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- W2897728459 abstract "Alzheimer's disease is the most frequent form of dementia, accounting for 70 to 80% of all cases. The greatest risk factor for AD is aging with an estimated 30 million people living with AD worldwide. The pathology of AD consists primarily of amyloid-beta plaques and neurofibrillary tangles composed of microtubule-associated protein tau. Mitochondrial dysfunction has been implicated in the pathogenesis of AD. Voltage dependent anion channel one (VDAC1) functions as the main mitochondrial membrane conduit for ions, ATP and other metabolites as well as acting as a sentinel between the cytoplasm and mitochondria. Proteomic analysis describes an increase in VDAC1 expression associated with the progression of AD. In AD, VDAC1 accumulates in plaques, dystrophic neurites, and in the neuronal soma, which may suggest that mitochondrial transport is impaired. In addition, two-month-old VDAC1 (+/-) heterozygous mice have been shown to have reduced mRNA levels of amyloid precursor protein (APP), presenilin 1 (PSEN1), presenilin 2 (PSEN2), and microtubule-associated protein tau. In order to investigate the role a reduction in VDAC1 plays in AD, we crossed VDAC1(+/-) and VDAC1 (-/-) in an APP/PSEN1 background. We hypothesize that reduction of VDAC1 in an APP/PSEN1 background will reduce plaque deposition. Mice: APP/PSEN1(APPswe/PSEN1DE9, Jackson: 34832) were crossed to VDAC(-/-)(provided by William Craigen) to produce VDAC1(+/+)/APP/PSEN1, VDAC1(+/-)/APP/PSEN1, and VDAC1(-/-) /APP/PSEN1. Plaques were analyzed using immunofluorescence staining with anti-Ab (CST) to determine differences in plaque count and size. Primary neuronal cultures expressing VDAC1(+/+), VDAC1(+/-), and VDAC1(-/-) were evaluated for sensitivity to Ab toxicity and changes in mitochondrial bioenergetics. We observe some changes in mitochondrial bioenergetics, which suggests a role of VDAC1 in AD. In 8-month old mice expressing reduced levels of VDAC1 in an APP/PSEN1 background there is an increase in plaque area in the hippocampus and cortex. With no decrease in plaque deposition associated with VDAC1 expression levels and only marginal changes in bioenergetics, the role of VDAC1 in AD needs further evaluation." @default.
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- W2897728459 date "2018-07-01" @default.
- W2897728459 modified "2023-10-16" @default.
- W2897728459 title "P1‐102: THE NEUROPROTECTIVE ROLE OF VDAC1 IN ALZHEIMER'S DISEASE" @default.
- W2897728459 doi "https://doi.org/10.1016/j.jalz.2018.06.105" @default.
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