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 D.
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.
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U2 - 10.1016/S0079-6123(08)61727-6
DO - 10.1016/S0079-6123(08)61727-6
M3 - Article
C2 - 1839068
AN - SCOPUS:0026338629
SN - 0079-6123
VL - 89
SP - 263
EP - 269
JO - Progress in brain research
JF - Progress in brain research
IS - C
ER -