TY - JOUR
T1 - Neuron number in the entorhinal cortex and CA1 in preclinical alzheimer disease
AU - Price, Joseph L.
AU - Ko, Andy I.
AU - Wade, Marcus J.
AU - Tsou, Sarah K.
AU - McKeel, Daniel W.
AU - Morris, John C.
PY - 2001
Y1 - 2001
N2 - Objectives: To determine whether nondemented subjects with pathological evidence of preclinical Alzheimer disease (AD) demonstrate neuronal loss in the entorhinal cortex and hippocampus, and whether the onset of cognitive deficits in AD coincides with the onset of neuronal degeneration. Methods: Preclinical AD cases have been defined by the absence of cognitive decline but with neuropathological evidence of AD. The hippocampus and entorhinal cortex were examined in 13 nondemented cases (Clinical Dementia Rating [CDR] 0) with healthy brains, 4 cases with preclinical AD, 8 cases with very mild symptomatic AD (CDR 0.5), and 4 cases with severe AD (CDR 3, hippocampus only). The volume and number of neurons were determined stereologically in 2 areas that are vulnerable to AD - the entorhinal cortex (as a whole and layer II alone) and hippocampal field CA1. Results: There was no significant decrease in neuron number or volume with age in the healthy nondemented group and little or none between the healthy and preclinical AD groups. Substantial decreases were found in the very mild AD group in neuron number (35% in the entorhinal cortex, 50% in layer II, and 46% in CA1) and volume (28% in the entorhinal cortex, 21% in layer II; and 29% in CA1). Greater decrements were observed in CA1 in the severe AD group. Conclusions: There is little or no neuronal loss in aging or preclinical AD but substantial loss in very mild AD. The findings indicate that AD results in clinical deficits only when it produces significant neuronal loss.
AB - Objectives: To determine whether nondemented subjects with pathological evidence of preclinical Alzheimer disease (AD) demonstrate neuronal loss in the entorhinal cortex and hippocampus, and whether the onset of cognitive deficits in AD coincides with the onset of neuronal degeneration. Methods: Preclinical AD cases have been defined by the absence of cognitive decline but with neuropathological evidence of AD. The hippocampus and entorhinal cortex were examined in 13 nondemented cases (Clinical Dementia Rating [CDR] 0) with healthy brains, 4 cases with preclinical AD, 8 cases with very mild symptomatic AD (CDR 0.5), and 4 cases with severe AD (CDR 3, hippocampus only). The volume and number of neurons were determined stereologically in 2 areas that are vulnerable to AD - the entorhinal cortex (as a whole and layer II alone) and hippocampal field CA1. Results: There was no significant decrease in neuron number or volume with age in the healthy nondemented group and little or none between the healthy and preclinical AD groups. Substantial decreases were found in the very mild AD group in neuron number (35% in the entorhinal cortex, 50% in layer II, and 46% in CA1) and volume (28% in the entorhinal cortex, 21% in layer II; and 29% in CA1). Greater decrements were observed in CA1 in the severe AD group. Conclusions: There is little or no neuronal loss in aging or preclinical AD but substantial loss in very mild AD. The findings indicate that AD results in clinical deficits only when it produces significant neuronal loss.
UR - http://www.scopus.com/inward/record.url?scp=0034849725&partnerID=8YFLogxK
U2 - 10.1001/archneur.58.9.1395
DO - 10.1001/archneur.58.9.1395
M3 - Article
C2 - 11559310
AN - SCOPUS:0034849725
SN - 0003-9942
VL - 58
SP - 1395
EP - 1402
JO - Archives of neurology
JF - Archives of neurology
IS - 9
ER -