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Fig. 2 | Acta Neuropathologica Communications

Fig. 2

From: Upregulation of calpain activity precedes tau phosphorylation and loss of synaptic proteins in Alzheimer’s disease brain

Fig. 2

Transient elevations of total APP amounts in early AD, and persistent accumulation of Aβ1-42 at end-stage disease. a Representative immunoblots of cortical homogenates from postmortem brain. Blots were probed with the 6E10 antibody to detect full-length amyloid precursor protein (APP) at 110 to 130 kDa. Blots were also probed with an anti-neuron-specific enolase (NSE, 45 kDa) as a loading control. b Bar graph shows APP amounts in brain following standardization to NSE protein in the same sample. Aβ ELISAs were used to measure Aβ1-40 and Aβ1-42 amounts in pg mg−1 in these tissues. Bar graphs show (c) Aβ1-40 and (d) Aβ1-42 amounts in each sample. e postmortem brain sections immunostained with an anti-Aβ antibody show the progressive development of amyloid plaque pathology in AD brain. CTRL: control (n = 5), Braak II AD (n = 4), Braak III AD (n = 3), Braak IV AD (n = 4), Braak V AD (n = 3), Braak VI AD (n = 5). Data is mean ± SEM. *p < 0.05, **p < 0.01

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