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Neurochemical Dissection of Synaptic Pathology in Alzheimer's Disease

Published online by Cambridge University Press:  10 January 2005

Pia Davidsson
Affiliation:
Department of Clinical Neuroscience, Unit of Neurochemistry, Sahlgrenska University Hospital, Mölndal, Sweden
Kaj Blennow
Affiliation:
Department of Clinical Neuroscience, Unit of Neurochemistry, Sahlgrenska University Hospital, Mölndal, Sweden
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Abstract

Synaptic pathology has attained increasing attention as being central in the pathogenesis of Alzheimer's disease (AD). To address the question whether synaptic pathology in AD involves the whole synapse, or is limited to specific components thereof, we studied three different synaptic vesicle proteins (rab3a, synaptotagmin, synaptophysin) and also the presynaptic membrane protein GAP-43 and the postsynaptic protein neurogranin. The material included post-mortem brain tissue (frontal cortex, hippocampus, and cerebellum) from 8 patients with early-onset AD (EAD), 11 patients with late-onset AD (LAD), 6 patients with vascular dementia (VAD), and 9 control subjects. A reduction of all synaptic proteins was found in AD, more pronounced in EAD than in LAD, in both the frontal cortex (EAD 30% to 70% vs. LAD 82% to 88% of control value) and hippocampus (EAD 22% to 82% vs. LAD 76% to 89% of control value), whereas only minor changes were found in VAD. The finding that all synaptic proteins were reduced in AD suggests a degeneration and loss of whole synaptic elements that are more pronounced in EAD than in LAD.

Type
Dementia
Copyright
© 1998 International Psychogeriatric Association

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