Is Brain Amyloid Production a Cause or a Result of Dementia of The Alzheimer's Type?

被引：73

作者：

Struble, Robert G. ^{[1
]}

Ala, Tom ^{[1
]}

Patrylo, Peter R. ^{[2
,4
]}

Brewer, Gregory J. ^{[3
]}

Yan, Xiao-Xin ^{[4
]}

机构：

[1] So Illinois Univ, Sch Med, Ctr Alzheimers Dis & Related Disorders, Carbondale, IL 62901 USA

[2] So Illinois Univ, Sch Med, Dept Physiol, Carbondale, IL 62901 USA

[3] So Illinois Univ, Sch Med, Dept Neurol & Med Microbiol Immunol & Cell Biol, Carbondale, IL 62901 USA

[4] So Illinois Univ, Sch Med, Dept Anat, Carbondale, IL 62901 USA

来源：

JOURNAL OF ALZHEIMERS DISEASE | 2010年 / 22卷 / 02期

关键词：

Amyloid-beta protein; apolipoprotein E; dementia; etiology; metabolism; mitochondria; pathology; olfactory pathways; therapeutics; GLUCOSE-METABOLISM; COGNITIVE IMPAIRMENT; SYNAPTIC PLASTICITY; DISEASE PATHOLOGY; OXIDATIVE STRESS; REGIONAL CHANGES; FRONTAL-CORTEX; BETA; SYSTEM; MOUSE;

D O I：

10.3233/JAD-2010-100846

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

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.

引用

页码：393 / 399

页数：7

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