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NEUROLOGY 2007;68:1501-1508
© 2007 American Academy of Neurology

Synaptic alterations in CA1 in mild Alzheimer disease and mild cognitive impairment

S. W. Scheff, PhD, D. A. Price, BA, F. A. Schmitt, PhD, S. T. DeKosky, MD and E. J. Mufson, PhD

From the Sanders-Brown Center on Aging and Alzheimer Disease Research Center (S.W.S., D.A.P., F.A.S.), University of Kentucky College of Medicine, Lexington, Department of Neurology (S.T.D.K.), University of Pittsburgh, PA, and Department of Neurological Sciences (E.J.M.), Rush University Medical Center, Chicago, IL.

Address correspondence and reprint requests to Dr Scheff, Sanders-Brown Center on Aging, 101 Sanders-Brown, Lexington, KY 40536-0230 sscheff{at}email.uky.edu

Objective: To evaluate the total number of synapses in the stratum radiatum (str rad) of the human hippocampal CA1 subfield in individuals with mild Alzheimer disease (mAD), mild cognitive impairment (MCI), or no cognitive impairment (NCI) and determine if synapse loss is an early event in the progression of the disease.

Methods: Short postmortem autopsy tissue was obtained, and an unbiased stereologic sampling scheme coupled with transmission electron microscopy was used to directly visualize synaptic contacts.

Results: Individuals with mAD had fewer synapses (55%) than the other two diagnostic groups. Individuals with MCI had a mean synaptic value that was 18% lower than the NCI group mean. The total number of synapses showed a correlation with several cognitive tests including those involving both immediate and delayed recall. Total synaptic numbers showed no relationship to the subject's Braak stage or to APOE genotype. The volume of the str rad was reduced in mAD vs the other two diagnostic groups that were not different from each other.

Conclusion: These results strongly support the concept that synapse loss is a structural correlate involved very early in cognitive decline in mild Alzheimer disease (mAD) and supports mild cognitive impairment as a transitional stage between mAD and no cognitive impairment.

Supported by grants from the NIH (National Institute on Aging, AG14449, AG10161, AG10688, AG19241, AG019241 and 5P50 AG05144).

Disclosure: The authors report no conflicts of interest.

Received August 21, 2006. Accepted in final form December 31, 2006.




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