Evidence map›Paper›PMID 37867176›Full record

ArticleSignal transduction and targeted therapy2023

Fe65-engineered neuronal exosomes encapsulating corynoxine-B ameliorate cognition and pathology of Alzheimer's disease.

Ashok Iyaswamy, Abhimanyu Thakur, Xin-Jie Guan, Senthilkumar Krishnamoorthi, Tsz Yan Fung, Kejia Lu, Isha Gaurav, Zhijun Yang, Cheng-Fu Su, Kwok-Fai Lau and 7 more

Open access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 1 pooled it
16.2field-weighted citation impact, top 1% 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

89 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.

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29 more citing papers are in PubMed but not listed here.

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

17 authors at 6 institutions in 4 countries.

Ashok Iyaswamy *Mr. & Mrs. Ko Chi-Ming Centre for Parkinson's Disease Research, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China. iashok@hkbu.edu.hk.ORCID http://orcid.org/0000-0003-0186-3863
Abhimanyu Thakur *Pritzker School of Molecular Engineering, The University of Chicago, Chicago, IL, USA. abhimanyu@uchicago.edu.ORCID http://orcid.org/0000-0002-0846-0998
Xin-Jie GuanMr. & Mrs. Ko Chi-Ming Centre for Parkinson's Disease Research, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Senthilkumar KrishnamoorthiMr. & Mrs. Ko Chi-Ming Centre for Parkinson's Disease Research, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Tsz Yan FungMr. & Mrs. Ko Chi-Ming Centre for Parkinson's Disease Research, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Kejia LuMr. & Mrs. Ko Chi-Ming Centre for Parkinson's Disease Research, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Isha GauravSchool of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Zhijun YangSchool of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Cheng-Fu SuMr. & Mrs. Ko Chi-Ming Centre for Parkinson's Disease Research, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Kwok-Fai LauSchool of Life Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China.
Kui ZhangPritzker School of Molecular Engineering, The University of Chicago, Chicago, IL, USA.
Roy Chun-Laam NgDivision of Neuroscience, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom.
Qizhou LianDepartment of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pok Fu Lam, Hong Kong SAR, China.
King-Ho CheungMr. & Mrs. Ko Chi-Ming Centre for Parkinson's Disease Research, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Keqiang YeFaculty of Life and Health Sciences, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.ORCID http://orcid.org/0000-0002-7657-8154
Huanhuan Joyce ChenPritzker School of Molecular Engineering, The University of Chicago, Chicago, IL, USA. joycechen@uchicago.edu.
Min LiMr. & Mrs. Ko Chi-Ming Centre for Parkinson's Disease Research, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China. limin@hkbu.edu.hk.ORCID http://orcid.org/0000-0002-7113-2700
Hong Kong Baptist University · HKUniversity of Chicago · USChinese University of Hong Kong · HKManchester Academic Health Science Centre · GBShenzhen Institutes of Advanced Technology · CNUniversity of Hong Kong · HK

Funding

Investigation of sub-lineages in pulmonary neuroendocrine cells and identification of the cells of origin of small cell lung cancerR00CA226353 · NCI · UNIVERSITY OF CHICAGO · PI CHEN, JOYCE HUANHUAN · 2020 to 2022
$747k
Investigation of sub-lineages in pulmonary neuroendocrine cells and identification of the cells of origin of small cell lung cancerK99CA226353 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHEN, JOYCE HUANHUAN · 2019 to 2019
$84k
NCI NIH HHS K99 CA226353NCI NIH HHS R00 CA226353
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the predominant impairment of neurons in the hippocampus and the formation of amyloid plaques, hyperphosphorylated tau protein, and neurofibrillary tangles in the brain. The overexpression of amyloid-β precursor protein (APP) in an AD brain results in the binding of APP intracellular domain (AICD) to Fe65 protein via the C-terminal Fe65-PTB2 interaction, which then triggers the secretion of amyloid-β and the consequent pathogenesis of AD. Apparently, targeting the interaction between APP and Fe65 can offer a promising therapeutic approach for AD. Recently, exosome, a type of extracellular vesicle with diameter around 30-200 nm, has gained much attention as a potential delivery tool for brain diseases, including AD, due to their ability to cross the blood-brain barrier, their efficient uptake by autologous cells, and their ability to be surface-modified with target-specific receptor ligands. Here, the engineering of hippocampus neuron cell-derived exosomes to overexpress Fe65, enabled the development of a novel exosome-based targeted drug delivery system, which carried Corynoxine-B (Cory-B, an autophagy inducer) to the APP overexpressed-neuron cells in the brain of AD mice. The Fe65-engineered HT22 hippocampus neuron cell-derived exosomes (Fe65-EXO) loaded with Cory-B (Fe65-EXO-Cory-B) hijacked the signaling and blocked the natural interaction between Fe65 and APP, enabling APP-targeted delivery of Cory-B. Notably, Fe65-EXO-Cory-B induced autophagy in APP-expressing neuronal cells, leading to amelioration of the cognitive decline and pathogenesis in AD mice, demonstrating the potential of Fe65-EXO-Cory-B as an effective therapeutic intervention for AD.

Indexed as

Alzheimer DiseaseExosomesAmyloid beta-Protein PrecursorAnimalsCognitionIndolesMiceNerve Tissue ProteinsNeuronsSpiro CompoundsAmyloid beta-Protein PrecursorcorynoxineIndolesNerve Tissue ProteinsSpiro Compounds

Identifiers

PMID37867176
PMCPMC10590775
OpenAlexW4387857159

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.