Cholesterol metabolism in the brain and its association with Parkinson’s disease.
Open accessAbstract
Parkinson's disease (PD) is the second most progressive neurodegenerative disorder of the aging population after Alzheimer's disease (AD). Defects in the lysosomal systems and mitochondria have been suspected to cause the pathogenesis of PD. Nevertheless, the pathogenesis of PD remains obscure. Abnormal cholesterol metabolism is linked to numerous disorders, including atherosclerosis. The brain contains the highest level of cholesterol in the body and abnormal cholesterol metabolism links also many neurodegenerative disorders such as AD, PD, Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS). The blood brain barrier effectively prevents uptake of lipoprotein-bound cholesterol from blood circulation. Accordingly, cholesterol level in the brain is independent from that in peripheral tissues. Because cholesterol metabolism in both peripheral tissue and the brain are quite different, cholesterol metabolism associated with neurodegeneration should be examined separately from that in peripheral tissues. Here, we review and compare cholesterol metabolism in the brain and peripheral tissues. Furthermore, the relationship between alterations in cholesterol metabolism and PD pathogenesis is reviewed.
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As neurons acquire maturity and brain total cholesterol reaches a plateau, astrocytes become largely responsible for maintaining lipid homeostasis in the brain.
“Neurons and astrocytes synthesize cholesterol in development, but as neurons acquire maturity and brain total cholesterol reaches a plateau stage, astrocytes become largely responsible for maintaining lipid homeostasis in the brain (Jin et al., 2019; Chen et al., 2023).”
From Astrocytes in fragile X syndrome (2024) · cites this paper as Jin et al., 2019
In “Cholesterol supply” (page not provided), the paper says that both neurons and glia synthesize cholesterol during embryogenesis, while differentiated adult neurons increasingly rely on cholesterol produced by glia. “Cholesterol transfer” (page not provided) also describes astrocytes as the suspected main producers of brain lipoproteins. These passages support a greater astrocyte role with neuronal maturity, but they do not say that total brain cholesterol reaches a plateau or establish that plateau as part of the transition. (LLM, conf=0.86)
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“Neurons and astrocytes synthesize cholesterol in development, but as neurons acquire maturity and brain total cholesterol reaches a plateau stage, astrocytes become largely responsible for maintaining lipid homeostasis in the brain (Jin et al., 2019; Chen et al., 2023).”
Background
- Authors
- Jin, U., Park, S. J., & Park, S. M.
- Affiliations
- Ajou University (KR)
- Department of Pharmacology, Ajou University School of Medicine, Suwon 16499, Korea
- Corresponding author
- Jin, Uram
- Venue
- Experimental Neurobiology
- Published
- 2019-10-31
- Volume
- 28
- Issue
- 5
- Pages
- 554-567
- ISSN
- 1226-2560 (ISSN-L)
- 2093-8144
- PMC
- PMC6844833
- OpenAlex
- W2988419602
- Cited by
- 169
- References
- 10
- Citations by year
- 2026: 18 · 2025: 28 · 2024: 35 · 2023: 28 · 2022: 26 · 2021: 22 · 2020: 12
- FWCI
- 3.09
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Licence
- cc-by-nc
- Locations
- Experimental Neurobiology (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- AJOU Open Repository (Ajou University) (submittedVersion, cc-by-nc)
- Funders
- National Research Foundation of Korea (NRF-2019R1A5A2026045)
- Ministry of Science, ICT and Future Planning (2017R1E1A1A91973713)
- Topics
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Health Sciences › Medicine › Physiology › Lysosomal Storage Disorders Research
- Keywords
- cholesterol metabolism, Parkinson's disease, brain cholesterol, neurodegeneration, blood-brain barrier, lysosomal dysfunction, mitochondrial dysfunction, neurodegenerative diseases, Huntington's disease, amyotrophic lateral sclerosis, Alzheimer's disease
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