Evidence map›Paper›PMID 42036573›Full record

ReviewAdvances in experimental medicine and biology2026

Complex Neurobiological Mechanisms and Risk Factors Underlying Late-Life Depression.

Kang Joon Lee, Yong-Ku Kim

Abstract readReview
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In one paragraph

Review in Advances in experimental medicine and biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Kang Joon LeeDepartment of Psychiatry, Inje University, College of Medicine, Ilsanpaik Hospital, Goyang, Republic of Korea. lkj@paik.ac.kr.
Yong-Ku KimDepartment of Psychiatry, College of Medicine, Korea University Ansan Hospital, Ansan, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Late-life depression (LLD) is a prevalent and debilitating disease closely associated with cognitive decline, exacerbation of chronic medical illness, decreased quality of life, and increased societal burden. This review explores the complex neurobiological mechanisms and key risk factors underlying LLD. Inflammation, particularly involving cytokines such as IL-6 and TNF-α and the activation of the NLRP3 inflammasome, plays a central role. Genetic vulnerability, including polymorphisms in serotonin-transporter-linked polymorphic region (5-HTTLPR), BDNF Val66Met, and methylenetetrahydrofolate reductase (MTHFR), interacts with environmental stressors to increase susceptibility. Dysregulation of neurotransmitters such as serotonin, dopamine, norepinephrine, glutamate, and GABA contributes to core depressive symptoms. LLD is also characterized by functional disruptions in large-scale brain networks and structural changes including cortical thinning and hippocampal atrophy. Additionally, HPA (hypothalamic-pituitary-adrenal) axis hyperactivity, gut microbiota dysbiosis, and metabolic disorders such as hypertension and diabetes further exacerbate LLD.LLD is a multifactorial disorder involving complex interactions among neurobiological systems. Effective prevention and management require an integrated, multidisciplinary approach that considers inflammation, genetics, neurotransmission, and brain structure alterations.

Indexed as

BrainDepressionAnimalsGenetic Predisposition to DiseaseHumansHypothalamo-Hypophyseal SystemNeurotransmitter AgentsRisk FactorsNeurotransmitter AgentsDysbiosisGeneticsGut–brain axisInflammationLate-life depressionNeurobiologyNeurotransmitter

Identifiers

What Socratic holds

Textmetadata
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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.