ArticleNeurology2021
Tripartite Relationship Among Synaptic, Amyloid, and Tau Proteins: An In Vivo and Postmortem Study.
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Article in Neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12citing papers in PubMed
1.3field-weighted citation impact, top 21% of its field
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12 citing papers in PubMed, 14 citations in OpenAlex.
- Plasma proteomics link menopause timing to brain aging and dementia risk.Research square · 2026Article
- Plasma proteomics link menopause timing to brain aging and dementia risk.medRxiv : the preprint server for health sciences · 2026Article
- Evidence for reduced synaptic protein SNAP-25 in cerebrospinal fluid in major depressive disorder and schizophrenia.BMJ mental health · 2025Article
- The interplay between age at menopause and synaptic integrity on Alzheimer's disease risk in women.Science advances · 2025Article
- Brain aging rejuvenation factors in adults with genetic and sporadic neurodegenerative disease.Brain communications · 2025Article
- GAP-43 is associated with faster amyloid-associated neurodegeneration and cognitive decline in Alzheimer's disease.Frontiers in neurology · 2025Article
- Complexin regulation of synaptic vesicle release: mechanisms in the central nervous system and specialized retinal ribbon synapses.Cell communication and signaling : CCS · 2024Review
- A multilayer network analysis of Alzheimer's disease pathogenesis: Roles for p-tau, synaptic peptides, and physical activity.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Sex-specific effects of SNAP-25 genotype on verbal memory and Alzheimer's disease biomarkers in clinically normal older adults.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- Association of CSF GAP-43 With the Rate of Cognitive Decline and Progression to Dementia in Amyloid-Positive Individuals.Neurology · 2023Article
- Synaptic Loss in Frontotemporal Dementia Revealed by [Annals of neurology · 2023Article
- Molecular pathology and synaptic loss in primary tauopathies: an 18F-AV-1451 and 11C-UCB-J PET study.Brain : a journal of neurology · 2022Observational
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Authors and funding
13 authors at 1 institution in 5 countries.
Kaitlin B CasalettoFrom the Memory and Aging Center (K.B.C., N.D., M.Y., S.W.-L., C.F., B.L.M., J.K.), Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco; Department of Psychiatry and Neurochemistry (H.Z., K.B., A.B.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B., A.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease (H.Z., K.B., A.B.), UCL Institute of Neurology, Queen ; UK Dementia Research Institute at UCL (H.Z.), London, UK; Department of Psychiatry (W.H.), University of British Columbia, Vancouver, Canada; and Department of Neurological Sciences (J.A.S., D.A.B.), Rush Medical College, Chicago, IL. kaitlin.casaletto@ucsf.edu.
Henrik ZetterbergFrom the Memory and Aging Center (K.B.C., N.D., M.Y., S.W.-L., C.F., B.L.M., J.K.), Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco; Department of Psychiatry and Neurochemistry (H.Z., K.B., A.B.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B., A.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease (H.Z., K.B., A.B.), UCL Institute of Neurology, Queen ; UK Dementia Research Institute at UCL (H.Z.), London, UK; Department of Psychiatry (W.H.), University of British Columbia, Vancouver, Canada; and Department of Neurological Sciences (J.A.S., D.A.B.), Rush Medical College, Chicago, IL.
Kaj BlennowFrom the Memory and Aging Center (K.B.C., N.D., M.Y., S.W.-L., C.F., B.L.M., J.K.), Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco; Department of Psychiatry and Neurochemistry (H.Z., K.B., A.B.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B., A.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease (H.Z., K.B., A.B.), UCL Institute of Neurology, Queen ; UK Dementia Research Institute at UCL (H.Z.), London, UK; Department of Psychiatry (W.H.), University of British Columbia, Vancouver, Canada; and Department of Neurological Sciences (J.A.S., D.A.B.), Rush Medical College, Chicago, IL.
