ApoE4 induces Alzheimer's disease through brain metabolic abnormalities

BI Danlei; SHEN Yong

doi:10.3981/j.issn.1000-7857.2021.20.008

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Science & Technology Review ›› 2021, Vol. 39 ›› Issue (20) : 92-100. DOI: 10.3981/j.issn.1000-7857.2021.20.008

Exclusive: Alzheimer's disease

ApoE4 induces Alzheimer's disease through brain metabolic abnormalities

Author information -

1. The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, Institute on Aging and Brain Disorders, University of Sciences and Technology of China, Hefei 230036, China;
2. Neurodegenerative Disease Research Center, University of Science and Technology of China, Hefei 230026, China;
3. Hefei National Laboratory for Physical Sciences at the Microscale, Neurodegenerative Disorder Research Center, CAS Key Laboratory of Brain Function and Disease, School of Life Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230026, China;
4. Institute of Brain-Intelligence Science and Technology, Shanghai 200031, China

Abstract

The Alzheimer's disease (AD), a neurodegenerative disease, is the major cause of dementia in senior people. The late-onset AD (LOAD) accounts for more than 95% of the total AD population. Apolipoprotein E ε4 (ApoE4) is the most prevalent risk gene in the LOAD. In this review, we discuss the mechanisms by which ApoE4 contributes to the alterations of the energy and the lipid metabolism. Alterations of metabolism, including the energy and the lipid, are frequently observed in the brains of individuals with a mild cognitive impairment and the AD. Therefore, ApoE4 induces the LOAD pathogenesis probably by impairing the metabolic homoestasis based on the clinical and basic researches. This could potentially provide new therapeutical targets in the drug development for the AD.

Key words

ApoE / Alzheimer's disease / metabolism

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BI Danlei, SHEN Yong. ApoE4 induces Alzheimer's disease through brain metabolic abnormalities[J]. Science & Technology Review, 2021, 39(20): 92-100 https://doi.org/10.3981/j.issn.1000-7857.2021.20.008

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