Evidence map›Paper›PMID 25009495›Full record

ReviewFrontiers in aging neuroscience2014

Glia and zinc in ageing and Alzheimer's disease: a mechanism for cognitive decline?

Sara M Hancock, David I Finkelstein, Paul A Adlard

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in aging neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Molecular mechanism of zinc neurotoxicity in Alzheimer's disease.Environmental science and pollution research international · 2020
    Review
  10. Crosstalk between zinc and free fatty acids in plasma.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2019
    Review
  11. Article
  12. Dietary Zinc Acts as a Sleep Modulator.International journal of molecular sciences · 2017
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. BRCA1 and p53 tumor suppressor molecules in Alzheimer's disease.International journal of molecular sciences · 2015
    Review
  18. Article
  19. Review
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 1 institution in 1 country.

Sara M HancockSynaptic Neurobiology Laboratory, Florey Institute of Neuroscience and Mental Health Parkville, VIC, Australia.
David I FinkelsteinParkinson's Disease Laboratory, Florey Institute of Neuroscience and Mental Health Parkville, VIC, Australia.
Paul A AdlardSynaptic Neurobiology Laboratory, Florey Institute of Neuroscience and Mental Health Parkville, VIC, Australia.
Florey Institute of Neuroscience and Mental Health · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Normal ageing is characterized by cognitive decline across a range of neurological functions, which are further impaired in Alzheimer's disease (AD). Recently, alterations in zinc (Zn) concentrations, particularly at the synapse, have emerged as a potential mechanism underlying the cognitive changes that occur in both ageing and AD. Zn is now accepted as a potent neuromodulator, affecting a variety of signaling pathways at the synapse that are critical to normal cognition. While the focus has principally been on the neuron: Zn interaction, there is a growing literature suggesting that glia may also play a modulatory role in maintaining both Zn ion homeostasis and the normal function of the synapse. Indeed, zinc transporters (ZnT's) have been demonstrated in glial cells where Zn has also been shown to have a role in signaling. Furthermore, there is increasing evidence that the pathogenesis of AD critically involves glial cells (such as astrocytes), which have been reported to contribute to amyloid-beta (Aβ) neurotoxicity. This review discusses the current evidence supporting a complex interplay of glia, Zn dyshomeostasis and synaptic function in ageing and AD.

Indexed as

ageing (aging)Alzheimer diseaseastrocyte-neuron interactionsmicrogliasynapse regulationzinc

Identifiers

PMID25009495
PMCPMC4069481
OpenAlexW2160685247

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.