ArticleInternational journal of molecular sciences2020
Elevated CLOCK and BMAL1 Contribute to the Impairment of Aerobic Glycolysis from Astrocytes in Alzheimer's Disease.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Pooled it
- HIF-1α and BMAL1 in bone regeneration: crosstalk between hypoxia response and circadian rhythm.Bone research · 2026Review
- The interplay between circadian rhythm components and apoptosis in health and disease.Human cell · 2026Review
- Core Circadian Protein BMAL1: Implication for Nervous System Functioning and Its Diseases.Brain sciences · 2025Review
- Advances of therapeutic strategies for Alzheimer's disease.Journal of neurology · 2025Review
- Hexokinase as a Central Hub in Neurodegeneration: From Metabolic Dysfunction to Therapeutic Innovation.Aging and disease · 2025Review
- The rhythm of decline: Circadian disruption in neurodegeneration.Journal of food and drug analysis · 2025Review
- The intersection of circadian rhythms and the blood-brain barrier with drug efficacy and delivery in neurological disorders.Advanced drug delivery reviews · 2025Review
- Importance of Gut Microbiota Dysbiosis and Circadian Disruption-Associated Biomarkers in Emergence of Alzheimer's Disease.Molecular neurobiology · 2025Review
- Visceral adiposity index, premature mortality, and life expectancy in US adults.Lipids in health and disease · 2025Article
- Dysregulation of the molecular clock by blood-borne factors in Alzheimer's disease patients.Journal of neurology · 2025Observational
- Unravelling the link between circadian clock genes and brain tumors: From pathological disruptions to potential therapeutic interventions.Frontiers in pharmacology · 2025Review
- Neuroglia and brain energy metabolism.Handbook of clinical neurology · 2025Review
- Circadian system disorder induced by aberrantly activated EFNB2-EPHB2 axis leads to facilitated liver metastasis in gastric cancer.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Indoxyl sulfate induces apoptotic cell death by inhibiting glycolysis in human astrocytes.Kidney research and clinical practice · 2024Article
- NOX4-mediated astrocyte ferroptosis in Alzheimer's disease.Cell & bioscience · 2024Article
- Sex-Dependent Effects of Chronic Circadian Disruption in AβPP/PS1 Mice.Journal of Alzheimer's disease : JAD · 2024Article
- Article
- Gut microbiota and circadian rhythm in Alzheimer's disease pathophysiology: a review and hypothesis on their association.npj aging · 2023Review
- Circadian rest-activity rhythm and longitudinal brain changes underlying late-life cognitive decline.Psychiatry and clinical neurosciences · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Altered glucose metabolism has been implicated in the pathogenesis of Alzheimer's disease (AD). Aerobic glycolysis from astrocytes is a critical metabolic pathway for brain energy metabolism. Disturbances of circadian rhythm have been associated with AD. While the role of circadian locomotor output cycles kaput (CLOCK) and brain muscle ARNT-like1 (BMAL1), the major components in the regulation of circadian rhythm, has been identified in the brain, the mechanism by which CLOCK and BMAL1 regulates the dysfunction of astrocytes in AD remains unclear. Here, we show that the protein levels of CLOCK and BMAL1 are significantly elevated in impaired astrocytes of cerebral cortex from patients with AD. We demonstrate that the over-expression of CLOCK and BMAL1 significantly suppresses aerobic glycolysis and lactate production by the reduction in hexokinase 1 (HK1) and lactate dehydrogenase A (LDHA) protein levels in human astrocytes. Moreover, the elevation of CLOCK and BMAL1 induces functional impairment by the suppression of glial fibrillary acidic protein (GFAP)-positive filaments in human astrocytes. Furthermore, the elevation of CLOCK and BMAL1 promotes cytotoxicity by the activation of caspase-3-dependent apoptosis in human astrocytes. These results suggest that the elevation of CLOCK and BMAL1 contributes to the impairment of astrocytes by inhibition of aerobic glycolysis in AD.
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Registered trials
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.