Evidence map›Paper›PMID 29933646›Full record

ReviewMedical sciences (Basel, Switzerland)2018

Circadian Rhythm and Alzheimer's Disease.

Jan Homolak, Monika Mudrovčić, Barbara Vukić, Karlo Toljan

Open access · goldAbstract readReview
In one paragraph

Review in Medical sciences (Basel, Switzerland), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.

  1. Pooled it
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  10. Sleep trajectories across three cognitive-aging pathways in community older adults.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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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

4 authors at 2 institutions in 1 country.

Jan HomolakDepartment of Pharmacology, University of Zagreb School of Medicine, Šalata 3, Zagreb 10 000, Croatia. homolakjan@gmail.com.ORCID 0000-0003-1508-3243
Monika MudrovčićUniversity Hospital for Infectious Diseases, Mirogojska cesta 8, Zagreb 10 000, Croatia. monikamudrovcic@yahoo.com.
Barbara VukićUniversity of Zagreb School of Medicine, Šalata 3, Zagreb 10 000, Croatia. bvukic1@gmail.com.
Karlo ToljanDepartment of Pathophysiology, University of Zagreb School of Medicine, Kišpaticeva 12, Zagreb 10 000, Croatia. karlo.toljan@gmail.com.ORCID 0000-0002-3189-9659
University of Zagreb · HRUniversity Hospital Centre Zagreb · HR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder with a growing epidemiological importance characterized by significant disease burden. Sleep-related pathological symptomatology often accompanies AD. The etiology and pathogenesis of disrupted circadian rhythm and AD share common factors, which also opens the perspective of viewing them as a mutually dependent process. This article focuses on the bi-directional relationship between these processes, discussing the pathophysiological links and clinical aspects. Common mechanisms linking both processes include neuroinflammation, neurodegeneration, and circadian rhythm desynchronization. Timely recognition of sleep-specific symptoms as components of AD could lead to an earlier and correct diagnosis with an opportunity of offering treatments at an earlier stage. Likewise, proper sleep hygiene and related treatments ought to be one of the priorities in the management of the patient population affected by AD. This narrative review brings a comprehensive approach to clearly demonstrate the underlying complexities linking AD and circadian rhythm disruption. Most clinical data are based on interventions including melatonin, but larger-scale research is still scarce. Following a pathophysiological reasoning backed by evidence gained from AD models, novel anti-inflammatory treatments and those targeting metabolic alterations in AD might prove useful for normalizing a disrupted circadian rhythm. By restoring it, benefits would be conferred for immunological, metabolic, and behavioral function in an affected individual. On the other hand, a balanced circadian rhythm should provide greater resilience to AD pathogenesis.

Indexed as

Alzheimer’s diseasecircadian rhythmmelatoninpathophysiologysleep

Identifiers

PMID29933646
PMCPMC6164904
OpenAlexW2809220022

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.