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Christopher M. Callahan - One of the best experts on this subject based on the ideXlab platform.
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Quality Improvement Research on Late Life Depression in Primary Care
Medical care, 2001Co-Authors: Christopher M. CallahanAbstract:Background. Two million older Americans suffer from Depression annually. Depression causes more functional impairment than many other common medical conditions and older adults have the highest rate of suicide in the United States. Although many of these patients fail to seek or fail to receive care for Depression, the majority will be seen in primary care for the treatment of other conditions. Objective. To review the health services research on quality improvement for Late Life Depression. Methods. Qualitative literature review. Results. During the past 30 years, multiple educational and quality improvement interventions have been designed and tested to improve the recognition and treatment of Depression in primary care settings. The findings from this large body of health services research suggest that: (1) the outcome of major Depression in the usual care of primary care is typically poor; this is particularly true of Late Life Depression; (2) informational support provided to primary care physicians is necessary but insufficient to improve the outcomes of Late Life Depression in primary care; achieving guideline-level therapy requires the substantial participation of an informed and motivated patient working in concert with a health care team and health care system designed to care for chronic conditions; (3) up to 30% of older primary care patients will fail to respond to excellent guideline-level therapy provided in primary care; and (4) the Latest quality improvement efforts focus not only on the clinical skills of primary care physicians, but also on patient’s self-care and on innovative strategies to improve the system of care. Conclusions. Late Life Depression is often a chronic disease and outcomes research demonstrates that quality improvement efforts that focus resources on improving systems of care and the active participation of patients offer the best evidence of improved patient outcomes.
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Primary care physicians' medical decision making for Late-Life Depression
Journal of general internal medicine, 1996Co-Authors: Christopher M. Callahan, Robert S. Dittus, William M. TierneyAbstract:OBJECTIVE: To describe primary care physicians’ clinical decision making regarding Late-Life Depression.
Howard J. Aizenstein - One of the best experts on this subject based on the ideXlab platform.
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Neuroimaging of Small Vessel Disease in Late-Life Depression
Advances in experimental medicine and biology, 2019Co-Authors: Nadim Farhat, Robert Theiss, Tales Santini, Tamer S. Ibrahim, Howard J. AizensteinAbstract:Cerebral small vessel disease is associated with Late-Life Depression, cognitive impairment, executive dysfunction, distress, and loss of Life for older adults. Late-Life Depression is becoming a substantial public health burden, and a considerable number of older adults presenting to primary care have significant clinical Depression. Even though white matter hyperintensities are linked with small vessel disease, white matter hyperintensities are nonspecific to small vessel disease and can co-occur with other brain diseases. Advanced neuroimaging techniques at the ultrahigh field magnetic resonance imaging are enabling improved characterization, identification of cerebral small vessel disease and are elucidating some of the mechanisms that associate small vessel disease with Late-Life Depression.
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machine learning approaches for integrating clinical and imaging features in Late Life Depression classification and response prediction
International Journal of Geriatric Psychiatry, 2015Co-Authors: Meenal J Patel, Charles F. Reynolds, Carmen Andreescu, Julie C Price, Kathryn L Edelman, Howard J. AizensteinAbstract:Objective Currently, Depression diagnosis relies primarily on behavioral symptoms and signs, and treatment is guided by trial and error instead of evaluating associated underlying brain characteristics. Unlike past studies, we attempted to estimate accurate prediction models for Late-Life Depression diagnosis and treatment response using multiple machine learning methods with inputs of multi-modal imaging and non-imaging whole brain and network-based features. Methods Late-Life Depression patients (medicated post-recruitment) (n = 33) and older non-depressed individuals (n = 35) were recruited. Their demographics and cognitive ability scores were recorded, and brain characteristics were acquired using multi-modal magnetic resonance imaging pretreatment. Linear and nonlinear learning methods were tested for estimating accurate prediction models. Results A learning method called alternating decision trees estimated the most accurate prediction models for Late-Life Depression diagnosis (87.27% accuracy) and treatment response (89.47% accuracy). The diagnosis model included measures of age, Mini-mental state examination score, and structural imaging (e.g. whole brain atrophy and global white mater hyperintensity burden). The treatment response model included measures of structural and functional connectivity. Conclusions Combinations of multi-modal imaging and/or non-imaging measures may help better predict Late-Life Depression diagnosis and treatment response. As a preliminary observation, we specuLate that the results may also suggest that different underlying brain characteristics defined by multi-modal imaging measures—rather than region-based differences—are associated with Depression versus Depression recovery because to our knowledge this is the first Depression study to accurately predict both using the same approach. These findings may help better understand Late-Life Depression and identify preliminary steps toward personalized Late-Life Depression treatment. Copyright © 2015 John Wiley & Sons, Ltd.
