Lewy bodies in the amygdala increase risk for major depression in subjects with Alzheimer disease

López, Oscar L.; Becker, James T.; Sweet, Robert A.; Martín-Sánchez, F.J.; Hamilton, Ronald L.

doi:10.1212/01.wnl.0000230161.28299.3c

Cited by 36 publications

(17 citation statements)

References 38 publications

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“…Samuels et al (2004) could not find cortical and subcortical Lewy body pathology associated with depression. In contrast, Lewy body density in the amygdalae was found to be associated with increased risk for major depression in subjects with AD (Lopez et al, 2006). Forstl et al (1992) explained the presence of depression in dementia by a loss of noradrenergic and cholinergic neurons in the Locus coeruleus and Nucleus basalis of Meynert.…”

Section: Discussionmentioning

confidence: 97%

Depression in mild dementia: associations with diagnosis, APOE genotype and clinical features

Fritze

Ehrt

Sønnesyn

et al. 2010

Int J Geriat Psychiatry

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Section: Discussionmentioning

confidence: 97%

Depression in mild dementia: associations with diagnosis, APOE genotype and clinical features

Fritze

Ehrt

Sønnesyn

et al. 2010

Int J Geriat Psychiatry

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“…However, this pathology did not occur in isolation, and all participants had evidence of either vascular or Lewy body pathology. Another study found higher rates of depression in individuals with comorbid AD and Lewy body pathologies compared to those with AD alone (Lopez et al, 2006). Despite the well-established relationship between LLD and vascular disease (Taylor et al, 2013), little is known about how vascular disease contributes to the pathologic basis of depression in dAD.…”

Section: Discussionmentioning

confidence: 99%

Clinicopathological correlates of depression in early Alzheimer's disease in the NACC

McCutcheon

Han

Troncoso

et al. 2016

Int J Geriat Psychiatry

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Objective Depression may be a prodrome to Alzheimer’s disease (AD). We assessed whether AD neuropathology is associated with depression in mild cognitive impairment (MCI) and mild dementia (dAD). Methods All clinical and neuropathological data for this study came from the National Alzheimer’s Coordinating Center (NACC). Healthy control (HC, n=120), MCI (n=77), and mild dAD (n=93) patients who underwent brain autopsy were included. In regression models with Geriatric Depression Scale (GDS) as the outcome, neuritic plaque (NP) score or Braak Stages of neurofibrillary (NF) pathology were covariates. Results GDS was not associated with cognitive status, NP score, Braak Stages, or their interaction. In both models, a history of TIAs, depression within the last 2 years, current benzodiazepine use, and greater severity of neuropsychiatric symptoms were associated with greater depression. In the Braak Stages model, less education was another significant predictor. Conclusions Depression in early AD appears to be independent of NP and NF pathology. Studies are needed to investigate other mechanisms that may be responsible for depression in MCI and dAD.

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“…Correspondingly, at least 59% of AD patients have LBs, usually restricted to amygdala and sparing the neocortical regions, with their number increasing as the disease progresses [30]. Interestingly, the presence of LBs in the amygdala appears to increase the risk for major depression in AD by nearly 5-fold [31]. Furthermore, in AD subjects with similar severity of cognitive impairment at baseline and comparable Braak stages at autopsy, those with concomitant neocortical LB pathology (referred to as Lewy body variant of AD) generally have faster cognitive decline and accelerated mortality compared to those with “pure” AD [32].…”

Section: Introductionmentioning

confidence: 99%

Cerebrospinal Fluid Biomarkers for Dementia with Lewy Bodies

Mukaetova‐Ladinska

Monteith

Perry

2010

International Journal of Alzheimer's Disease

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More than 750,000 of the UK population suffer from some form of cognitive impairment and dementia. Of these, 5–20% will have Dementia with Lewy Bodies (DLB). Clinico-pathological studies have shown that it is the low frequency of DLB clinical core features that makes the DLB diagnosis hardly recognisable during life, and easily misdiagnosed for other forms of dementia. This has an impact on the treatment and long-term care of the affected subjects. Having a biochemical test, based on quantification of a specific DLB biomarker within Cerebrospinal Fluid (CSF) could be an effective diagnostic method to improve the differential diagnosis. Although some of the investigated DLB CSF biomarkers are well within the clinical criteria for sensitivity and specificity (>90%), they all seem to be confounded by the contradictory data for each of the major groups of biomarkers (α-synuclein, tau and amyloid proteins). However, a combination of CSF measures appear to emerge, that may well be able to differentiate DLB from other dementias: α-synuclein reduction in early DLB, a correlation between CSF α-synuclein and Aβ42 measures (characteristic for DLB only), and t-tau and p-tau181 profile (differentiating AD from DLB).

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Lewy bodies in the amygdala increase risk for major depression in subjects with Alzheimer disease

Cited by 36 publications

References 38 publications

Depression in mild dementia: associations with diagnosis, APOE genotype and clinical features

Depression in mild dementia: associations with diagnosis, APOE genotype and clinical features

Clinicopathological correlates of depression in early Alzheimer's disease in the NACC

Cerebrospinal Fluid Biomarkers for Dementia with Lewy Bodies

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