Evidence map›Paper›PMID 38281031›Full record

ArticleAlzheimer's research & therapy2024

A nonhuman primate model with Alzheimer's disease-like pathology induced by hippocampal overexpression of human tau.

Zhouquan Jiang, Jing Wang, Yongpeng Qin, Shanggong Liu, Bin Luo, Fan Bai, Huiyi Wei, Shaojuan Zhang, Junjie Wei, Guoyu Ding and 10 more

Open access · goldAbstract read
In one paragraph

Article in Alzheimer's research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

20 citing papers in PubMed, 22 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

20 authors at 2 institutions in 1 country.

Zhouquan Jiang *Guangdong-Hong Kong-Macau Institute of CNS Regeneration, Jinan University, Guangzhou, 510630, Guangdong, China.
Jing Wang *Department of Neurosurgery, the First Affiliated Hospital, Jinan University, Guangzhou, 510630, Guangdong, China.
Yongpeng QinGuangdong-Hong Kong-Macau Institute of CNS Regeneration, Jinan University, Guangzhou, 510630, Guangdong, China.
Shanggong LiuGuangdong-Hong Kong-Macau Institute of CNS Regeneration, Jinan University, Guangzhou, 510630, Guangdong, China.
Bin LuoGuangdong-Hong Kong-Macau Institute of CNS Regeneration, Jinan University, Guangzhou, 510630, Guangdong, China.
Fan BaiGuangdong-Hong Kong-Macau Institute of CNS Regeneration, Jinan University, Guangzhou, 510630, Guangdong, China.
Huiyi WeiDepartment of Nuclear Medicine and PET/CT-MRI Centre, the First Affiliated Hospital, Jinan University, Guangzhou, 510630, Guangdong, China.
Shaojuan ZhangDepartment of Nuclear Medicine and PET/CT-MRI Centre, the First Affiliated Hospital, Jinan University, Guangzhou, 510630, Guangdong, China.
Junjie WeiDepartment of Nuclear Medicine and PET/CT-MRI Centre, the First Affiliated Hospital, Jinan University, Guangzhou, 510630, Guangdong, China.
Guoyu DingGuangdong-Hong Kong-Macau Institute of CNS Regeneration, Jinan University, Guangzhou, 510630, Guangdong, China.
Long MaGuangdong-Hong Kong-Macau Institute of CNS Regeneration, Jinan University, Guangzhou, 510630, Guangdong, China.
Shu HeGuangdong-Hong Kong-Macau Institute of CNS Regeneration, Jinan University, Guangzhou, 510630, Guangdong, China.
Rongjie ChenGuangdong-Hong Kong-Macau Institute of CNS Regeneration, Jinan University, Guangzhou, 510630, Guangdong, China.
Ying SunGuangdong-Hong Kong-Macau Institute of CNS Regeneration, Jinan University, Guangzhou, 510630, Guangdong, China.
Yi ChenGuangdong-Hong Kong-Macau Institute of CNS Regeneration, Jinan University, Guangzhou, 510630, Guangdong, China.
Lu WangDepartment of Nuclear Medicine and PET/CT-MRI Centre, the First Affiliated Hospital, Jinan University, Guangzhou, 510630, Guangdong, China.
Hao XuDepartment of Nuclear Medicine and PET/CT-MRI Centre, the First Affiliated Hospital, Jinan University, Guangzhou, 510630, Guangdong, China.
Xiangyu WangDepartment of Neurosurgery, the First Affiliated Hospital, Jinan University, Guangzhou, 510630, Guangdong, China.
Gong ChenGuangdong-Hong Kong-Macau Institute of CNS Regeneration, Jinan University, Guangzhou, 510630, Guangdong, China. gongchen@jnu.edu.cn.
Wenliang LeiGuangdong-Hong Kong-Macau Institute of CNS Regeneration, Jinan University, Guangzhou, 510630, Guangdong, China. leiwenliang@jnu.edu.cn.
Jinan University · CNFirst Affiliated Hospital of Jinan University · CN

Funding

Guangdong Provincial Department of Science and Technology 2018B030332001Guangzhou Municipal Science and Technology Bureau 202206060002National Natural Science Foundation of China 31970906Natural Science Foundation of Guangdong Province 2020A1515010083
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is one of the most burdening diseases of the century with no disease-modifying treatment at this time. Nonhuman primates (NHPs) share genetic, anatomical, and physiological similarities with humans, making them ideal model animals for investigating the pathogenesis of AD and potential therapies. However, the use of NHPs in AD research has been hindered by the paucity of AD monkey models due to their long generation time, ethical considerations, and technical challenges in genetically modifying monkeys.

methodsHere, we developed an AD-like NHP model by overexpressing human tau in the bilateral hippocampi of adult rhesus macaque monkeys. We evaluated the pathological features of these monkeys with immunostaining, Nissl staining, cerebrospinal fluid (CSF) analysis, magnetic resonance imaging (MRI), positron emission tomography (PET), and behavioural tests.

resultsWe demonstrated that after hippocampal overexpression of tau protein, these monkeys displayed multiple pathological features of AD, including 3-repeat (3R)/4-repeat (4R) tau accumulation, tau hyperphosphorylation, tau propagation, neuronal loss, hippocampal atrophy, neuroinflammation, Aβ clearance deficits, blood vessel damage, and cognitive decline. More interestingly, the accumulation of both 3R and 4R tau is specific to NHPs but not found in adult rodents.

conclusionsThis work establishes a tau-induced AD-like NHP model with many key pathological and behavioural features of AD. In addition, our model may potentially become one of the AD NHP models adopted by researchers worldwide since it can be generated within 2 ~ 3 months through a single injection of AAVs into the monkey brains. Hence, our model NHPs may facilitate mechanistic studies and therapeutic treatments for AD.

Indexed as

Alzheimer DiseaseCognitive DysfunctionAmyloid beta-PeptidesAnimalsHippocampusHumansMacaca mulattatau ProteinsAmyloid beta-Peptidestau Proteins3R tau4R tauAlzheimer’s diseaseBlood vessel damageCognitive declineHuman tauNeuroinflammationNonhuman primateTau hyperphosphorylation

Identifiers

PMID38281031
PMCPMC10821564
OpenAlexW4391278301

What OpenQuestion holds

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LicenceCC BY
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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.