Evidence map›Paper›PMID 19076369›Full record

ReviewAnnals of the New York Academy of Sciences2008

Glutamate and neurotrophic factors in neuronal plasticity and disease.

Mark P Mattson

Open access · greenAbstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 262 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
262citing papers in PubMed, 5 pooled it
12.0field-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

262 citing papers in PubMed, 5 syntheses or guidelines pooled it, 634 citations in OpenAlex.

  1. Pooled it
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  13. Protective effect of the aqueous extract ofIBRO neuroscience reports · 2026
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202 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

1 author at 1 institution in 1 country.

Mark P MattsonLaboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA. mattsonm@grc.nia.nih.gov
National Institutes of Health · US

Funding

Synaptic Plasticity In Aging And Neurodegenerative DisordersZIAAG000317 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$8.5M
Neuroprotective And Neurorestorative Signaling Mechanisms in Alzheimer's DiseaseZIAAG000314 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$6.7M
Synaptic Plasticity In Aging And Neurodegenerative DisordersZ01AG000317 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK P · 2001 to 2008
$1.7M
Intramural NIH HHS Z01 AG000317
6 · The paper itself

Abstract

Glutamate's role as a neurotransmitter at synapses has been known for 40 years, but glutamate has since been shown to regulate neurogenesis, neurite outgrowth, synaptogenesis, and neuron survival in the developing and adult mammalian nervous system. Cell-surface glutamate receptors are coupled to Ca(2+) influx and release from endoplasmic reticulum stores, which causes rapid (kinase- and protease-mediated) and delayed (transcription-dependent) responses that change the structure and function of neurons. Neurotrophic factors and glutamate interact to regulate developmental and adult neuroplasticity. For example, glutamate stimulates the production of brain-derived neurotrophic factor (BDNF), which, in turn, modifies neuronal glutamate sensitivity, Ca(2+) homeostasis, and plasticity. Neurotrophic factors may modify glutamate signaling directly, by changing the expression of glutamate receptor subunits and Ca(2+)-regulating proteins, and also indirectly by inducing the production of antioxidant enzymes, energy-regulating proteins, and antiapoptotic Bcl-2 family members. Excessive activation of glutamate receptors, under conditions of oxidative and metabolic stress, may contribute to neuronal dysfunction and degeneration in diseases ranging from stroke and Alzheimer's disease to psychiatric disorders. By enhancing neurotrophic factor signaling, environmental factors such as exercise and dietary energy restriction, and chemicals such as antidepressants may optimize glutamatergic signaling and protect against neurological disorders.

Indexed as

Alzheimer DiseaseAnimalsBrain-Derived Neurotrophic FactorBrain DiseasesGlutamic AcidHumansNerve Growth FactorsNeuritesNeurogenesisNeuronal PlasticityNeuronsParkinson DiseaseReceptors, GlutamateReceptors, Nerve Growth FactorSignal TransductionStrokeBrain-Derived Neurotrophic FactorGlutamic AcidNerve Growth FactorsReceptors, GlutamateReceptors, Nerve Growth Factor

Identifiers

PMID19076369
PMCPMC2614307
OpenAlexW2032444015

What OpenQuestion holds

Textmetadata
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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.