Alzheimer 's Disease ( Ad )

1068 WordsMar 31, 20175 Pages
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by β-amyloid plaque formation caused by aggregation of β-amyloid42 within the brain leading to a progressive decline in cognitive function and memory loss (2). Hyperphosphorylated tau protein is occasionally found in brains of AD patients with advanced pathology however, it is not necessarily an indicator of AD but considered a sign of disease severity (2, 4, Kosik et al, 1986). AD is separated into two subcategories following the simple sporadic and familial disease classifications, early-onset AD (EOAD) which develops in individuals between 30 and 60+ years of age and late-onset AD (LOAD) which develops in individuals 60 years of age or older (2). Familial AD may…show more content…
β-amyloid aggregation spread from the site of injection to include both hemispheres of the brain further displaying the potentiation induced by aggregates within the brain homogenates (Stöhr et al, 2012). Under transmission electron microscopy, purified β-amyloid aggregates from transgenic mice revealed densely bundled fibrils; which were observed to increase levels of GFAP, Aβ(1-40) and Aβ(1-42) in bigenic mice at 300 days post injection via ELISA and immunoblotting (Stöhr et al, 2012). Crude brain homogenate exhibited approximately 15-20 times less β-amyloid than the purified homogenates (Stöhr et al, 2012). BLI of bigenic mouse brains injected with purified homogenate exhibited an early time of detection with signals at 161 + 7 [Tg(APP23)] and 173 + 9 [Tg(CRND8)] days (Stöhr et al, 2012). (FIGURE). Synthetic β-amyloid aggregates, wild-type Aβ(1-40) and mutant Aβ(AβS26C)2, were used to determine if prior results from purified brain homogenate could have contained any cofactors which would affect propagation of pathology (Stöhr et al, 2012). Results from the injection of synthetic fibrils into bigenic mice revealed similar β-amyloid aggregation, however pathology was less severe than purified brain homogenates from transgenic models (Stöhr et al, 2012). BLI of synthetic fibrils revealed a decrease in

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