Cited by 100Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsNeuroscience and Neuropharmacology Research

Cognitive reserve, presynaptic proteins, and dementia in the elderly

Open access
Honer, W G, Barr, A M, Sawada, K, Thornton, A E, Morris, M C, Leurgans, S E, Schneider, J A, Bennett, D A·2012·Translational Psychiatry

Abstract

Differences in cognitive reserve may contribute to the wide range of likelihood of dementia in people with similar amounts of age-related neuropathology. The amounts and interactions of presynaptic proteins could be molecular components of cognitive reserve, contributing resistance to the expression of pathology as cognitive impairment. We carried out a prospective study with yearly assessments of N = 253 participants without dementia at study entry. Six distinct presynaptic proteins, and the protein-protein interaction between synaptosomal-associated protein 25 (SNAP-25) and syntaxin, were measured in post-mortem brains. We assessed the contributions of Alzheimer's disease (AD) pathology, cerebral infarcts and presynaptic proteins to odds of dementia, level of cognitive function and cortical atrophy. Clinical dementia was present in N = 97 (38.3%), a pathologic diagnosis of AD in N = 142 (56.1%) and cerebral infarcts in N = 77 (30.4%). After accounting for AD pathology and infarcts, greater amounts of vesicle-associated membrane protein, complexins I and II and the SNAP-25/syntaxin interaction were associated with lower odds of dementia (odds ratio = 0.36-0.68, P < 0.001 to P = 0.03) and better cognitive function (P < 0.001 to P = 0.03). Greater cortical atrophy, a putative dementia biomarker, was not associated with AD pathology, but was associated with lower complexin-II (P = 0.01) and lower SNAP-25/syntaxin interaction (P < 0.001). In conclusion, greater amounts of specific presynaptic proteins and distinct protein-protein interactions may be structural or functional components of cognitive reserve that reduce the risk of dementia with aging.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1038/tp.2012.38

Cites

40 of 40 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Honer, W. G., Barr, A. M., Sawada, K., Thornton, A. E., Morris, M. C., Leurgans, S. E., Schneider, J. A., & Bennett, D. A.
Affiliations
  • University of British Columbia (CA)
  • Simon Fraser University (CA)
  • Rush University Medical Center (US)
Corresponding author
Honer, W G
Venue
Translational Psychiatry
Published
2012-05-15
Volume
2
Issue
5
Pages
e114-e114
ISSN
2158-3188 (ISSN-L)
OpenAlex
W2043488532
Cited by
100
References
40
Citations by year
2025: 6 · 2024: 4 · 2023: 10 · 2022: 5 · 2021: 9 · 2020: 6 · 2019: 9 · 2018: 7 · 2017: 4 · 2016: 4 · 2015: 10 · 2014: 8 · 2013: 15 · 2012: 3
FWCI
8.22
Type
journal article
Language
en
Open access
Locations
  • Translational Psychiatry (publishedVersion, cc-by-nc-nd)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
Funders
  • Scottish Rite Charitable Foundation of Canada
  • Canadian Institutes of Health Research (R01AG17917, CBG101827)
  • National Institute on Aging (R01AG017917, R01AG031553)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
cognitive reserve, presynaptic proteins, dementia, Alzheimer's disease pathology, cerebral infarction, SNAP-25, syntaxin, VAMP, complexin, protein-protein interaction, cortical atrophy, cognitive function, aging, postmortem brain
MeSH terms
Aged, Aged, 80 and over, Alzheimer Disease, Atrophy, Brain, Cerebral Cortex, Cerebral Infarction, Female, Humans, Longitudinal Studies, Male, Membrane Proteins, Nerve Tissue Proteins, Reference Values, Synapses, Risk Assessment, Adaptor Proteins, Vesicular Transport, R-SNARE Proteins, Qa-SNARE Proteins, Synaptosomal-Associated Protein 25, Protein Interaction Domains and Motifs, Cognitive Reserve, Cognitive Dysfunction

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review