Ann BrinkmalmFrom the Memory and Aging Center (K.B.C., N.D., M.Y., S.W.-L., C.F., B.L.M., J.K.), Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco; Department of Psychiatry and Neurochemistry (H.Z., K.B., A.B.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B., A.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease (H.Z., K.B., A.B.), UCL Institute of Neurology, Queen ; UK Dementia Research Institute at UCL (H.Z.), London, UK; Department of Psychiatry (W.H.), University of British Columbia, Vancouver, Canada; and Department of Neurological Sciences (J.A.S., D.A.B.), Rush Medical College, Chicago, IL.
William HonerFrom the Memory and Aging Center (K.B.C., N.D., M.Y., S.W.-L., C.F., B.L.M., J.K.), Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco; Department of Psychiatry and Neurochemistry (H.Z., K.B., A.B.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B., A.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease (H.Z., K.B., A.B.), UCL Institute of Neurology, Queen ; UK Dementia Research Institute at UCL (H.Z.), London, UK; Department of Psychiatry (W.H.), University of British Columbia, Vancouver, Canada; and Department of Neurological Sciences (J.A.S., D.A.B.), Rush Medical College, Chicago, IL.
Julie A SchneiderFrom the Memory and Aging Center (K.B.C., N.D., M.Y., S.W.-L., C.F., B.L.M., J.K.), Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco; Department of Psychiatry and Neurochemistry (H.Z., K.B., A.B.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B., A.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease (H.Z., K.B., A.B.), UCL Institute of Neurology, Queen ; UK Dementia Research Institute at UCL (H.Z.), London, UK; Department of Psychiatry (W.H.), University of British Columbia, Vancouver, Canada; and Department of Neurological Sciences (J.A.S., D.A.B.), Rush Medical College, Chicago, IL.
David A BennettFrom the Memory and Aging Center (K.B.C., N.D., M.Y., S.W.-L., C.F., B.L.M., J.K.), Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco; Department of Psychiatry and Neurochemistry (H.Z., K.B., A.B.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B., A.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease (H.Z., K.B., A.B.), UCL Institute of Neurology, Queen ; UK Dementia Research Institute at UCL (H.Z.), London, UK; Department of Psychiatry (W.H.), University of British Columbia, Vancouver, Canada; and Department of Neurological Sciences (J.A.S., D.A.B.), Rush Medical College, Chicago, IL.
Nina DjukicFrom the Memory and Aging Center (K.B.C., N.D., M.Y., S.W.-L., C.F., B.L.M., J.K.), Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco; Department of Psychiatry and Neurochemistry (H.Z., K.B., A.B.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B., A.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease (H.Z., K.B., A.B.), UCL Institute of Neurology, Queen ; UK Dementia Research Institute at UCL (H.Z.), London, UK; Department of Psychiatry (W.H.), University of British Columbia, Vancouver, Canada; and Department of Neurological Sciences (J.A.S., D.A.B.), Rush Medical College, Chicago, IL.
Michelle YouFrom the Memory and Aging Center (K.B.C., N.D., M.Y., S.W.-L., C.F., B.L.M., J.K.), Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco; Department of Psychiatry and Neurochemistry (H.Z., K.B., A.B.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B., A.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease (H.Z., K.B., A.B.), UCL Institute of Neurology, Queen ; UK Dementia Research Institute at UCL (H.Z.), London, UK; Department of Psychiatry (W.H.), University of British Columbia, Vancouver, Canada; and Department of Neurological Sciences (J.A.S., D.A.B.), Rush Medical College, Chicago, IL.
