Evidence map›Paper›PMID 38716507›Full record

ArticleAging cell2024

Amygdala neuronal dyshomeostasis via 5-HT receptors mediates mood and cognitive defects in Alzheimer's disease.

Xin-Rong Wu, Xiao-Na Zhu, Yuan-Bo Pan, Xue Gu, Xian-Dong Liu, Si Chen, Yu Zhang, Tian-Le Xu, Nan-Jie Xu, Suya Sun

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
  2. 5-HTZoological research · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Foods (Basel, Switzerland) · 2025
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. 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

10 authors.

Xin-Rong WuDepartment of Neurology, Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiao-Na ZhuDepartment of Anatomy and Physiology, Collaborative Innovation Center for Brain Science, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yuan-Bo PanDepartment of Neurosurgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xue GuDepartment of Anatomy and Physiology, Collaborative Innovation Center for Brain Science, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xian-Dong LiuDepartment of Neurology, Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Si ChenDepartment of Anatomy and Physiology, Collaborative Innovation Center for Brain Science, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yu ZhangDepartment of Anatomy and Physiology, Collaborative Innovation Center for Brain Science, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Tian-Le XuDepartment of Anatomy and Physiology, Collaborative Innovation Center for Brain Science, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Nan-Jie XuDepartment of Anatomy and Physiology, Collaborative Innovation Center for Brain Science, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Suya SunDepartment of Neurology, Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0001-8967-7883

Funding

National Natural Science Foundation of China 32030042National Natural Science Foundation of China 32271009Science and Technology Innovation 2030 Major Projects 2021ZD0202801Shanghai Outstanding Academic Leaders Program 21XD1401800
6 · The paper itself

Abstract

Behavioral changes or neuropsychiatric symptoms (NPSs) are common features in dementia and are associated with accelerated cognitive impairment and earlier deaths. However, how NPSs are intertwined with cognitive decline remains elusive. In this study, we identify that the basolateral amygdala (BLA) is a key brain region that is associated with mood disorders and memory decline in the AD course. During the process from pre- to post-onset in AD, the dysfunction of parvalbumin (PV) interneurons and pyramidal neurons in the amygdala leads to hyperactivity of pyramidal neurons in the basal state and insensitivity to external stimuli. We further demonstrate that serotonin (5-HT) receptors in distinct neurons synergistically regulate the BLA microcircuit of AD rather than 5-HT levels, in which both restrained inhibitory inputs by excessive 5-HT

Indexed as

Alzheimer DiseaseReceptors, SerotoninAffectAmygdalaAnimalsBasolateral Nuclear ComplexHomeostasisHumansInterneuronsMaleMiceMice, Inbred C57BLNeuronsReceptors, Serotonin5‐HT receptorsAlzheimer's diseasebasolateral amygdalamood and cognitive defectsneuronal hyperactivity

Identifiers

PMID38716507
PMCPMC11320345

What OpenQuestion holds

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Registered trials

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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.