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plasma biosignature and brain pathology reLated to persistent cognitive impairment in Late Life Depression
Molecular Psychiatry, 2015Co-Authors: Breno S. Diniz, Howard J. Aizenstein, Etienne Sibille, Ying Ding, George C Tseng, Francis E Lotrich, James T Becker, Oscar L Lopez, Michael T Lotze, William E KlunkAbstract:Plasma biosignature and brain pathology reLated to persistent cognitive impairment in Late-Life Depression
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pathways linking Late Life Depression to persistent cognitive impairment and dementia
Dialogues in clinical neuroscience, 2008Co-Authors: Meryl A. Butters, Howard J. Aizenstein, Benoit H. Mulsant, Charles F. Reynolds, Jeffrey Young, Oscar Ramos Lopez, Steven T Dekosky, James T BeckerAbstract:There is a strong association between Late-Life Depression, cognitive impairment, cerebrovascular disease, and poor cognitive outcomes, including progressive dementia, especially Alzheimer's disease. While neuroimaging evidence suggests that cerebrovascular disease plays a prominent role, it seems that Depression alone may also confer substantial risk for developing Alzheimer's disease. The relationships between the prominent cerebrovascular changes, other structural abnormalities, specific forms of cognitive dysfunction, and increased risk for developing Alzheimer's disease among those with Late-Life Depression have been difficult to reconcile. The varied findings suggest that there are likely multiple pathways to poor cognitive outcomes. We present a framework outlining multiple, non-mutually exclusive etiologic links between Depression, cognitive impairment, and progressive decline, including dementia. Importantly, the model is both testable and falsifiable. Going forward, using models such as this to inform research should accelerate knowledge acquisition on the Depression/dementia relationship that may be useful for dementia prevention, monitoring the impact of Depression treatment on clinical status and course of illness.
Warren D. Taylor - One of the best experts on this subject based on the ideXlab platform.
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Nicotine and networks: Potential for enhancement of mood and cognition in Late-Life Depression.
Neuroscience and biobehavioral reviews, 2017Co-Authors: Jason A. Gandelman, Paul A. Newhouse, Warren D. TaylorAbstract:Late-Life Depression is characterized by both lower mood and poor cognitive performance, symptoms that often do not fully respond to current antidepressant medications. Nicotinic acetylcholine receptor (nAChR) agonists such as nicotine may serve as a novel therapeutic approach for this population. Both preclinical and preliminary clinical studies suggest that nAChR agonists can improve depressive behavior in animal models and improve mood in depressed individuals. Substantial literature also supports that nAChR agonists benefit cognitive performance, particularly in older populations. These potential benefits may be mediated by the effects of nAChR stimulation on neural network function and connectivity. Functional neuroimaging studies detail effects of nAChR agonists on the default mode network, central-executive network, and salience network that may oppose or reverse network changes seen in Depression. We propose that, given the existent literature and the clinical presentation of Late-Life Depression, nicotine or other nAChR agonists may have unique therapeutic benefits in this population and that clinical trials examining nicotine effects on mood, cognition, and network dynamics in Late-Life Depression are justified.
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Cognition as a therapeutic target in Late-Life Depression: potential for nicotinic therapeutics.
