Cited by 105Alzheimer's disease research and treatmentsNeuroscience and Neuropharmacology ResearchDementia and Cognitive Impairment Research

Gain-of-function mutations in protein kinase Cα (PKCα) may promote synaptic defects in Alzheimer’s disease

Open access
Alfonso, Stephanie I., Callender, Julia A., Hooli, Basavaraj, Antal, Corina E., Mullin, Kristina, Sherman, Mathew A., Lesné, Sylvain E., Leitges, Michael +3 more·2016·Science Signaling

Abstract

PKCα variants in some patients with Alzheimer’s disease may mediate the pathological effects of amyloid-β.

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Integrity signals

Registry

Crossref · 10.1126/scisignal.aaf6209

Cites

54 of 54 references verified0 citation errors · 0 not checkable

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  • The PRKCA gene encodes protein kinase Cα (PKCα), which participates in synaptic loss resulting from the accumulation of amyloid-β in AD neuropathology.

    “The PRKCA gene encodes protein kinase Cα (PKCα), which participates in synaptic loss resulting from the accumulation of amyloid-β (Aβ) in AD neuropathology [73, 74].”

    From Sex-specific DNA methylation differences in Alzheimer’s disease pathology (2021) · cites this paper as [73]

    The Abstract identifies PRKCA as the gene encoding PKCα, and the Results (‘PKCα is necessary for the synaptic effects of Aβ’) show that PKCα is required for Aβ-related synaptic depression in mouse hippocampal slices. The Discussion links Aβ accumulation with synaptic loss in AD, but the study does not directly show that PKCα causes synaptic loss in human AD. (LLM, conf=0.82)

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Research works printed but not linked: 1

  1. [14]Alfonso S Kessels HW Banos CC Chan TR Lin ET Kumaravel G Scannevin RH Rhodes KJ Huganir R Guckian KM Dunah AW Malinow R Synapto-depressive effects of amyloid beta require PICK1 Eur J Neurosci 39 1225 1233 2014 24713001 PMC3983572

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Authors
Alfonso, S. I., Callender, J. A., Hooli, B., Antal, C. E., Mullin, K., Sherman, M. A., Lesné, S. E., Leitges, M., Newton, A. C., Tanzi, R. E., & Malinow, R.
Affiliations
  • University of California San Diego (US)
  • Harvard University (US)
  • University of Minnesota (US)
  • University of Oslo (NO)
Corresponding author
  • Alfonso, Stephanie I.
  • Callender, Julia A.
  • Hooli, Basavaraj
  • Antal, Corina E.
  • Newton, Alexandra C.
  • Tanzi, Rudolph E.
  • Malinow, Roberto
Venue
Science Signaling
Published
2016-05-10
Volume
9
Issue
427
Pages
ra47-ra47
ISSN
  • 1937-9145 (ISSN-L)
  • 1945-0877
OpenAlex
W2359021079
Cited by
103
References
54
Citations by year
2026: 7 · 2025: 11 · 2024: 4 · 2023: 12 · 2022: 11 · 2021: 14 · 2020: 9 · 2019: 12 · 2018: 7 · 2017: 11 · 2016: 5
FWCI
9.39
Type
journal article
Language
en
Open access
Locations
  • Science Signaling (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
Funders
  • NIH (GM43154, MH060009, AG032132, GM007752, DGE1144086)
  • Cure Alzheimer's Fund
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, protein kinase C alpha, gain-of-function mutations, amyloid-beta, synaptic dysfunction, late-onset Alzheimer's disease, familial Alzheimer's disease, synaptic depression, hippocampus
MeSH terms
Protein Domains, Alzheimer Disease, Animals, Chlorocebus aethiops, Family Health, Hippocampus, Humans, Mutation, Neoplasms, Synapses, Genome, Human, Genome, COS Cells, Neurodegenerative Diseases, Mice, Protein Kinase C-alpha

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