Recent advances on the molecular mechanisms of exercise-induced improvements of cognitive dysfunction

Translational Neurodegeneration, Journal Year: 2023, Volume and Issue: 12(1)

Published: Feb. 27, 2023

Abstract Physical exercise is of great significance for maintaining human health. Exercise can provide varying degrees benefits to cognitive function at all stages life cycle. Currently, with the aging world’s population and increase expectancy, dysfunction has gradually become a disease high incidence, which accompanied by neurodegenerative diseases in elderly individuals. Patients often exhibit memory loss, aphasia weakening orientation once diagnosed, are unable have normal life. Cognitive largely affects physical mental health, reduces quality life, causes economic burden society. At present, most interventions aimed maintain current level delay deterioration cognition. In contrast, as nonpharmacological therapy advantages its nontoxicity, low cost universal application. The molecular mechanisms underlying effect on cognition complex, studies been extensively centered neural plasticity, direct target brain. addition, mitochondrial stability energy metabolism essential brain status. Meanwhile, organ-brain axis responds induces release cytokines related this review, we summarize latest evidence effects cognition, point out directions future research.

Language: Английский

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Exercise therapy to prevent and treat Alzheimer’s disease

Frontiers in Aging Neuroscience, Journal Year: 2023, Volume and Issue: 15

Published: Aug. 4, 2023

Alzheimer’s disease (AD) is a progressive neurodegenerative in the elderly with dementia, memory loss, and severe cognitive impairment that imposes high medical costs on individuals. The causes of AD include increased deposition amyloid beta (Aβ) phosphorylated tau, age, mitochondrial defects, neuroinflammation, decreased synaptic connections, nerve growth factors (NGF). While animals moderate-intensity exercise restores hippocampal amygdala through levels p-AKT, p-TrkB, p-PKC Aβ, tau phosphorylation, precursor proteins (APP) AD. Aerobic (with an intensity 50–75% VO2 max) prevents volume reduction, spatial learning reduction increasing flexibility. Exercise training induces binding brain-derived neurotrophic factor (BDNF) to TrkB NGF TrkA induce cell survival neuronal plasticity. After aerobic high-intensity interval training, increase VEGF, angiopoietin 1 2, NO, tPA, HCAR1 cerebral vessels blood flow angiogenesis cerebellum, motor cortex, striatum, hippocampus. In hippocampus, decreases fragmentation, DRP1, FIS1, improving OPA1, MFN1, MFN2, morphology. humans, acute as anti-inflammatory condition IL-6 such IL-1RA IL-10. Moderate-intensity also inhibits inflammatory markers IFN-γ, IL-1β, IL-6, CRP, TNF-α, sTNFR1, COX-2, NF-κB. significantly increases plasma BDNF, factor, plasticity, activity, memory, exploratory behavior subjects. Irisin myokine released from skeletal muscle during protects hippocampus by suppressing Aβ accumulation promoting proliferation STAT3 signaling. Therefore, combined strength balance coordination social activities seems provide important benefits for people

Language: Английский

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Non-pharmacological treatment of Alzheimer’s disease: an update

Frontiers in Aging Neuroscience, Journal Year: 2025, Volume and Issue: 17

Published: Feb. 13, 2025

Alzheimer’s disease (AD) is a neurodegenerative disorder that significantly impairs memory, cognitive function, and the ability to perform daily tasks. The pathological features of AD include β-amyloid plaques, neurofibrillary tangles, neuronal loss. Current treatments target changes but often fail noticeably slow progression can cause severe complications, limiting their effectiveness. In addition therapies targeting core pathology AD, more comprehensive approach may be needed for its treatment. recent years, non-pharmacological such as physical therapy, exercise cell nanoparticles have shown great potential in mitigating alleviating clinical symptoms. This article reviews advances treatment approaches highlighting contributions management facilitating exploration novel therapeutic strategies.

Language: Английский

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Aerobic exercise regulates GPR81 signal pathway and mediates complement- microglia axis homeostasis on synaptic protection in the early stage of Alzheimer's disease

Life Sciences, Journal Year: 2023, Volume and Issue: 331, P. 122042 - 122042

Published: Aug. 25, 2023

Language: Английский

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Bisphenol S impairs mitochondrial function by targeting Myo19/oxidative phosphorylation pathway contributing to axonal and dendritic injury

Environment International, Journal Year: 2024, Volume and Issue: 186, P. 108643 - 108643

Published: April 1, 2024

Exposure to bisphenol S (BPS) is known adversely affect neuronal development. As pivotal components of polarization, axons and dendrites are indispensable structures within neurons, crucial for the maintenance nervous system function. Here, we investigated impact BPS exposure on axonal dendritic development both in vivo vitro. Our results revealed that during pregnancy lactation led a reduction complexity, density, length prefrontal cortex (PFC) offspring. Employing RNA sequencing technology elucidate underlying mechanisms damage induced by BPS, Kyoto Encyclopedia Genes Genomes (KEGG) analysis highlighted significant alteration oxidative phosphorylation (OXPHOS) pathway, essential mitochondrial Subsequent experiments demonstrate BPS-induced impairment function, including damaged morphology, decreased adenosine triphosphate (ATP) superoxide dismutase (SOD) levels, increased reactive oxygen species malondialdehyde (MDA). These alterations coincided with downregulated expression OXPHOS pathway-related genes (ATP6V1B1, ATP5K, NDUFC1, NDUFC2, NDUFA3, COX6B1) Myosin 19 (Myo19). Notably, Myo19 overexpression restored dysfunction alleviating inhibition pathway. Consequently, this amelioration was associated injury observed cultured neurons PFC.