Biochemical pharmacology, 2013Co-Authors: Lilia Zurkovsky, Warren D. Taylor, Paul A. NewhouseAbstract:Depression is associated with impairments to cognition and brain function at any age, but such impairments in the elderly are particularly problematic because of the additional burden of normal cognitive aging and in some cases, structural brain pathology. Individuals with Late-Life Depression exhibit impairments in cognition and brain structural integrity, alongside mood dysfunction. Antidepressant treatment improves symptoms in some but not all patients, and those who benefit may not return to the cognitive and functional level of nondepressed elderly. Thus, for comprehensive treatment of Late-Life Depression, it may be necessary to address both the affective and cognitive deficits. In this review, we propose a model for the treatment of Late-Life Depression in which nicotinic stimulation is used to improve cognitive performance and improve the efficacy of an antidepressant treatment of the syndrome of Late-Life Depression. The cholinergic system is well-established as important to cognition. Although muscarinic stimulation may exacerbate depressive symptoms, nicotinic stimulation may improve cognition and neural functioning without a detriment to mood. While some studies of nicotinic subtype specific receptor agonists have shown promise in improving cognitive performance, less is known regarding how nicotinic receptor stimulation affects cognition in depressed elderly patients. Late-Life Depression thus represents a new therapeutic target for the development of nicotinic agonist drugs. Parallel treatment of cognitive dysfunction along with medical and psychological approaches to treating mood dysfunction may be necessary to ensure full resolution of depressive illness in aging.
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Neuroimaging in Late-Life Depression
International review of psychiatry (Abingdon England), 2006Co-Authors: Sandeep Vaishnavi, Warren D. TaylorAbstract:Late-Life Depression may be associated with vasculopathy. Neuroimaging has been a critical tool in exploring the relationship between this form of Depression and vascular factors. Magnetic resonance imaging has been the most widely used tool, but there is potential to use other structural imaging techniques as well as functional neuroimaging methodologies. Neuroimaging may potentially be utilized at some point as a biomarker for Late-Life Depression, thus helping with diagnosis and guiding treatment.
David C. Steffens - One of the best experts on this subject based on the ideXlab platform.
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Neurobiology and Risk Factors of Late-Life Depression
Understanding Depression, 2017Co-Authors: Neha Jain, David C. SteffensAbstract:Depressive disorders are a common cause of emotional suffering, increased disability, premature mortality, increased healthcare utilization costs, and cognitive decline in the elderly. There appear to be multiple unique pathophysiological pathways to Late-Life Depression. This chapter seeks to review the research performed in this field over the last several decades, describing disturbances in fronto-subcortical function, genetic polymorphisms, chronic stress and inflammation, as well as vascular pathology. We also discuss structural and functional neuroimaging studies of Late-Life Depression. Future research must explore outcomes of early intervention strategies combined with a personalized approach to the depressed elderly patient.
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What Are the Causes of Late-Life Depression?
The Psychiatric clinics of North America, 2013Co-Authors: Rehan Aziz, David C. SteffensAbstract:Depression, including MDD, remains a serious public health concern across the Lifespan and especially in the elderly. Despite a lower overall percentage of depressed elders, when compared with their younger counterparts,3 the expected increasing numbers of seniors point to an even greater necessity for health professionals to be aware of the specialized needs of elders. The consequences of untreated or partially treated Late-Life Depression are dire. There are higher mortality rates from both suicide4 and medical illness.5,6 Geriatric Depression is also costly. In one study, total health care costs were 47% to 51% higher and outpatient costs were 43% to 52% higher for depressed elders when compared with non-depressed patients, even after adjustment for chronic medical illness. This increase was seen in every component of health care costs, with only a small percentage caused by mental health treatment.7 This issue of the Psychiatric Clinics of North America offers a comprehensive review of Late-Life Depression. This article appraises several facets of geriatric Depression, including a description of geriatric Depression and recent epidemiologic studies highlighting the incidence and prevalence of old-age Depression. The evidence regarding the cause of Late-Life Depression is addressed from a biopsychosocial perspective. This review is crafted to be extensive, although not exhaustive. Particular attention is focused on vascular Depression and the relationship between Depression and cognitive impairment.
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FoLate metabolism genes, dietary foLate and response to antidepressant medications in Late-Life Depression.
International journal of geriatric psychiatry, 2012Co-Authors: Brenda D. Jamerson, Martha E. Payne, Melanie E. Garrett, Allison E. Ashley-koch, Marcy C. Speer, David C. SteffensAbstract:Objective The primary aims of this study were to 1) determine whether foLate metabolism genetic polymorphisms predict age of onset and occurrence of Late Life Depression and 2) determine whether foLate metabolism genetic polymorphisms predict response to antidepressant medications in Late-Life Depression.