Sophia Weiner-LightFrom the Memory and Aging Center (K.B.C., N.D., M.Y., S.W.-L., C.F., B.L.M., J.K.), Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco; Department of Psychiatry and Neurochemistry (H.Z., K.B., A.B.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B., A.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease (H.Z., K.B., A.B.), UCL Institute of Neurology, Queen ; UK Dementia Research Institute at UCL (H.Z.), London, UK; Department of Psychiatry (W.H.), University of British Columbia, Vancouver, Canada; and Department of Neurological Sciences (J.A.S., D.A.B.), Rush Medical College, Chicago, IL.ORCID http://orcid.org/0000-0002-8522-8869
Corrina FonsecaFrom the Memory and Aging Center (K.B.C., N.D., M.Y., S.W.-L., C.F., B.L.M., J.K.), Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco; Department of Psychiatry and Neurochemistry (H.Z., K.B., A.B.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B., A.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease (H.Z., K.B., A.B.), UCL Institute of Neurology, Queen ; UK Dementia Research Institute at UCL (H.Z.), London, UK; Department of Psychiatry (W.H.), University of British Columbia, Vancouver, Canada; and Department of Neurological Sciences (J.A.S., D.A.B.), Rush Medical College, Chicago, IL.
Bruce L MillerFrom the Memory and Aging Center (K.B.C., N.D., M.Y., S.W.-L., C.F., B.L.M., J.K.), Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco; Department of Psychiatry and Neurochemistry (H.Z., K.B., A.B.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B., A.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease (H.Z., K.B., A.B.), UCL Institute of Neurology, Queen ; UK Dementia Research Institute at UCL (H.Z.), London, UK; Department of Psychiatry (W.H.), University of British Columbia, Vancouver, Canada; and Department of Neurological Sciences (J.A.S., D.A.B.), Rush Medical College, Chicago, IL.
Joel KramerFrom the Memory and Aging Center (K.B.C., N.D., M.Y., S.W.-L., C.F., B.L.M., J.K.), Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco; Department of Psychiatry and Neurochemistry (H.Z., K.B., A.B.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B., A.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease (H.Z., K.B., A.B.), UCL Institute of Neurology, Queen ; UK Dementia Research Institute at UCL (H.Z.), London, UK; Department of Psychiatry (W.H.), University of British Columbia, Vancouver, Canada; and Department of Neurological Sciences (J.A.S., D.A.B.), Rush Medical College, Chicago, IL.
Rush University Medical Center · US
Funding
Research Education ComponentP30AG062422 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HOWARD J ROSEN · 2019 to 2026
$36.9MMechanisms of Executive Decline in Normal AgingR01AG032289 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Kaitlin B Casaletto, JOEL H KRAMER · 2009 to 2026
$8.3MEffects of chronic inflammation on brain structure and functionR01AG048234 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KRAMER, JOEL H · 2015 to 2019
$3.2MCan Behavior Shape Neural Health? Identifying Modifiable Factors to Prevent Cognitive Decline in AgeK23AG058752 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CASALETTO, KAITLIN B · 2018 to 2022
$994kNIA NIH HHS K23 AG058752NIA NIH HHS P30 AG062422NIA NIH HHS R01 AG032289NIA NIH HHS R01 AG048234
Abstract
objectiveTo test the hypothesis that fundamental relationships along the amyloid, tau, and neurodegeneration (A/T/N) cascade depend on synaptic integrity in older adults in vivo and postmortem.
methodsThe 2 independent observational, cross-sectional cohorts included (1) in vivo community-dwelling, clinically normal adults from the University of California, San Francisco Memory and Aging Center who completed lumbar puncture and MRI (exclusion criteria, Clinical Dementia Rating score >0) and (2) postmortem decedents from the Rush Memory and Aging Project (exclusion criteria, inability to sign informed consent). In vivo measures included CSF synaptic proteins (synaptotagmin-1, synaptosome associated protein-25, neurogranin, and growth associated protein-43), β-amyloid (Aβ
resultsSixty-eight in vivo older adults (age 71 years, 43% female) and 633 decedents (age 90 years, 68% female, 34% clinically normal) were included. Each in vivo CSF synaptic protein moderated the relationship between Aβ
conclusionsPathogenic relationships of Aβ and tau may depend on synaptic state. Synaptic markers may help identify risk or resilience to AD proteinopathy.
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