Evidence map›Paper›PMID 15056725›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004

Neuronal zinc exchange with the blood vessel wall promotes cerebral amyloid angiopathy in an animal model of Alzheimer's disease.

Avi L Friedlich, Joo-Yong Lee, Thomas van Groen, Robert A Cherny, Irene Volitakis, Toby B Cole, Richard D Palmiter, Jae-Young Koh, Ashley I Bush

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

55 citing papers in PubMed, 138 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. PTPRM Is Critical for Synapse Formation Regulated by Zinc Ion.Frontiers in molecular neuroscience · 2022
    Article
  7. Novel Biomarkers of Alzheimer's Disease: Based Upon N-methyl-D-aspartate Receptor Hypoactivation and Oxidative Stress.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2021
    Review
  8. Article
  9. Article
  10. β-Amyloid aggregation and heterogeneous nucleation.Protein science : a publication of the Protein Society · 2019
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Oxidative Stress, Synaptic Dysfunction, and Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2017
    Review
  17. Article
  18. Vascular cognitive impairment and dementia.Biochimica et biophysica acta · 2016
    Review
  19. Review
  20. Article
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

9 authors at 6 institutions in 4 countries.

Avi L FriedlichLaboratory for Oxidation Biology, Genetics and Aging Research Unit, Massachusetts General Hospital, and Department of Psychiatry, Harvard Medical School, Charlestown, Massachusetts 02129-4404, USA.
Joo-Yong Lee
Thomas van Groen
Robert A Cherny
Irene Volitakis
Toby B Cole
Richard D Palmiter
Jae-Young Koh
Ashley I Bush
Howard Hughes Medical Institute · USMental Health Research Institute · AUUlsan College · KRHarvard University · USMassachusetts General Hospital · USUniversity of Eastern Finland · FI

Funding

ZINC AND ALZHEIMERS DISEASE PATHOPHYSIOLOGYR01AG012686 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI BUSH, ASHLEY I · 1998 to 2004
$1.3M
ENERGY METABOLISM IN HUNTINGTON'S DISEASEF32NS010874 · NINDS · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI FRIEDLICH, AVI L · 1999 to 2002
$77k
NIA NIH HHS 5R01AG12686-09NIA NIH HHS R01 AG012686NINDS NIH HHS F32 NS010874NINDS NIH HHS F32NS10874
6 · The paper itself

Abstract

Cerebral amyloid angiopathy (CAA) is common in Alzheimer's disease (AD) and may contribute to dementia and cerebral hemorrhage. Parenchymal beta-amyloid deposition is dependent on the activity of zinc transporter 3 (ZnT3), a neocortical synaptic vesicle membrane protein that causes enrichment of exchangeable Zn2+ in the vesicle, which is externalized on neurotransmission. However, the contribution of zinc to vascular beta-amyloid deposition remains unclear. Here, we identify for the first time an exchangeable pool of Zn2+ in the cerebrovascular wall of normal mice. This histochemically reactive Zn2+ is enriched in CAA in a transgenic mouse model of AD (Tg2576), and a dramatic reduction of CAA occurs after targeted disruption of the Znt3 gene in these mice. Also, in Znt3 knock-out mice, the amount of exchangeable Zn2+ [detected by N-(6-methoxy-8-quinolyl)-p-carboxybenzoylsulphonamide (TFL-Zn)] in the perivascular space was significantly decreased in the neocortex but not in peripheral organs. ZnT3 was not detected in the cerebral vessel walls or in blood components of wild-type mice. Thus, synaptic ZnT3 activity may promote CAA by indirectly raising exchangeable Zn2+ concentrations in the perivascular spaces of the brain.

Indexed as

Cation Transport ProteinsAlzheimer DiseaseAnimalsBlood VesselsCarrier ProteinsCerebral Amyloid AngiopathyCopperDisease Models, AnimalGenetic Predisposition to DiseaseHumansMembrane ProteinsMembrane Transport ProteinsMiceMice, TransgenicNeocortexOrgan SpecificityCarrier ProteinsCation Transport ProteinsCopperMembrane ProteinsMembrane Transport ProteinsSLC30A3 protein, humanSlc30a3 protein, mouseZinc

Identifiers

PMID15056725
PMCPMC6730042
OpenAlexW2070214311

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.