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Cited by 575

β-Secretase Protein and Activity Are Increased in the Neocortex in Alzheimer Disease

Fukumoto, Hiroaki·2002·Archives of Neurology
DOI 10.1001/archneur.59.9.1381
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Abstract

Context Amyloid plaques, a major pathological feature of Alzheimer disease (AD), are composed of an internal fragment of amyloid precursor protein (APP): the 4-kd amyloid-beta protein (Abeta). The metabolic processing of APP that results in Abeta formation requires 2 enzymatic cleavage events, a gamma-secretase cleavage dependent on presenilin, and a beta-secretase cleavage by the aspartyl protease beta-site APP-cleaving enzyme (BACE). Objective To test the hypothesis that BACE protein and activity are increased in regions of the brain that develop amyloid plaques in AD. Methods We developed an antibody capture system to measure BACE protein level and BACE-specific beta-secretase activity in frontal, temporal, and cerebellar brain homogenates from 61 brains with AD and 33 control brains. Results In the brains with AD, BACE activity and protein were significantly increased (P Conclusions The BACE protein and activity levels are increased in brain regions affected by amyloid deposition and remain increased despite significant neuronal and synaptic loss in AD.

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  • BACE1 activity is increased in postmortem brains of Alzheimer's disease patients and in brains of Alzheimer's disease mouse models.

    “BACE1 activity is increased in postmortem brains of AD patients and in brains of AD mouse models (Fukumoto et al., 2002; Yang et al., 2003).”

    From VPS35 haploinsufficiency increases Alzheimer’s disease neuropathology (2011) · cites this paper as Fukumoto et al., 2002

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Authors
Fukumoto, H.
Venue
Archives of Neurology
Publisher
American Medical Association (AMA)
Published
2002-09-01
Volume
59
Issue
9
Pages
1381
ISSN
0003-9942
DOI
10.1001/archneur.59.9.1381
Cited by
575
References
5
Language
en

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