期刊
FEBS JOURNAL
卷 289, 期 24, 页码 7688-7709出版社
WILEY
DOI: 10.1111/febs.16175
关键词
amyotrophic lateral sclerosis; apolipoprotein E; blood-brain barrier; cholesterol esters; cholesterol metabolism; frontotemporal dementia; low-density lipoprotein receptor; oxysterol; sterol regulatory element-binding factor 2; TAR DNA-binding protein 43 KDa
资金
- Swee Liew-Wadsworth Endowment fund
- National University of Singapore (NUS)
- National Medical Research Council [NMRC/OFIRG/0001/2016, NMRC/OFIRG/0042/2017]
- National Research Foundation, Singapore [NRF2019-NRF-ISF003-3221]
ALS is a common adult-onset motor neuron disease characterized by selective degeneration of motor neurons. Dyslipidemia, particularly abnormal cholesterol levels, has been reported in ALS patients, but its specific role in the disease remains unclear. Further research is needed to understand the potential contribution of cholesterol metabolism to ALS.
Amyotrophic lateral sclerosis (ALS), the most common adult-onset motor neuron disease, is characterized by the selective degeneration of motor neurons leading to paralysis and eventual death. Multiple pathogenic mechanisms, including systemic dysmetabolism, have been proposed to contribute to ALS. Among them, dyslipidemia, i.e., abnormal level of cholesterol and other lipids in the circulation and central nervous system (CNS), has been reported in ALS patients, but without a consensus. Cholesterol is a constituent of cellular membranes and a precursor of steroid hormones, oxysterols, and bile acids. Consequently, optimal cholesterol levels are essential for health. Due to the blood-brain barrier (BBB), cholesterol cannot move between the CNS and the rest of the body. As such, cholesterol metabolism in the CNS is proposed to operate autonomously. Despite its importance, it remains elusive how cholesterol dyshomeostasis may contribute to ALS. In this review, we aim to describe the current state of cholesterol metabolism research in ALS, identify unresolved issues, and provide potential directions.
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