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• W2896291867 abstract "Depression and dementia are both common diseases. Although new cases of depression are more common in younger adults there is a second peak at the age of 50 years suggesting a different pathological process.(Eaton et al 1997) It has been estimated that late-life depression doubles the risk of dementia. (Takayanagi et al 2015) Despite two decades of research on the link between depression and dementia it remains unclear whether depression represents a dementia prodrome or is a true risk factor for its development. The most common substrates of dementia are Alzheimer's disease (AD) and Lewy body pathology, and ischaemic brain damage. These often overlap, and share pathophysiological determinants. (Love et al 2016) We hypothesised that later-life depression is a prodromal manifestation of these disease processes and would therefore be associated with more AD, Lewy body and/or ischaemic brain abnormalities than are present in earlier-life depression or in age- and sex-matched controls. For assessment, we chose the orbitofrontal cortex (OFC), an area important in mood regulation (Brookes et al 2014) and severely affected in AD.(Van Hoesen et al 2000). We studied orbitofrontal cortex obtained post-mortem from 145 individuals in 4 groups: 28 18-50-year-olds with depression, 30 older individuals (ages 51-90) with depression, 28 with early AD (Braak stages 3-4) and 57 matched controls (17 early-life, 42 later-life). Levels of Aβ (plaque-associated or total insoluble), phospho-tau and α-synuclein were measured by immunohistochemistry and ELISA (adjusted for protein content).(Ashby et al 2012) To quantify chronic ischaemia, VEGF, MAG and PLP were measured by ELISA.(Barker et al 2013) To assess pericyte damage, PDGFRB was measured by ELISA. To assess blood-brain barrier leakiness, fibrinogen was measured by ELISA and adjusted for haemoglobin content, determined by colorimetic assay.(Miners et al 2017). As expected both Aβ40 and Aβ42 were increased in the AD group. There was no evidence of cerebral hypoperfusion or increased Aβ in either depression group. Further analysis of data is ongoing. Our initial findings suggest that later life depression does not represent prodromal AD. The results are more supportive of its being a risk factor for AD." @default.
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• W2896291867 date "2018-07-01" @default.
• W2896291867 modified "2023-10-16" @default.
• W2896291867 title "P4‐252: IS LATER LIFE DEPRESSION A RISK FACTOR FOR AD OR A PRODROMAL AD SYMPTOM?" @default.
• W2896291867 doi "https://doi.org/10.1016/j.jalz.2018.07.074" @default.
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