Evidence map›Paper›PMID 30568576›Full record

ReviewFrontiers in cellular neuroscience2018

Disorders of Body Weight, Sleep and Circadian Rhythm as Manifestations of Hypothalamic Dysfunction in Alzheimer's Disease.

Abigail J Hiller, Makoto Ishii

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in cellular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
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  6. Article
  7. Nutrition: A non-negligible factor in the pathogenesis and treatment of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
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  14. Snoring and risk of dementia: a prospective cohort and Mendelian randomization study.medRxiv : the preprint server for health sciences · 2023
    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

2 authors at 1 institution in 1 country.

Abigail J HillerFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, Cornell University, New York, NY, United States.
Makoto IshiiFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, Cornell University, New York, NY, United States.
MIND Research Institute · US

Funding

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 AG051179
6 · The paper itself

Abstract

While cognitive decline and memory loss are the major clinical manifestations of Alzheimer's disease (AD), they are now recognized as late features of the disease. Recent failures in clinical drug trials highlight the importance of evaluating and treating patients with AD as early as possible and the difficulties in developing effective therapies once the disease progresses. Since the pathological hallmarks of AD including the abnormal aggregation of amyloid-beta (Aβ) and tau can occur decades before any significant cognitive decline in the preclinical stage of AD, it is important to identify the earliest clinical manifestations of AD and elucidate their underlying cellular and molecular mechanisms. Importantly, metabolic and non-cognitive manifestations of AD such as weight loss and alterations of peripheral metabolic signals can occur before the onset of cognitive symptoms and worsen with disease progression. Accumulating evidence suggests that the major culprit behind these early metabolic and non-cognitive manifestations of AD is AD pathology causing dysfunction of the hypothalamus, a brain region critical for integrating peripheral signals with essential homeostatic physiological functions. Here, we aim to highlight recent developments that address the role of AD pathology in the development of hypothalamic dysfunction associated with metabolic and non-cognitive manifestations seen in AD. Understanding the mechanisms underlying hypothalamic dysfunction in AD could give key new insights into the development of novel biomarkers and therapeutic targets.

Indexed as

amyloid-betacircadian rhythmdementiadiabeteshypothalamusobesitysleeptau

Identifiers

PMID30568576
PMCPMC6289975
OpenAlexW2902077545

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.