Evidence map›Paper›PMID 26136654›Full record

ReviewFrontiers in neuroscience2015

Noradrenergic dysfunction in Alzheimer's disease.

Mary Gannon, Pulin Che, Yunjia Chen, Kai Jiao, Erik D Roberson, Qin Wang

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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

110 citing papers in PubMed, 1 synthesis or guideline pooled it, 205 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Brexpiprazole for the Treatment of Agitation Associated with Dementia due to Alzheimer's Disease: Clinical Perspectives.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2026
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Role of NLRP3 Inflammasome in Chronic Pain and Alzheimer's Disease-A Review.Journal of biochemical and molecular toxicology · 2025
    Review
  20. Article

50 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

6 authors at 1 institution in 1 country.

Mary GannonDepartment of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham Birmingham, AL, USA.
Pulin CheDepartment of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham Birmingham, AL, USA.
Yunjia ChenDepartment of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham Birmingham, AL, USA.
Kai JiaoDepartment of Genetics, University of Alabama at Birmingham Birmingham, AL, USA.
Erik D RobersonDepartment of Neurology, University of Alabama at Birmingham Birmingham, AL, USA.
Qin WangDepartment of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham Birmingham, AL, USA.
University of Alabama at Birmingham · US

Funding

Regulation of novel alpha2A adrenergic receptor signaling by spinophilinR01MH081917 · NIMH · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WANG, QIN · 2009 to 2019
$3.9M
Preclinical test for the efficacy of adrenergic agents in treatment of ADR21AG042716 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WANG, QIN · 2012 to 2013
$393k
NIA NIH HHS R21 AG042716NIMH NIH HHS R01 MH081917
6 · The paper itself

Abstract

The brain noradrenergic system supplies the neurotransmitter norepinephrine throughout the brain via widespread efferent projections, and plays a pivotal role in modulating cognitive activities in the cortex. Profound noradrenergic degeneration in Alzheimer's disease (AD) patients has been observed for decades, with recent research suggesting that the locus coeruleus (where noradrenergic neurons are mainly located) is a predominant site where AD-related pathology begins. Mounting evidence indicates that the loss of noradrenergic innervation greatly exacerbates AD pathogenesis and progression, although the precise roles of noradrenergic components in AD pathogenesis remain unclear. The aim of this review is to summarize current findings on noradrenergic dysfunction in AD, as well as to point out deficiencies in our knowledge where more research is needed.

Indexed as

adrenergic receptorsdegenerationdysfunctionnoradrenergic systemnorepinephrine

Identifiers

PMID26136654
PMCPMC4469831
OpenAlexW1583810538

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.