Language: Английский

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Molecular mechanisms underlying the neural correlates of working memory

BMC Biology, Journal Year: 2024, Volume and Issue: 22(1)

Published: Oct. 21, 2024

Language: Английский

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Management of cognitive frailty: A network meta‐analysis of randomized controlled trials

International Journal of Geriatric Psychiatry, Journal Year: 2023, Volume and Issue: 38(9)

Published: Sept. 1, 2023

We aimed to compare the effectiveness of interventions in cognitive function and frailty status rank these interventions.Data Sources-We searched PubMed, Embase, CINAHL, PsycINFO, Web Science, Cochrane Library, Central Register Controlled Trials (CENTRAL), CNKI, Wanfang, VIP Google scholar. Data synthesis-The risk bias was assessed using assessment tool. Statistical heterogeneity Chi-square test quantified by I2 . The results were pooled standardized mean difference (SMD). probability for each intervention calculated surface under cumulative ranking curve (SUCRA). Additionally, quality evidence evaluated GRADE approach.A total 10 randomized controlled trials (RCTs) involving 1110 patients included our analysis. network map comprised 9 RCTs with 1347 participants, examining eight different interventions. Nutritional support (SUCRA = 99.9%, SMD 3.02, 95% CI: 2.53, 3.51) may be most effective improve function. (including 1017 participants interventions) suggested that multicomponent exercises 96.4%, -5.10, -5.96, -4.23) tended have a greater effect.Community-based shown significant benefits improving older adults, moderate certainty. For hospitalized Cognitive (CF), current suggests nutritional yields improvement. aerobic exercise dual-task training proven managing CF. Further studies are needed validate preliminary findings exploring more accessible physical prevent CF aging.

Language: Английский

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FGF21 Exhibits Neuroprotective Effects by Promoting 5-HT1AR-FGFR1 Heteroreceptor Complexes and Triggering MEK1/2-ERK1/2 Signaling Pathway

Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 10, 2025

Language: Английский

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L-Lactate Administration Improved Synaptic Plasticity and Cognition in Early 3xTg-AD Mice

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(4), P. 1486 - 1486

Published: Feb. 11, 2025

Synaptic plasticity impairment and behavioral deficits constitute classical pathological hallmarks in early-stage Alzheimer’s disease (AD). Emerging evidence suggests these synaptic dysfunctions may stem from metabolic dysregulation, particularly impaired aerobic glycolysis. As a key product of astrocyte-mediated glycolysis, lactate serves dual roles as both an energy substrate signaling molecule, playing critical regulatory role long-term memory formation. This study investigated whether exogenous L-lactate supplementation could ameliorate dysfunction cognitive AD models. Our findings reveal significant reductions hippocampal levels experimental mice. Systemic administration (200 mg/kg) effectively restored physiological concentrations tissue cerebrospinal fluid (CSF). Chronic treatment significantly improved spatial learning performance assessments. Electrophysiological recordings demonstrated that either acute bath application (2 mM) to slices or chronic intraperitoneal enhanced high-frequency stimulation (HFS)-induced potentiation (LTP) magnitude 3xTg-AD Ultrastructural analysis revealed density morphological features synapses. At the molecular level, upregulated marker synaptophysin (SYP) expression while downregulating activity-regulated cytoskeletal-associated protein (ARC) These multimodal demonstrate restores function mice through concurrent improvements at behavioral, structural, levels.

Language: Английский

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Aerobic exercise training improves learning and memory performance in hypoxic-exposed rats by activating the hippocampal PKA–CREB–BDNF signaling pathway

BMC Neuroscience, Journal Year: 2025, Volume and Issue: 26(1)

Published: Feb. 21, 2025

Abstract Background This study aims to investigate the effects of aerobic exercise training on learning and memory (L&M) performance in rats exposed altitude hypoxia its relationship with hippocampal plasticity PKA–CREB–BDNF signaling pathway. Methods Male Sprague–Dawley were 14.2% or without 60 min non-weight-bearing swimming for 8 weeks. The L&M was evaluated using Morris water maze, mRNA expression PSD95, SYP, PKA, CREB, CBP, BDNF hippocampus detected. Results Chronic exposure significantly impaired reduced BDNF. Aerobic effectively reversed these changes by enhancing synaptic through activation Conclusion can alleviate decline caused exposure, possibly

Language: Английский

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