Evidence map›Paper›PMID 35525980›Full record

ReviewMolecular neurodegeneration2022

Circadian clocks, cognition, and Alzheimer's disease: synaptic mechanisms, signaling effectors, and chronotherapeutics.

Kari R Hoyt, Karl Obrietan

Open access · goldAbstract readReview
In one paragraph

Review in Molecular neurodegeneration, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 2 pooled it
6.3field-weighted citation impact, top 2% 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

45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.

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  20. Intestinal Clock Promotes Cognitive Memory Through Adenosine Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    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

2 authors at 1 institution in 1 country.

Kari R HoytDivision of Pharmaceutics and Pharmacology, Ohio State University, 412 Riffe Building, 12th Ave, Columbus, OH, 43210, USA. Hoyt.31@osu.edu.
Karl ObrietanDepartment of Neuroscience, Ohio State University, Graves Hall, 333 W. 10th Ave, Columbus, OH, 43210, USA. Obrietan.1@osu.edu.ORCID 0000-0002-7525-7121
The Ohio State University · US

Funding

Alzheimer's disease pathogenesis and the desynchronization of cortico-limbic circadian rhythmsR01AG065830 · NIA · OHIO STATE UNIVERSITY · PI HOYT, KARI RENE, OBRIETAN, KARL H · 2020 to 2024
$3.5M
Hippocampal Cellular RhythmsR01MH103361 · NIMH · OHIO STATE UNIVERSITY · PI OBRIETAN, KARL H · 2014 to 2018
$2.0M
MAPK signaling: gates, oscillators and circadian timingR01GM133032 · NIGMS · OHIO STATE UNIVERSITY · PI HOYT, KARI RENE, OBRIETAN, KARL H · 2020 to 2023
$1.9M
NIA NIH HHS R01 AG065830NIGMS NIH HHS R01 GM133032NIMH NIH HHS R01 MH103361
6 · The paper itself

Abstract

Modulation of basic biochemical and physiological processes by the circadian timing system is now recognized as a fundamental feature of all mammalian organ systems. Within the central nervous system, these clock-modulating effects are reflected in some of the most complex behavioral states including learning, memory, and mood. How the clock shapes these behavioral processes is only now beginning to be realized. In this review we describe recent findings regarding the complex set of cellular signaling events, including kinase pathways, gene networks, and synaptic circuits that are under the influence of the clock timing system and how this, in turn, shapes cognitive capacity over the circadian cycle. Further, we discuss the functional roles of the master circadian clock located in the suprachiasmatic nucleus, and peripheral oscillator populations within cortical and limbic circuits, in the gating of synaptic plasticity and memory over the circadian cycle. These findings are then used as the basis to discuss the connection between clock dysregulation and cognitive impairments resulting from Alzheimer's disease (AD). In addition, we discuss the conceptually novel idea that in AD, there is a selective disruption of circadian timing within cortical and limbic circuits, and that it is the disruption/desynchronization of these regions from the phase-entraining effects of the SCN that underlies aspects of the early- and mid-stage cognitive deficits in AD. Further, we discuss the prospect that the disruption of circadian timing in AD could produce a self-reinforcing feedback loop, where disruption of timing accelerates AD pathogenesis (e.g., amyloid deposition, oxidative stress and cell death) that in turn leads to a further disruption of the circadian timing system. Lastly, we address potential therapeutic approaches that could be used to strengthen cellular timing networks and, in turn, how these approaches could be used to improve cognitive capacity in Alzheimer's patients.

Indexed as

Alzheimer DiseaseCircadian ClocksAnimalsCircadian RhythmCognitionDrug ChronotherapyHumansMammalsAlzheimer’s diseaseChronotherapeuticsCircadianCortexLimbic systemMemorySuprachiasmatic nucleus

Identifiers

PMID35525980
PMCPMC9078023
OpenAlexW4229016791

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.