Journal
JOURNAL OF ALZHEIMERS DISEASE
Volume 22, Issue 2, Pages 393-399Publisher
IOS PRESS
DOI: 10.3233/JAD-2010-100846
Keywords
Amyloid-beta protein; apolipoprotein E; dementia; etiology; metabolism; mitochondria; pathology; olfactory pathways; therapeutics
Categories
Funding
- State of Illinois
- Wyeth Pharmaceuticals Inc
- Janssen Alzheimer Immunotherapy
- NATIONAL INSTITUTE ON AGING [R01AG032431, R56AG013435] Funding Source: NIH RePORTER
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The amyloid cascade hypothesis has guided much of the research into Alzheimer's disease (AD) over the last 25 years. We argue that the hypothesis of amyloid-beta (A beta) as the primary cause of dementia may not be fully correct. Rather, we propose that decline in brain metabolic activity, which is tightly linked to synaptic activity, actually underlies both the cognitive decline in AD and the deposition of A beta. A beta may further exacerbate metabolic decline and result in a downward spiral of cognitive function, leading to dementia. This novel interpretation can tie the disparate risk factors for dementia to a unifying hypothesis and present a roadmap for interventions to decrease the prevalence of dementia in the elderly population.
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