Evidence mapPaperPMID 42327728Full record

ReviewFrontiers in immunology2026

Agitation, Alzheimer's disease, and autophagy: mechanistic insights into aging pathways, gut microbiome, and artificial intelligence.

Kenneth Maiese

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

1 author.

Kenneth MaieseInnovation and Commercialization, National Institutes of Health, Bethesda, MD, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The presentation of mood disorders that involve agitation and anxiety in patients with cognitive loss represent significant challenges for the care of patients with Alzheimer's disease (AD). Additional concerns rest with the rising lifespan and aging of the global population with expectations that over the next two decades more than 50 percent of the elderly population will suffer from mental health disease and at least 30 million of these individuals will also succumb to cognitive loss with AD. Although current treatments for mood disorders and cognitive loss can have a multi-modal approach with behavioral therapy, cognitive training sessions, physical exercise, nutritional care, environmental changes, and disease modifying agents, these therapies are primarily symptomatic in nature that do not halt disease progression and possess risks for further nervous system insults. Given these consideration, novel work that addresses the shared underlying pathways for mood disorders and cognitive loss with autophagy and related mechanisms of programmed cell death, aging and cellular senescence, perivascular system dysfunction, inflammatory microglial cell dynamics, oxidative stress, metabolic pathways that involve diabetes mellitus and apolipoprotein E, the gut microbiota, glucagon-like peptide-1 receptor agonism, innovative diagnostic strategies, artificial intelligence, and machine learning can offer rewarding avenues for the innovative development of therapeutic strategies that address disease onset and progression of these disorders. These pathways that oversee mood disorders and cognitive are both critical and complex in their intimate relationships and warrant in-depth knowledge of the mechanisms that can influence biological outcome for clinical translation.

Indexed as

AgingAlzheimer DiseaseArtificial IntelligenceAutophagyGastrointestinal MicrobiomeAnimalsHumansAlzheimer’s diseaseautophagycell senescencediabetes mellitusgut microbiotamechanistic target of rapamycin (mTOR)mood disordersoxidative stress

Identifiers

PMID42327728
PMCPMC13278926

What Socratic holds

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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 Socratic graph.