Cited by 167Alzheimer's disease research and treatmentsNeuroscience and Neuropharmacology ResearchCalcium signaling and nucleotide metabolism

Calcium signalling and Alzheimer's disease

Berridge, Michael J.·2011·Neurochemical Research

Abstract

New insights into how Ca(2+) regulates learning and memory have begun to provide clues as to how the amyloid-dependent remodelling of neuronal Ca(2+) signalling pathways can disrupt the mechanisms of learning and memory in Alzheimer's disease (AD). The calcium hypothesis of AD proposes that activation of the amyloidogenic pathway remodels the neuronal Ca(2+) signalling pathways responsible for cognition by enhancing the entry of Ca(2+) and/or the release of internal Ca(2+) by ryanodine receptors or InsP(3) receptors. The specific proposal is that Ca(2+) signalling remodelling results in a persistent elevation in the level of Ca(2+) that constantly erases newly acquired memories by enhancing the mechanism of long-term depression (LTD). Neurons can still form memories through the process of LTP, but this stored information is rapidly removed by the persistent activation of LTD. Further dysregulation in Ca(2+) signalling will then go on to induce the neurodegeneration that characterizes the later stages of dementia.

Integrity signals

Registry

Crossref · 10.1007/s11064-010-0371-4

Cites

53 of 53 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

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?

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Berridge, M. J.
Affiliations
Babraham Institute (GB)
Corresponding author
Berridge, Michael J.
Venue
Neurochemical Research
Published
2010-12-24
Volume
36
Issue
7
Pages
1149-1156
ISSN
  • 0364-3190 (ISSN-L)
  • 1573-6903
OpenAlex
W2086253463
Cited by
167
References
53
Citations by year
2026: 2 · 2025: 5 · 2024: 2 · 2023: 15 · 2022: 10 · 2021: 14 · 2020: 15 · 2019: 11 · 2018: 12 · 2017: 8 · 2016: 11 · 2015: 17 · 2014: 10 · 2013: 13 · 2012: 13
FWCI
7.37
Type
journal article
Language
en
Open access
closed
Locations
  • Neurochemical Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
Biotechnology and Biological Sciences Research Council (BBS/E/B/0000C134)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
Keywords
calcium signaling, Alzheimer's disease, calcium hypothesis, amyloid, ryanodine receptor, IP3 receptor, long-term depression, long-term potentiation, memory consolidation, neurodegeneration, learning and memory
MeSH terms
Actins, Alzheimer Disease, Amyloid, Calcium, Humans, Learning, Memory, Neurons, Amyloid beta-Peptides, Long-Term Potentiation, Receptors, AMPA, Ryanodine Receptor Calcium Release Channel, Calcium Signaling

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