TAI + Hx rats; however, EPO prevented this loss, and maintained MAP2 density over time. EPO administration elicited an early enhanced expression of EpoR 1 day after TAI + Hx compared with a 7-day peak in vehicle controls. Furthermore, EPO reduced IL-1β to sham levels 2 hours after TAI + Hx, concomitant to a decrease in CD68 positive cells at 7 and 14 days. When administered EPO, TAI + Hx rats had improved behavioural and Cognitive performance, attenuated white matter damage, resolution of neuronal damage spanning from the axon to the dendrite, and suppressed neuroinflammation, alongside enhanced expression of EpoR. These data provide compelling evidence of EPO’s neuroprotective capability. Few benefits were observed when EPO was administered to TAI rats without hypoxia, indicating that EPO’s neuroprotective capacity is bolstered under hypoxic conditions, which may be an important consideration when EPO is employed for neuroprotection in the clinic.
Fabrizio Michetti - One of the best experts on this subject based on the ideXlab platform.
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canine Cognitive Deficit correlates with diffuse plaque maturation and s100β astrocytosis but not with insulin cerebrospinal fluid level
Acta Neuropathologica, 2006Co-Authors: Marco Pugliese, Maria Concetta Geloso, Josep Lluís Carrasco, Joan Mascort, Fabrizio Michetti, Nicole MahyAbstract:Like humans, canines develop with aging β-amyloid (Aβ) plaques and a progressive Cognitive Deficit on tasks similar to those used in diagnosis and follow-up of Alzheimer’s disease. Owing to that, dogs are quite unique to investigate the early events taking place in the diffuse Aβ plaque maturation and its relationship with Cognitive Deficit. The aim of the present investigation was to study the link between the diffuse Aβ plaque maturation and the astro- and microglial reactivity. The involvement of insulin and beta-subunit of S100 protein (S100β) overexpression in the process was also investigated. Aβ plaques were measured and counted in prefrontal cortex of 16 pet dogs of different breeds, weight and sex, classified as control and with a light or severe Cognitive Deficit. A correlation between canine graded Cognitive Deficit, diffuse plaque maturation, and S100β (−) astrocytosis, but not with cerebrospinal fluid insulin level, was found that may reflect the very early events of Aβ deposition in Alzheimer’s disease.
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canine Cognitive Deficit correlates with diffuse plaque maturation and s100beta astrocytosis but not with insulin cerebrospinal fluid level
Acta Neuropathologica, 2006Co-Authors: Marco Pugliese, Maria Concetta Geloso, Josep Lluís Carrasco, Joan Mascort, Fabrizio Michetti, Nicole MahyAbstract:Like humans, canines develop with aging β-amyloid (Aβ) plaques and a progressive Cognitive Deficit on tasks similar to those used in diagnosis and follow-up of Alzheimer’s disease. Owing to that, dogs are quite unique to investigate the early events taking place in the diffuse Aβ plaque maturation and its relationship with Cognitive Deficit. The aim of the present investigation was to study the link between the diffuse Aβ plaque maturation and the astro- and microglial reactivity. The involvement of insulin and beta-subunit of S100 protein (S100β) overexpression in the process was also investigated. Aβ plaques were measured and counted in prefrontal cortex of 16 pet dogs of different breeds, weight and sex, classified as control and with a light or severe Cognitive Deficit. A correlation between canine graded Cognitive Deficit, diffuse plaque maturation, and S100β (−) astrocytosis, but not with cerebrospinal fluid insulin level, was found that may reflect the very early events of Aβ deposition in Alzheimer’s disease.