Chapter 17

The neuropil and GAP-43/B-50 in normally aging and Alzheimer's disease human brain

Paul Coleman, Kathryn E. Rogers, Dorothy G. Flood

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Morphological studies of dendritic extent in normal aging and Alzheimer's disease (AD) have suggested the hypotheses that normally aging neurons are able to mount plastic, compensatory responses to the death of their neighbors. In AD, dendritic extent has been found to not increase with increasing age, even in regions where there is normally an age-related increase in dendritic extent, suggesting the hypothesis that one of the neurobiological deficits of AD is reduced neuronal plasticity. This chapter examines GAP-43/B50/F1 message levels as a potential marker of neuronal plasticity. Prevalence of this message as a function of normal aging also shows regional differences, with area 9 showing a decrease in GAP message level in normal aging, whereas data obtained from area 11 suggest no significant change of message level per cell in normal aging. Any decreases in GAP-43 message level found in AD brain may be accounted for on the basis of excess neuron loss in AD. However, preliminary data suggest that there may be defective posttranslational processing of GAP-43 in AD.

Original languageEnglish (US)
Pages (from-to)263-269
Number of pages7
JournalProgress in Brain Research
Volume89
Issue numberC
DOIs
StatePublished - Jan 1 1991
Externally publishedYes

Fingerprint

GAP-43 Protein
Neuropil
Alzheimer Disease
Brain
Neuronal Plasticity
Neurons
Plastics

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Chapter 17 : The neuropil and GAP-43/B-50 in normally aging and Alzheimer's disease human brain. / Coleman, Paul; Rogers, Kathryn E.; Flood, Dorothy G.

In: Progress in Brain Research, Vol. 89, No. C, 01.01.1991, p. 263-269.

Research output: Contribution to journalArticle

@article{df25259a3da34c89a8d36d9cf1003599,
title = "Chapter 17: The neuropil and GAP-43/B-50 in normally aging and Alzheimer's disease human brain",
abstract = "Morphological studies of dendritic extent in normal aging and Alzheimer's disease (AD) have suggested the hypotheses that normally aging neurons are able to mount plastic, compensatory responses to the death of their neighbors. In AD, dendritic extent has been found to not increase with increasing age, even in regions where there is normally an age-related increase in dendritic extent, suggesting the hypothesis that one of the neurobiological deficits of AD is reduced neuronal plasticity. This chapter examines GAP-43/B50/F1 message levels as a potential marker of neuronal plasticity. Prevalence of this message as a function of normal aging also shows regional differences, with area 9 showing a decrease in GAP message level in normal aging, whereas data obtained from area 11 suggest no significant change of message level per cell in normal aging. Any decreases in GAP-43 message level found in AD brain may be accounted for on the basis of excess neuron loss in AD. However, preliminary data suggest that there may be defective posttranslational processing of GAP-43 in AD.",
author = "Paul Coleman and Rogers, {Kathryn E.} and Flood, {Dorothy G.}",
year = "1991",
month = "1",
day = "1",
doi = "10.1016/S0079-6123(08)61727-6",
language = "English (US)",
volume = "89",
pages = "263--269",
journal = "Progress in Brain Research",
issn = "0079-6123",
publisher = "Elsevier",
number = "C",

}

TY - JOUR

T1 - Chapter 17

T2 - The neuropil and GAP-43/B-50 in normally aging and Alzheimer's disease human brain

AU - Coleman, Paul

AU - Rogers, Kathryn E.

AU - Flood, Dorothy G.

PY - 1991/1/1

Y1 - 1991/1/1

N2 - Morphological studies of dendritic extent in normal aging and Alzheimer's disease (AD) have suggested the hypotheses that normally aging neurons are able to mount plastic, compensatory responses to the death of their neighbors. In AD, dendritic extent has been found to not increase with increasing age, even in regions where there is normally an age-related increase in dendritic extent, suggesting the hypothesis that one of the neurobiological deficits of AD is reduced neuronal plasticity. This chapter examines GAP-43/B50/F1 message levels as a potential marker of neuronal plasticity. Prevalence of this message as a function of normal aging also shows regional differences, with area 9 showing a decrease in GAP message level in normal aging, whereas data obtained from area 11 suggest no significant change of message level per cell in normal aging. Any decreases in GAP-43 message level found in AD brain may be accounted for on the basis of excess neuron loss in AD. However, preliminary data suggest that there may be defective posttranslational processing of GAP-43 in AD.

AB - Morphological studies of dendritic extent in normal aging and Alzheimer's disease (AD) have suggested the hypotheses that normally aging neurons are able to mount plastic, compensatory responses to the death of their neighbors. In AD, dendritic extent has been found to not increase with increasing age, even in regions where there is normally an age-related increase in dendritic extent, suggesting the hypothesis that one of the neurobiological deficits of AD is reduced neuronal plasticity. This chapter examines GAP-43/B50/F1 message levels as a potential marker of neuronal plasticity. Prevalence of this message as a function of normal aging also shows regional differences, with area 9 showing a decrease in GAP message level in normal aging, whereas data obtained from area 11 suggest no significant change of message level per cell in normal aging. Any decreases in GAP-43 message level found in AD brain may be accounted for on the basis of excess neuron loss in AD. However, preliminary data suggest that there may be defective posttranslational processing of GAP-43 in AD.

UR - http://www.scopus.com/inward/record.url?scp=0026338629&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026338629&partnerID=8YFLogxK

U2 - 10.1016/S0079-6123(08)61727-6

DO - 10.1016/S0079-6123(08)61727-6

M3 - Article

VL - 89

SP - 263

EP - 269

JO - Progress in Brain Research

JF - Progress in Brain Research

SN - 0079-6123

IS - C

ER -