Association between family history of affective disorder and the depressive syndrome of Alzheimer??s disease

The recently shown association between apolipoprotein E (APOE) genotype and depressive illness has been challenged by subsequent studies. However, controversial results may derive from the different diagnostic criteria used for depression and from the small numbers of depressed patients included in the studies. We examined the association between depression and the genetic polymorphism of APOE in a large sample of depressed patients, Alzheimer’s disease (AD) patients, and healthy controls following clear definitions for late-life depression. The cumulative incidence of depression depending on the age at onset of the first episode was examined by survival analysis. Our data do not disconfirm the hypothesis of depression sharing some common pathophysiologic features with AD, however, it seems very unlikely that the APOE genotype will elucidate the assumed common mechanisms.

Section: Discussionmentioning

confidence: 99%

Early-Onset and Late-Onset Depression Are Independent of the Genetic Polymorphism of Apolipoprotein E

Papassotiropoulos

Bagli

Jessen

et al. 1999

“…A family history of mood disorder in a first-degree relative appears to be a strong risk factor for depression in AD in most relevant AD Dement Geriatr Cogn Disord 2004;17:55-64 57 studies [Pearlson et al, 1990, Lyketsos et al, 1996Fahim et al, 1998], but not in others [Heun et al, 2001]. A search for specific susceptibility loci for depression in AD initially focused on the apolipoprotein E gene (ApoE4).…”

Section: Etiopathogenesis and Genetics Of Depression In Admentioning

confidence: 99%

Diagnosis and Treatment of Depression in Alzheimer’s Disease

Lyketsos

Lee

2003

123

Over 80% of patients with Alzheimer’s disease (AD) develop ‘noncognitive’ neuropsychiatric symptoms at some point during the course of their illness. Depression is among the most frequent of such comorbidities. Affecting up to 50% of AD patients, depression is associated with severe negative consequences for patients and caregivers. Despite having a presentation in the context of AD that differs from typical ‘geriatric’ depression, it can be detected and quantified reliably, and can be differentiated from the other neuropsychiatric symptoms of AD. Several effective treatment modalities for depression in AD are available. In many cases, these reduce its adverse impact on patients and caregivers. This paper provides an overview of current knowledge regarding depression in AD for the clinician. It is followed by a practical discussion of the detection, evaluation, quantification, differential diagnosis and treatment of depression in AD.

“…These losses may result from known genetic risk factors for AD or involve the action of distinct genetic risk factors for psychiatric illness assuming clinical significance within the degenerated Alzheimer brain. If known genetic risk factors are responsible, behavioural symptoms would be seen to accompany either a family history of AD or conventional markers such as apolipoprotein E. Lack of association between the presence of depression in AD and a family history of dementia has been documented in two studies [6,7] and the role of apolipoprotein E Â4 in the aetiology of depression in dementia seems conflicting. Two large studies found no evidence for apolipoprotein E Â4 in depression [8,9].…”

Section: Introductionmentioning

confidence: 99%

Association Analysis of Apolipoprotein E Genotype and Risk of Depressive Symptoms in Alzheimer’s Disease

Craig¹,

Hart²,

McIlroy³

et al. 2005

Objectives: Behavioural and psychological symptoms of dementia (BPSD) are potent predictors of carer distress and admission to institutional care. In Alzheimer’s disease (AD), depressive symptoms are one of the most common complaints affecting around 50% of all patients. There is speculation these symptoms result from known genetic risk factors for AD, therefore we investigated the role of apolipoprotein E Ε4 in the aetiology of depression in AD. Methods: In this well-characterised cohort (n = 404) from the relatively genetically homogeneous Northern Ireland population, we tested the hypothesis that genetic variants of apolipoprotein E influence the risk for depressive symptoms in AD patients using the Neuropsychiatric Inventory (NPI-D) to determine the presence of depressive symptoms during the dementing illness. Results: A total of 55% of patients exhibited a history of depression/dysphoria during the course of the illness as gathered by the NPI-D questionnaire. Forty-six percent were suffering from depression/dysphoria when the analysis was restricted to the month prior to interview. No statistically significant association between genotypes or alleles of apolipoprotein E and depression/dysphoria in AD was observed, nor was any association noted between the presence of severe symptoms and genotypes/alleles of apolipoprotein E. Conclusions: These results suggest apolipoprotein E genotype creates no additional risk for depressive symptoms in AD.