Dendritic changes in Alzheimer's disease and factors that may underlie these changes

被引：89

作者：

Anderton, BH

Callahan, L

Coleman, P

Davies, P

Flood, D

Jicha, GA

Ohm, T

Weaver, C

机构：

[1] Inst Psychiat, Dept Neurosci, London SE5 8AF, England

[2] Univ Rochester, Med Ctr, Rush Alzheimers Dis Ctr, Rochester, NY 14642 USA

[3] Yeshiva Univ Albert Einstein Coll Med, Dept Pathol, Bronx, NY 10461 USA

[4] Yeshiva Univ Albert Einstein Coll Med, Dept Neurosci, Bronx, NY 10461 USA

[5] Charite Univ Clin, Dept Cell Neurobiol, D-10115 Berlin, Germany

来源：

PROGRESS IN NEUROBIOLOGY | 1998年 / 55卷 / 06期

关键词：

D O I：

10.1016/S0301-0082(98)00022-7

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

It seems likely that the Alzheimer disease (AD)-related dendritic changes addressed in this article are induced by two principally different processes. One process is linked to the plastic response associated with deafferentation, that is, long-lasting transneuronally induced regressive changes in dendritic geometry and structure. The other process is associated with severe alterations of the dendritic- and perikaryal cytoskeleton as seen in neurons with the neurofibrillary pathology of AD, that is, the formation of paired helical filaments formed by hyperphosphorylated microtubule-associated protein tau. As the development of dendritic and cytoskeletal abnormalities are at least mediated by alterations in signal transduction. this article also reviews changes in signal pathways in AD. We also discuss transgenic approaches developed to model and understand cytoskeletal abnormalities. (C) 1998 Elsevier Science Ltd. All rights reserved.

引用

页码：595 / 609

页数：15

共 193 条

[1]

Arendt T, 1997, J NEUROSCI, V17, P516

[2] Transfer of beta-amyloid precursor protein gene using adenovirus vector causes mitochondrial abnormalities in cultured normal human muscle [J].