Brain Research, Journal Year: 2024, Volume and Issue: unknown, P. 149348 - 149348
Published: Nov. 1, 2024
Language: Английский
Brain Research, Journal Year: 2024, Volume and Issue: unknown, P. 149348 - 149348
Published: Nov. 1, 2024
Language: Английский
Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 7, 2025
Language: Английский
Citations
1Translational Neurodegeneration, Journal Year: 2024, Volume and Issue: 13(1)
Published: Sept. 6, 2024
Language: Английский
Citations
4IntechOpen eBooks, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 13, 2025
Intermittent fasting, a cleansing activity that severely restricts calorie intake, is an effective means of activating autophagy. As dietary pattern, intermittent fasting can delay aging and reduce the risk age-related diseases. helps maintain homeostasis body through series hormonal metabolic changes, protecting variety diseases preventing chronic And it has been shown to improve efficacy weight loss obesity-related non-alcoholic fatty liver disease health indicators. There are still some challenges in area fasting’s effects, further long-term clinical studies needed.
Language: Английский
Citations
0PLoS ONE, Journal Year: 2025, Volume and Issue: 20(3), P. e0319253 - e0319253
Published: March 25, 2025
Huntington’s disease (HD) is a devastating neurodegenerative disorder characterized by variety of debilitating symptoms including abnormal motor control, cognitive impairment, and psychiatric disturbances. Despite significant efforts, efficacious treatments to alter the course HD remain elusive, highlighting need explore new therapeutic strategies, lifestyle changes that may delay onset slow progression. Recent research indicates time-restricted eating (TRE), type intermittent fasting where caloric intake confined specific time window each day, be beneficial in treating diseases like HD. TRE has been found enhance mitochondrial function, stimulate autophagy, lower oxidative stress, improve performance. Although shown potential animal models non-HD populations, it yet analyzed for safety, feasibility, efficacy persons with Therefore, we propose prospective interventional, open-label, single-arm, pilot study 25 participants late prodromal early manifest evaluate participant adherence diet – specifically, maintaining 6-8-hour every day 12 weeks. Secondary measures will include pre- versus post-intervention assessment body composition via bioelectrical impedance analysis, vital signs safety labs, serum biomarkers neurodegeneration, standard behavioral, cognitive, function clinical scales. Additional exploratory sleep quality, physical activity, mood, dietary composition, function. We expect safe, feasible, also progression anticipate this lay foundation future large-scale trials further This registered on July 8, 2024 ClinicalTrials.gov registration number NCT06490367 ( https://clinicaltrials.gov/study/NCT06490367 ).
Language: Английский
Citations
0Life, Journal Year: 2025, Volume and Issue: 15(4), P. 577 - 577
Published: April 1, 2025
Huntington’s disease (HD) is a detrimental neurodegenerative caused by the expansion of CAG triplet in HTT gene. This mutation leads to production mutant Huntingtin (Htt) protein with toxic gain-of-function. The mHtt responsible several ways for establishment an intricate pathogenetic scenario affected cells, particularly HD neurons. Among features HD, oxidative stress plays relevant role progression at cellular level. Mitochondrial dysfunction, bioenergetic deficits, Reactive Oxygen Species (ROS) production, neuroinflammation, and general reduction antioxidant levels are all involved promotion environment, eventually causing cell death. Nonetheless, neuronal cells exert molecules build up defense mechanisms. Key components these defensive mechanisms nuclear factor erythroid 2-related 2 (NRF2) peroxisome proliferator-activated receptor gamma coactivator-1 α (PGC-1α). Thus, this review aims describe involvement exploring roles NRF2 PGC-1α, crucial actors play. Finally, therapeutic strategies targeting such markers discussed.
