OBJECTIVE: To use stereological methods for estimating the total number of neurons in hippocampi of non-Alzheimer demented patients. MATERIAL AND METHODS: Hippocampi from six women with severely impaired memory but without Alzheimer pathology were compared with six mentally intact age-matched female controls. The total number of neurons was estimated in the granule cell layer of the dentate gyrus, the hilus of the dentate gyrus, the pyramidal cell layer of CA3 and CA2, the pyramidal cell layer of CA1 and the cellular layer of subiculum using the optical fractionator. RESULTS: The total neuron number was the same in the dementia cases, 22.4 x 106, compared with 22.7 x 106 in the controls (P = 0.85). No region-specific group differences or side difference were found. Two cases without clinical signs of dementia but with abundant plaques and tangles in hippocampus and neocortex had total neuron numbers within normal limits. CONCLUSION: Our results indicate that severely impaired memory can occur in the presence of intact numbers of hippocampal neurons in non-Alzheimer dementia and that nerve cell loss in the hippocampus might be characteristic for Alzheimer's disease, and perhaps other forms of primary cortical dementia.
OBJECTIVE: To use stereological methods for estimating the total number of neurons in hippocampi of non-Alzheimer dementedpatients. MATERIAL AND METHODS: Hippocampi from six women with severely impaired memory but without Alzheimer pathology were compared with six mentally intact age-matched female controls. The total number of neurons was estimated in the granule cell layer of the dentate gyrus, the hilus of the dentate gyrus, the pyramidal cell layer of CA3 and CA2, the pyramidal cell layer of CA1 and the cellular layer of subiculum using the optical fractionator. RESULTS: The total neuron number was the same in the dementia cases, 22.4 x 106, compared with 22.7 x 106 in the controls (P = 0.85). No region-specific group differences or side difference were found. Two cases without clinical signs of dementia but with abundant plaques and tangles in hippocampus and neocortex had total neuron numbers within normal limits. CONCLUSION: Our results indicate that severely impaired memory can occur in the presence of intact numbers of hippocampal neurons in non-Alzheimer dementia and that nerve cell loss in the hippocampus might be characteristic for Alzheimer's disease, and perhaps other forms of primary cortical dementia.
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