Evidence map›Paper›PMID 21234391›Full record

ArticleInternational journal of Alzheimer's disease2010

Insight into glutamate excitotoxicity from synaptic zinc homeostasis.

Atsushi Takeda

Open access · hybridAbstract read
In one paragraph

Article in International journal of Alzheimer's disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 39 citations in OpenAlex.

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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

1 author at 1 institution in 1 country.

Atsushi TakedaDepartment of Medical Biochemistry, School of Pharmaceutical Sciences, University of Shizuoka, Global COE, 52-1 Yada, Suruga-ku, Shizuoka 422-8526, Japan.
University of Shizuoka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Zinc is released from glutamatergic (zincergic) neuron terminals in the hippocampus, followed by the increase in Zn(2+) concentration in the intracellular (cytosol) compartment, as well as that in the extracellular compartment. The increase in Zn(2+) concentration in the intracellular compartment during synaptic excitation is mainly due to Zn(2+) influx through calcium-permeable channels and serves as Zn(2+) signaling as well as the case in the extracellular compartment. Synaptic Zn(2+) homeostasis is important for glutamate signaling and altered under numerous pathological processes such as Alzheimer's disease. Synaptic Zn(2+) homeostasis might be altered in old age, and this alteration might be involved in the pathogenesis and progression of Alzheimer's disease; Zinc may play as a key-mediating factor in the pathophysiology of Alzheimer's disease. This paper summarizes the role of Zn(2+) signaling in glutamate excitotoxicity, which is involved in Alzheimer's disease, to understand the significance of synaptic Zn(2+) homeostasis in the pathophysiology of Alzheimer's disease.

Identifiers

PMID21234391
PMCPMC3017909
OpenAlexW2013838286

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.