Failed Compensatory Dendritic Growth as a Pathophysiological Process in Alzheimer's Disease

Dorothy G. Flood, Paul Coleman

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

In normal human aging the remaining neurons of two areas of the hippocampal region have been found to compensate for age-related neuronal loss by proliferating new dendrites. In Alzheimer's disease (AD) the layer II pyramidal neurons of the parahippocampal gyrus fail to show this compensatory response, in spite of a probable, exaggerated disease-related loss of neurons. In AD the dentate gyrus granule cells of the hippocampus also show a reduced amount of the compensatory response. This failure of the AD brain to show the normal compensatory plastic response, seen in normal aging as dendritic growth, may be viewed as one of the pathophysiological processes of the disease.

Original languageEnglish (US)
Pages (from-to)475-479
Number of pages5
JournalCanadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques
Volume13
Issue numberS4
DOIs
StatePublished - Jan 1 1986
Externally publishedYes

Fingerprint

Alzheimer Disease
Growth
Neurons
Parahippocampal Gyrus
Pyramidal Cells
Dentate Gyrus
Dendrites
Plastics
Hippocampus
Brain

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

Cite this

@article{b50394fa7bc0448183733c4444871ea1,
title = "Failed Compensatory Dendritic Growth as a Pathophysiological Process in Alzheimer's Disease",
abstract = "In normal human aging the remaining neurons of two areas of the hippocampal region have been found to compensate for age-related neuronal loss by proliferating new dendrites. In Alzheimer's disease (AD) the layer II pyramidal neurons of the parahippocampal gyrus fail to show this compensatory response, in spite of a probable, exaggerated disease-related loss of neurons. In AD the dentate gyrus granule cells of the hippocampus also show a reduced amount of the compensatory response. This failure of the AD brain to show the normal compensatory plastic response, seen in normal aging as dendritic growth, may be viewed as one of the pathophysiological processes of the disease.",
author = "Flood, {Dorothy G.} and Paul Coleman",
year = "1986",
month = "1",
day = "1",
doi = "10.1017/S031716710003715X",
language = "English (US)",
volume = "13",
pages = "475--479",
journal = "Canadian Journal of Neurological Sciences",
issn = "0317-1671",
publisher = "Canadian Journal of Neurological Sciences",
number = "S4",

}

TY - JOUR

T1 - Failed Compensatory Dendritic Growth as a Pathophysiological Process in Alzheimer's Disease

AU - Flood, Dorothy G.

AU - Coleman, Paul

PY - 1986/1/1

Y1 - 1986/1/1

N2 - In normal human aging the remaining neurons of two areas of the hippocampal region have been found to compensate for age-related neuronal loss by proliferating new dendrites. In Alzheimer's disease (AD) the layer II pyramidal neurons of the parahippocampal gyrus fail to show this compensatory response, in spite of a probable, exaggerated disease-related loss of neurons. In AD the dentate gyrus granule cells of the hippocampus also show a reduced amount of the compensatory response. This failure of the AD brain to show the normal compensatory plastic response, seen in normal aging as dendritic growth, may be viewed as one of the pathophysiological processes of the disease.

AB - In normal human aging the remaining neurons of two areas of the hippocampal region have been found to compensate for age-related neuronal loss by proliferating new dendrites. In Alzheimer's disease (AD) the layer II pyramidal neurons of the parahippocampal gyrus fail to show this compensatory response, in spite of a probable, exaggerated disease-related loss of neurons. In AD the dentate gyrus granule cells of the hippocampus also show a reduced amount of the compensatory response. This failure of the AD brain to show the normal compensatory plastic response, seen in normal aging as dendritic growth, may be viewed as one of the pathophysiological processes of the disease.

UR - http://www.scopus.com/inward/record.url?scp=0022973690&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0022973690&partnerID=8YFLogxK

U2 - 10.1017/S031716710003715X

DO - 10.1017/S031716710003715X

M3 - Article

C2 - 3791064

AN - SCOPUS:0022973690

VL - 13

SP - 475

EP - 479

JO - Canadian Journal of Neurological Sciences

JF - Canadian Journal of Neurological Sciences

SN - 0317-1671

IS - S4

ER -