Evidence map›Paper›PMID 31537707›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019

Amyloid-Beta Modulates Low-Threshold Activated Voltage-Gated L-Type Calcium Channels of Arcuate Neuropeptide Y Neurons Leading to Calcium Dysregulation and Hypothalamic Dysfunction.

Makoto Ishii, Abigail J Hiller, Laurie Pham, Matthew J McGuire, Costantino Iadecola, Gang Wang

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Crosstalk between bone and brain in Alzheimer's disease: Mechanisms, applications, and perspectives.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Amyloid AβInternational journal of molecular sciences · 2022
    Article
  10. Article
  11. Article
  12. CaInternational journal of molecular sciences · 2022
    Review
  13. Potential mechanisms underlying lithium treatment for Alzheimer's disease and COVID-19.European review for medical and pharmacological sciences · 2022
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Makoto IshiiFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, New York 10065, and mishii@med.cornell.edu.ORCID 0000-0003-3397-9908
Abigail J HillerFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, New York 10065, and.
Laurie PhamFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, New York 10065, and.
Matthew J McGuireFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, New York 10065, and.
Costantino IadecolaFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, New York 10065, and.
Gang WangFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, New York 10065, and.
Cornell University · US

Funding

Overexpression of the amyloid precursor protein and cerebrovascular regulationR01NS037853 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI Costantino Iadecola · 1998 to 2026
$10.6M
Pathobiology of Hypothalamic and Metabolic Dysfunction in Normal Aging and Alzheimer's DiseaseK08AG051179 · NIA · WEILL MEDICAL COLL OF CORNELL UNIV · PI ISHII, MAKOTO · 2015 to 2019
$864k
NIA NIH HHS K08 AG051179NINDS NIH HHS R01 NS037853
6 · The paper itself

Abstract

Weight loss is an early manifestation of Alzheimer's disease that can precede the cognitive decline, raising the possibility that amyloid-β (Aβ) disrupts hypothalamic neurons critical for the regulation of body weight. We previously reported that, in young transgenic mice overexpressing mutated amyloid precursor protein (Tg2576), Aβ causes dysfunction in neuropeptide Y (NPY)-expressing hypothalamic arcuate neurons before plaque formation. In this study, we examined whether Aβ causes arcuate NPY neuronal dysfunction by disrupting intracellular Ca

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsArcuate Nucleus of HypothalamusCalciumCalcium Channels, L-TypeFeeding BehaviorFemaleGhrelinHomeostasisMaleMembrane PotentialsMice, TransgenicNeuronsNeuropeptide YPeptide FragmentsAmyloid beta-Peptidesamyloid beta-protein (1-42)CalciumCalcium Channels, L-TypeGhrelinNeuropeptide YPeptide FragmentsAlzheimer's diseaseelectrophysiologyghrelinhypothalamusleptinneuropeptide Y

Identifiers

PMID31537707
PMCPMC6820205
OpenAlexW2974222077

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.