Journal
NEUROLOGY
Volume 75, Issue 20, Pages 1803-1809Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0b013e3181fd6328
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Funding
- Marabou Foundation, Sweden
- Psychiatry Research Trust UK
- Alzheimer's Research Trust UK
- American Alzheimer's Association USA
- H. Lundbeck A/S
- Novartis
- Eisai Inc.
- Acadia Pharmaceuticals
- NIHR (UK)
- MRC
- Alzheimer's Society
- Alzheimer Research Trust
- BUPA Foundation
- Research into Ageing
- Edmund J Safra Foundation
- Wellcome Trust
- Dunhill Medical Trust
- Medical Research Council UK
- Alzheimers Research UK [ART-PhD2009-2] Funding Source: researchfish
- Medical Research Council [G0502157, G0400074, G0500247, G0700718B, G0900652] Funding Source: researchfish
- MRC [G0900652, G0502157, G0400074, G0500247] Funding Source: UKRI
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Objectives: Vascular dementia (VaD) accounts for approximately 15%-20% of all dementias, but the relationship of progressive cognitive impairment to neurochemical changes is poorly understood. We have therefore investigated glutamatergic synaptic markers in VaD. Methods: We used homogenates prepared from gray matter from 2 neocortical regions (Brodmann area [BA] 9 and BA 20) and Western blotting to determine the concentrations of key components of the glutamatergic neurotransmitter system, vesicular glutamate transporter 1 (VGLUT1) and excitatory amino acid transporter EAAT2 (GLT-1), and the ubiquitous synaptic protein, synaptophysin, in 73 individuals-48 patients with cerebrovascular disease with and without dementia, 10 patients with AD, and 15 controls-in a case-control design. Results: VGLUT1 concentrations in BA 20 and BA 9 were correlated with CAMCOG total (Rs 0.525, p = 0.018, n = 20; Rs 0.560, p = 0.002, n = 27) and CAMCOG memory scores (Rs 0.616, p = 0.004, n = 20; Rs 0.675, p = 0.000, n = 27). VGLUT1 concentration in BA 9 differed between the different dementia groups and the stroke no dementia group (1-way analysis of variance F = 6.69, p = 0.001 and Bonferroni p = 0.01 in each case), with subjects with stroke who did not develop dementia exhibiting the highest mean value for VGLUT1. Conclusions: These data suggest that loss of glutamatergic synapses is a feature of VaD and Alzheimer disease but the preservation of synapses, in particular glutamatergic synapses, in the frontal cortex against the temporal cortex plays a role in sustaining cognition and protecting against dementia following a stroke. Neurology (R) 2010;75:1803-1809
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