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Association of AGTR1 With 18-Month Treatment Outcome in Late-Life Depression
The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry, 2007Co-Authors: Douglas G. Kondo, Marcy C. Speer, K. Ranga Rama Krishnan, Douglas R. Mcquoid, Susan H. Slifer, Carl F. Pieper, Ashley V. Billups, David C. SteffensAbstract:Objective Converging lines of evidence implicate vascular factors in Late-Life Depression, and argue that Late-Life Depression is a distinct entity among the mood disorders. The A1166C polymorphism in the angiotensin II receptor, vascular type 1 (AGTR1) gene has been associated with a range of vascular diseases. This study investigated the association of AGTR1 genotype on 18-month treatment outcome in Late-Life Depression. Methods In a large, prospective cohort study, patients with Late-Life Depression received individualized treatment using a standardized algorithm. The authors genotyped participants at the AGTR1 A1166C single nucleotide polymorphism (SNP) using standardized methodology, then used survival analysis to estimate the impact of A1166C and demographic variables on time to remission during 18 months of follow-up. Results The hazard ratio for AGTR1 homozygous C/C status was 0.37. The A1166C SNP showed evidence for genotypic and allelic association in a comparison of remitted and unremitted/censored subjects. Conclusion Consistent with its association with numerous vascular disorders, AGTR1 is associated with treatment outcome in Late-Life Depression. Further studies are needed to replicate this finding, and to investigate the impact of other genetic markers of vascular disease on Late-Life Depression outcome.
Paul A. Newhouse - One of the best experts on this subject based on the ideXlab platform.
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Nicotine and networks: Potential for enhancement of mood and cognition in Late-Life Depression.
Neuroscience and biobehavioral reviews, 2017Co-Authors: Jason A. Gandelman, Paul A. Newhouse, Warren D. TaylorAbstract:Late-Life Depression is characterized by both lower mood and poor cognitive performance, symptoms that often do not fully respond to current antidepressant medications. Nicotinic acetylcholine receptor (nAChR) agonists such as nicotine may serve as a novel therapeutic approach for this population. Both preclinical and preliminary clinical studies suggest that nAChR agonists can improve depressive behavior in animal models and improve mood in depressed individuals. Substantial literature also supports that nAChR agonists benefit cognitive performance, particularly in older populations. These potential benefits may be mediated by the effects of nAChR stimulation on neural network function and connectivity. Functional neuroimaging studies detail effects of nAChR agonists on the default mode network, central-executive network, and salience network that may oppose or reverse network changes seen in Depression. We propose that, given the existent literature and the clinical presentation of Late-Life Depression, nicotine or other nAChR agonists may have unique therapeutic benefits in this population and that clinical trials examining nicotine effects on mood, cognition, and network dynamics in Late-Life Depression are justified.
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Cognition as a therapeutic target in Late-Life Depression: potential for nicotinic therapeutics.
Biochemical pharmacology, 2013Co-Authors: Lilia Zurkovsky, Warren D. Taylor, Paul A. NewhouseAbstract:Depression is associated with impairments to cognition and brain function at any age, but such impairments in the elderly are particularly problematic because of the additional burden of normal cognitive aging and in some cases, structural brain pathology. Individuals with Late-Life Depression exhibit impairments in cognition and brain structural integrity, alongside mood dysfunction. Antidepressant treatment improves symptoms in some but not all patients, and those who benefit may not return to the cognitive and functional level of nondepressed elderly. Thus, for comprehensive treatment of Late-Life Depression, it may be necessary to address both the affective and cognitive deficits. In this review, we propose a model for the treatment of Late-Life Depression in which nicotinic stimulation is used to improve cognitive performance and improve the efficacy of an antidepressant treatment of the syndrome of Late-Life Depression. The cholinergic system is well-established as important to cognition. Although muscarinic stimulation may exacerbate depressive symptoms, nicotinic stimulation may improve cognition and neural functioning without a detriment to mood. While some studies of nicotinic subtype specific receptor agonists have shown promise in improving cognitive performance, less is known regarding how nicotinic receptor stimulation affects cognition in depressed elderly patients. Late-Life Depression thus represents a new therapeutic target for the development of nicotinic agonist drugs. Parallel treatment of cognitive dysfunction along with medical and psychological approaches to treating mood dysfunction may be necessary to ensure full resolution of depressive illness in aging.