Language: Английский
Citations
0Exploration, Journal Year: 2025, Volume and Issue: unknown
Published: April 1, 2025
ABSTRACT Selenium (Se) is a crucial element in selenoproteins, key biomolecules for physiological function vivo. As selenium‐rich organ, the central nervous system can express all 25 kinds of which protect neurons by reducing oxidative stress and inflammatory response. However, decreased Se levels are prevalent variety neurological disorders, not conducive to treatment prognosis patients. Thus, biological study has emerged as focal point investigating pivotal role trace elements neuroprotection. This paper presents comprehensive review pathogenic mechanism diseases, protective Se, selenoproteins. Additionally, application neuroprotective agent disorder therapy, including ischemic stroke, Alzheimer's, Parkinson's, other summarized. The present aims offer novel insights methodologies prevention disorders with providing scientific basis development innovative Se‐based neuroprotectants promote their clinical against diseases.
Language: Английский
Citations
0Acta Pharmaceutica Sinica B, Journal Year: 2025, Volume and Issue: unknown
Published: April 1, 2025
Language: Английский
Citations
0Published: July 24, 2024
Some of neurodegenerative diseases may be characterized by continuing behavioral and cognitive dysfunction that contains memory loss and/or apathy. Alzheimer's disease is the most typical type such deficit cognition alteration behavior. Despite huge efforts against disease, there has been yet no successful treatment for this disease. Interestingly, several possible risk genes to are frequently expressed within brain cells, which also linked cholesterol metabolism, lipid transport, exosomes caveolae formation, suggesting a therapeutic target consider dysfunctions. modulation autophagy/mitophagy with glucagon-like peptide-1 (GLP-1) N-methyl-d-aspartate (NMDA) receptors signaling offer novel approach prevent alleviate dysfunction. A paradigm both GLP-1 NMDA at sites promising crucial dysfunctions presented here, might able modify progression This research direction open potential move clinical care toward disease-modifying strategies maximal benefits patients without detrimental adverse events diseases.
Language: Английский
Citations
2International Journal of Physiology Pathophysiology and Pharmacology, Journal Year: 2024, Volume and Issue: 16(5), P. 96 - 110
Published: Jan. 1, 2024
Alzheimer's disease is the most general type of cognitive impairments. Until recently, strategies that prevent its clinical progression have remained more elusive. Consequently, research direction should be for finding effective neuroprotective agents. It has been suggested oxidative stress, mitochondrial injury, and inflammation level might lead to brain cell death in many neurological disorders. Therefore, several autophagy-targeted bioactive compounds may promising candidate therapeutics prevention damage. Interestingly, some risk genes are expressed within cells, which linked cholesterol metabolism, lipid transport, endocytosis, exocytosis and/or caveolae formation, suggesting a fruitful therapeutic target improve This review would highlight latest advances technologies treatment disease. In particular, paradigm serotonin N-methyl-d-aspartate (NMDA) receptors agonist/antagonist structure possibly impairment. cellular membrane biophysics our understanding pathology dysfunction associated with Here, this purpose therapy open potential move care toward disease-modifying certain benefits patients.
Language: Английский
Citations
1Molecules, Journal Year: 2024, Volume and Issue: 29(16), P. 3922 - 3922
Published: Aug. 20, 2024
Some neurodegenerative diseases may be characterized by continuing behavioral and cognitive dysfunction that encompasses memory loss and/or apathy. Alzheimer’s disease is the most typical type of such are deficits cognition alterations behavior. Despite huge efforts against disease, there has yet been no successful treatment for this disease. Interestingly, several possible risk genes frequently expressed within brain cells, which also linked to cholesterol metabolism, lipid transport, exosomes, caveolae formation, suggesting a therapeutic target dysfunctions. modulation autophagy/mitophagy with alteration glucagon-like peptide-1 (GLP-1) N-methyl-d-aspartate (NMDA) receptor signaling offer novel approach preventing alleviating dysfunction. A paradigm showing both GLP-1 NMDA receptors at sites promising crucial targets dysfunctions presented here, able modify progression This research direction create potential move clinical care toward disease-modifying strategies maximal benefits patients without detrimental adverse events diseases.
Language: Английский
Citations
0