Evidence map›Paper›PMID 39460876›Full record

ReviewHuman cell2024

Brain inflammaging in the pathogenesis of late-life depression.

Toshiaki Ishizuka, Wataru Nagata, Keiichi Nakagawa, Sayaka Takahashi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Human cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
–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

9 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  4. Review
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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.

Toshiaki IshizukaDepartment of Pharmacology, National Defense Medical College, 3-2, Namiki, Tokorozawa, Saitama, 359-8513, Japan. tishizu@ndmc.ac.jp.ORCID http://orcid.org/0000-0002-7887-8150
Wataru NagataDepartment of Pharmacology, National Defense Medical College, 3-2, Namiki, Tokorozawa, Saitama, 359-8513, Japan.
Keiichi NakagawaDepartment of Pharmacology, National Defense Medical College, 3-2, Namiki, Tokorozawa, Saitama, 359-8513, Japan.
Sayaka TakahashiDepartment of Pharmacology, National Defense Medical College, 3-2, Namiki, Tokorozawa, Saitama, 359-8513, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Late-life depression (LLD) is a prevalent mental disorder among older adults. Previous studies revealed that many pathologic factors are associated with the onset and development of LLD. However, the precise mechanisms that cause LLD remain elusive. Aging induces chronic inflammatory changes mediated by alterations of immune responses. The chronic systemic inflammation termed "inflammaging" is linked to the etiology of aging-related disorders. Aged microglia induce senescence-associated secretory phenotype (SASP) and transition to M1-phenotype, cause neuroinflammation, and diminish neuroprotective effects. In addition, there is an age-dependent loss of blood-brain barrier (BBB) integrity. As the BBB breakdown can lead to invasion of immune cells into brain parenchyma, peripheral immunosenescence may cause microglial activation and neuroinflammation. Therefore, it is suggested that these mechanisms related to brain inflammaging may be involved in the pathogenesis of LLD. In this review, we described the role of brain inflammaging in LLD. Pharmacologic approaches to prevent brain inflammaging appears to be a promising strategy for treating LLD.

Indexed as

BrainDepressionAgingAnimalsBlood-Brain BarrierFemaleHumansMaleMetabolic ReprogrammingMicrogliaTh17 CellsBBB breakdownInflammasome activationLate-life depressionMetabolic reprogrammingSenescence-associated secretory phenotype (SASP)

Identifiers

What OpenQuestion holds

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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.