Evidence map›Paper›PMID 20212036›Full record

ReviewThe Journal of biological chemistry2010

Calcium signaling and amyloid toxicity in Alzheimer disease.

Angelo Demuro, Ian Parker, Grace E Stutzmann

Open access · hybridAbstract readReview
In one paragraph

Review in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 191 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
191citing papers in PubMed, 1 pooled it
19.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

191 citing papers in PubMed, 1 synthesis or guideline pooled it, 404 citations in OpenAlex.

  1. Pooled it
  2. Randomized phase 2a trial assessing a novel septin molecular glue in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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131 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Angelo DemuroDepartment of Neurobiology and Behavior, University of California, Irvine, California 92697, USA.
Ian Parker
Grace E Stutzmann
University of California, Irvine · USRosalind Franklin University of Medicine and Science · US

Funding

UC Irvine Alzheimer's Disease Research Center Induced Pluripotent Stem Cell CoreP50AG016573 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI LAFERLA, FRANK M · 2000 to 2019
$37.0M
Elementary Events of Intracellular Calcium SignalingR37GM048071 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI PARKER, IAN · 2011 to 2020
$5.3M
SPATIAL AND TEMPORAL ASPECTS OF INSP3 SIGNALLINGR01GM048071 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI PARKER, IAN · 1992 to 2010
$3.9M
Neuronal Calcium Dysregulation in Aging and Alzheimer's diseaseR01AG030205 · NIA · ROSALIND FRANKLIN UNIV OF MEDICINE & SCI · PI STUTZMANN, GRACE E. · 2008 to 2012
$1.4M
NIA NIH HHS AG30205NIA NIH HHS P50 AG016573NIA NIH HHS P50-AG16573NIA NIH HHS R01 AG030205NIGMS NIH HHS GM48071NIGMS NIH HHS R01 GM048071NIGMS NIH HHS R37 GM048071
6 · The paper itself

Abstract

Intracellular Ca(2+) signaling is fundamental to neuronal physiology and viability. Because of its ubiquitous roles, disruptions in Ca(2+) homeostasis are implicated in diverse disease processes and have become a major focus of study in multifactorial neurodegenerative diseases such as Alzheimer disease (AD). A hallmark of AD is the excessive production of beta-amyloid (Abeta) and its massive accumulation in amyloid plaques. In this minireview, we highlight the pathogenic interactions between altered cellular Ca(2+) signaling and Abeta in its different aggregation states and how these elements coalesce to alter the course of the neurodegenerative disease. Ca(2+) and Abeta intersect at several functional levels and temporal stages of AD, thereby altering neurotransmitter receptor properties, disrupting membrane integrity, and initiating apoptotic signaling cascades. Notably, there are reciprocal interactions between Ca(2+) pathways and amyloid pathology; altered Ca(2+) signaling accelerates Abeta formation, whereas Abeta peptides, particularly in soluble oligomeric forms, induce Ca(2+) disruptions. A degenerative feed-forward cycle of toxic Abeta generation and Ca(2+) perturbations results, which in turn can spin off to accelerate more global neuropathological cascades, ultimately leading to synaptic breakdown, cell death, and devastating memory loss. Although no cause or cure is currently known, targeting Ca(2+) dyshomeostasis as an underlying and integral component of AD pathology may result in novel and effective treatments for AD.

Indexed as

Calcium SignalingAlzheimer DiseaseAmyloid beta-PeptidesAnimalsCell DeathHomeostasisHumansPeptidesReceptors, NeurotransmitterSynapsesAmyloid beta-PeptidesPeptidesReceptors, Neurotransmitter

Identifiers

PMID20212036
PMCPMC2857063
OpenAlexW2009828191

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.