Evidence map›Paper›PMID 38012054›Full record

ArticleBrain pathology (Zurich, Switzerland)2024

Reduced neurogenesis in human hippocampus with Alzheimer's disease.

Yan Cao, Pan Liu, Hongfei Bian, Sixuan Jin, Jiaqi Liu, Ning Yu, Huan Cui, Fengrun Sun, Xiaojing Qian, Wenying Qiu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 25 citations in OpenAlex.

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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

11 authors at 1 institution in 1 country.

Yan CaoNational Human Brain Bank for Development and Function, Department of Human Anatomy, Histology and Embryology, Neuroscience Center, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, China.ORCID 0009-0001-3978-8144
Pan LiuNational Human Brain Bank for Development and Function, Department of Human Anatomy, Histology and Embryology, Neuroscience Center, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, China.
Hongfei BianNational Human Brain Bank for Development and Function, Department of Human Anatomy, Histology and Embryology, Neuroscience Center, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, China.
Sixuan JinNational Human Brain Bank for Development and Function, Department of Human Anatomy, Histology and Embryology, Neuroscience Center, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, China.
Jiaqi LiuNational Human Brain Bank for Development and Function, Department of Human Anatomy, Histology and Embryology, Neuroscience Center, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, China.
Ning YuNational Human Brain Bank for Development and Function, Department of Human Anatomy, Histology and Embryology, Neuroscience Center, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, China.
Huan CuiNational Human Brain Bank for Development and Function, Department of Human Anatomy, Histology and Embryology, Neuroscience Center, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, China.
Fengrun SunNational Human Brain Bank for Development and Function, Department of Human Anatomy, Histology and Embryology, Neuroscience Center, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, China.
Xiaojing QianNational Human Brain Bank for Development and Function, Department of Human Anatomy, Histology and Embryology, Neuroscience Center, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, China.
Wenying QiuNational Human Brain Bank for Development and Function, Department of Human Anatomy, Histology and Embryology, Neuroscience Center, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, China.
Chao MaNational Human Brain Bank for Development and Function, Department of Human Anatomy, Histology and Embryology, Neuroscience Center, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, China.ORCID 0000-0003-1346-6961
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

STI2030-Major Project #2021ZD0201100STI2030-Major Project Task1#2021ZD0201101The CAMS Innovation Fund for Medical Sciences (CIFMS) #2021-I2M-1-025
6 · The paper itself

Abstract

Adult hippocampal neurogenesis (AHN), essential for the plasticity of hippocampal structure and function, may be disrupted in Alzheimer's disease (AD). However, the relationship between the changes in AHN and AD-related pathology in humans remains uncertain. By utilizing advanced immunostaining techniques, we could identify multiple biomarkers representing different stages of AHN in postmortem human hippocampal tissue that exhibited various AD-related neuropathological changes. In this study, we observed a significant presence of neurogenic cells in the hippocampus's dentate gyrus (DG) region in 30 individuals, including 14 individuals diagnosed with AD-related neuropathological changes and the remaining 16 individuals without any neurological diseases. Further investigation revealed that patients with AD exhibited pronounced astrogliosis and reduced neurogenesis. Specifically, the number of neuroblasts, immature and early mature granule cells decreased significantly as AD advanced. Although the number of neural stem cells (NSCs) remained unchanged in AD patients compared with mentally healthy individuals, they tended to be more quiescent state regulated by Notch and bone morphogenetic protein (BMP) signaling pathways. These abnormalities were strongly associated with the neuropathological alterations in AD patients. These research findings provide potential insights into the underlying mechanisms that underpin the pathogenesis of AD.

Indexed as

Alzheimer DiseaseNeural Stem CellsAdultHippocampusHumansNeurogenesisNeuronsadult hippocampal neurogenesisAlzheimer diseasehuman brain

Identifiers

PMID38012054
PMCPMC11007046
OpenAlexW4389068631

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.