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ACAT1 as a Therapeutic Target and its Genetic Relationship with Alzheimer's Disease

Alavez-Rubio, Jessica Sarahi, Juarez-Cedillo, Teresa·2019·Current Alzheimer Research
DOI 10.2174/1567205016666190823125245
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Abstract

Background: Alzheimer´s disease (AD) is a chronic and progressive disease which impacts caregivers, families and societies physically, psychologically and economically. Currently available drugs can only improve cognitive symptoms, have no impact on progression and are not curative, so identifying and studying new drug targets is important. There are evidences which indicate disturbances in cholesterol homeostasis can be related with AD pathology, especially the compartmentation of intracellular cholesterol and cytoplasmic cholesterol esters formed by acyl-CoA: cholesterol acyltransferase 1 (ACAT1) can be implicated in the regulation of amyloid-beta (Aβ) peptide, involved in AD. Blocking ACAT1 activity, beneficial effects are obtained, so it has been suggested that ACAT1 can be a potential new therapeutic target. The present review discusses the role of cholesterol homeostasis in AD pathology, especially with ACAT inhibitors, and how they have been raised as a therapeutic approach. In addition, the genetic relationship of ACAT and AD is discussed. Conclusion: Although there are several lines of evidence from cell-based and animal studies that suggest that ACAT inhibition is an effective way of reducing cerebral Aβ, there is still an information gap in terms of mechanisms and concerns to cover before passing to the next level. Additionally, an area of interest that may be useful in understanding AD to subsequently propose new therapeutic approaches is pharmacogenetics; however, there is still a lot of missing information in this area.

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  • Previous studies using commercial ACAT inhibitors including AVAS, and ACAT-knockout mice, show reduced AD-like pathology and APP processing in familial AD-transgenic mice.

    “Previous studies using commercial ACAT inhibitors, including avasimibe (AVAS), as well as ACAT-knock out (KO) mice, exhibit reduced AD-like pathology and amyloid precursor protein (APP) processing in familial AD (FAD)-transgenic (Tg) mice.”

    From Inhibition of ACAT as a Therapeutic Target for Alzheimer's Disease Is Independent of ApoE4 Lipidation (2023) · cites this paper as [70]

  • Cholesterol mobilization by ACAT inhibition in microglia can promote autophagy and lysosomal biogenesis, leading to increased clearance of oAβ.

    “cholesterol mobilization by ACAT inhibition in microglia can promote autophagy and lysosomal biogenesis, leading to an increased clearance of oAβ [69–71, 77].”

    From Inhibition of ACAT as a Therapeutic Target for Alzheimer's Disease Is Independent of ApoE4 Lipidation (2023) · cites this paper as [70]

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Metadata

Authors
Alavez-Rubio, J. S., & Juarez-Cedillo, T.
Affiliations
  • Universidad Nacional Autonoma de México, Mexico City, Mexico
  • Unidad de Investigacion Epidemiologica y en Servicios de Salud, Area Envejecimiento, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social (Actualmente comisionada en la Unidad de Investigacion en Epidemiologia, Clínica, Hospital Regional, Num. 1 Dr. Carlos MacGregor Sanchez Navarro IMSS), Mexico
Venue
Current Alzheimer Research
Publisher
Bentham Science Publishers Ltd.
Published
2019-10-11
Volume
16
Issue
8
Pages
699-709
ISSN
1567-2050
DOI
10.2174/1567205016666190823125245
Cited by
12
References
16
Language
en
Funders
Fondo Sectorial de Investigación en Salud y Seguridad Social FONSEC (SSA/IMSS/ISSSTE-CONACYT Salud-233065)

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