We are analyzing https://link.springer.com/article/10.1007/s10571-025-01559-9.

Title:
Let-7 Family as a Mediator of Exercise on Alzheimer’s Disease | Cellular and Molecular Neurobiology
Description:
Memory loss, and behavioral impairments. Hallmark pathological features include amyloid-beta (Aβ) plaques, tau neurofibrillary tangles, chronic inflammation, and impaired neuronal signaling. Physical exercise is increasingly recognized as a non-pharmacological intervention to attenuate Alzheimer’s disease (AD) risk and progression by enhancing neuroplasticity, improving mitochondrial function, and modulating immune responses. The let-7 family of microRNAs is critically involved in AD pathology. Elevated levels of let-7b and let-7e have been reported in the cerebrospinal fluid of AD patients, with let-7b levels correlating positively with total tau and phosphorylated tau concentrations. Overexpression of let-7a enhances Aβ-induced neurotoxicity, increases neuronal apoptosis by up to 45%, and alters autophagy-related signaling via the PI3K/Akt/mTOR pathway, as shown by 1.8-fold increases in LC3-II/I ratios and 2.2-fold upregulation of Beclin-1 expression. Exercise modulates let-7 expression in a tissue-specific and context-dependent manner. Aerobic training reduces skeletal muscle expression of let-7b-5p by 30–35%, while increasing its suppressor Lin28a by 40%, thereby improving mitochondrial respiration. Overall, modulation of let-7 by exercise influences neuronal survival, autophagy, and inflammation, offering a potential mechanism through which physical activity exerts neuroprotective effects in AD. Quantitative characterization of let-7 expression patterns may support its use as a diagnostic and therapeutic biomarker, though further research is needed to establish optimal modulation strategies.
Website Age:
28 years and 1 months (reg. 1997-05-29).

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Keywords {🔍}

pubmed, article, google, scholar, cas, exercise, alzheimers, disease, central, expression, levels, cell, mirnas, cells, cancer, microrna, activity, physical, role, wang, cognitive, pathways, family, leta, impact, research, signaling, pathway, liu, micrornas, study, tlr, studies, mirna, chen, function, increased, effects, protein, letb, brain, tau, training, potential, aerobic, individuals, regulation, gene, progression, autophagy,

Topics {✒️}

t-tau-p-tau logistic regression au-rich-element-mediated upregulation k-ras/hmga2/snail axis taq-man qrt-pcr analyses radiation-induced micro-rna modulation conduct long-term investigations article download pdf de la rosa eukaryotic rna-interference machinery tlr-mediated signal transduction control long-term modifications n6-methyladenylated ggac sequences short-term interval training hsa-let7 g-5p compared rna polymerase ii/iii high-intensity interval training antisense-mediated depletion reveal org/cgi-bin/browse zeb1 induced mir-99b/ t-maze alternation percentage high-fat diet resulted hsa-let7 g-5p mirnas alzheimer’s-related synaptic dysfunction hcv-mediated hepatocellular carcinoma tlr4/pi3k/akt signaling microrna-mediated gene silencing pi3k/akt/mtor pathway stem cell-derived cardiomyocytes central nervous system /akt/mtor signaling pathway large case–control study rna-sensing protein tlr7 pten/akt/foxo1 pathway directly targeting k-ras sample collection post-exercise modeling late-onset alzheimer alters autophagy-related signaling 7e-5p regulates igf2bp2 yuwen wan contributed de la longrais growth factor-ii expression increased p-tau concentration exacerbate aβ1–40-induced neurotoxicity exacerbate aβ-induced neurotoxicity long-term studies privacy choices/manage cookies ago2-mediated microrna biogenesis alters autophagy-related pathways induces muscle atrophy ruiz-pérez

Questions {❓}

Leng F, Edison P (2021) Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here?

Schema {🗺️}

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      description:Memory loss, and behavioral impairments. Hallmark pathological features include amyloid-beta (Aβ) plaques, tau neurofibrillary tangles, chronic inflammation, and impaired neuronal signaling. Physical exercise is increasingly recognized as a non-pharmacological intervention to attenuate Alzheimer’s disease (AD) risk and progression by enhancing neuroplasticity, improving mitochondrial function, and modulating immune responses. The let-7 family of microRNAs is critically involved in AD pathology. Elevated levels of let-7b and let-7e have been reported in the cerebrospinal fluid of AD patients, with let-7b levels correlating positively with total tau and phosphorylated tau concentrations. Overexpression of let-7a enhances Aβ-induced neurotoxicity, increases neuronal apoptosis by up to 45%, and alters autophagy-related signaling via the PI3K/Akt/mTOR pathway, as shown by 1.8-fold increases in LC3-II/I ratios and 2.2-fold upregulation of Beclin-1 expression. Exercise modulates let-7 expression in a tissue-specific and context-dependent manner. Aerobic training reduces skeletal muscle expression of let-7b-5p by 30–35%, while increasing its suppressor Lin28a by 40%, thereby improving mitochondrial respiration. Overall, modulation of let-7 by exercise influences neuronal survival, autophagy, and inflammation, offering a potential mechanism through which physical activity exerts neuroprotective effects in AD. Quantitative characterization of let-7 expression patterns may support its use as a diagnostic and therapeutic biomarker, though further research is needed to establish optimal modulation strategies.
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