Loss of proteins regulating synaptic plasticity in normal aging of the human brain and in Alzheimer disease

Kimmo Hatanpää; Krystyna R. Isaacs; Tomoaki Shirao; Daniel R. Brady; Stanley I. Rapoport

doi:10.1097/00005072-199906000-00008

Loss of proteins regulating synaptic plasticity in normal aging of the human brain and in Alzheimer disease

Kimmo Hatanpää, Krystyna R. Isaacs, Tomoaki Shirao, Daniel R. Brady, Stanley I. Rapoport

Research output: Contribution to journal › Article › peer-review

178 Scopus citations

Abstract

Recent studies suggest that the cognitive impairment associated with normal aging is due to neuronal dysfunction rather than to loss of neurons or synapses. To characterize this dysfunction, molecular indices of neuronal function were quantified in autopsy samples of cerebral cortex. During normal aging, the most dramatic decline was found in levels of synaptic proteins involved in structural plasticity (remodeling) of axons and dendrites. Alzheimer disease, the most common cause of dementia in the elderly, was associated with an additional 81% decrease in levels of drebrin, a protein regulating postsynaptic plasticity. Disturbed mechanisms of plasticity may contribute to cognitive dysfunction during aging and in Alzheimer disease.

Original language	English (US)
Pages (from-to)	637-643
Number of pages	7
Journal	Journal of neuropathology and experimental neurology
Volume	58
Issue number	6
DOIs	https://doi.org/10.1097/00005072-199906000-00008
State	Published - Jun 1999

Keywords

Cytochrome oxidase
Drebrin
Energy metabolism
GAP-43
Neuron specific-enolase
Synaptophysin
β-tubulin

ASJC Scopus subject areas

Pathology and Forensic Medicine
Neurology
Clinical Neurology
Cellular and Molecular Neuroscience

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10.1097/00005072-199906000-00008

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abstract = "Recent studies suggest that the cognitive impairment associated with normal aging is due to neuronal dysfunction rather than to loss of neurons or synapses. To characterize this dysfunction, molecular indices of neuronal function were quantified in autopsy samples of cerebral cortex. During normal aging, the most dramatic decline was found in levels of synaptic proteins involved in structural plasticity (remodeling) of axons and dendrites. Alzheimer disease, the most common cause of dementia in the elderly, was associated with an additional 81% decrease in levels of drebrin, a protein regulating postsynaptic plasticity. Disturbed mechanisms of plasticity may contribute to cognitive dysfunction during aging and in Alzheimer disease.",

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AU - Shirao, Tomoaki

AU - Brady, Daniel R.

AU - Rapoport, Stanley I.

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KW - Energy metabolism

KW - GAP-43

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Loss of proteins regulating synaptic plasticity in normal aging of the human brain and in Alzheimer disease

Abstract

Keywords

ASJC Scopus subject areas

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