Journal of Neuroinflammation, Год журнала: 2024, Номер 21(1)
Опубликована: Сен. 28, 2024
Язык: Английский
Frontiers in Pharmacology, Год журнала: 2024, Номер 15
Опубликована: Сен. 17, 2024
Background Alzheimer’s disease (AD) is a neurodegenerative characterized by progressive decline in cognitive function, which significantly increases pain and social burden. However, few therapeutic interventions are effective preventing or mitigating the progression of AD. An increasing number recent studies support hypothesis that gut microbiome its metabolites may be associated with upstream regulators AD pathology. Methods In this review, we comprehensively explore potential mechanisms currently available targeting for improvement Our discussion structured around modern research advancements AD, bidirectional communication between brain, multi-target regulatory effects microbial on strategies aimed at modulating microbiota to manage Results The plays crucial role pathogenesis through continuous via microbiota-gut-brain axis. Among these, such as lipids, amino acids, bile acids neurotransmitters, especially sphingolipids phospholipids, serve central components gut-brain axis, regulating AD-related pathogenic including β-amyloid metabolism, Tau protein phosphorylation, neuroinflammation. Additionally, probiotic administration, fecal transplantation, antibiotic use have also provided evidence supporting association At same time, propose an innovative strategy treating AD: healthy lifestyle combined targeted probiotics other interventions, aiming restore intestinal ecology balance. Conclusion Despite previous efforts, molecular microbes act yet fully described. microorganisms become essential target connecting axis improving symptoms it requires joint exploration multiple centers disciplines.
Язык: Английский
Процитировано
2
Cells, Год журнала: 2024, Номер 13(19), С. 1608 - 1608
Опубликована: Сен. 25, 2024
Accumulating evidence underscores exercise as a straightforward and cost-effective lifestyle intervention capable of mitigating the risk slowing emergence progression Alzheimer’s disease (AD). However, intricate cellular molecular mechanisms mediating these exercise-induced benefits in AD remain elusive. The present study delved into impact treadmill on memory retrieval performance, hippocampal synaptic plasticity, morphology, expression activity α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic receptors (AMPARs) 6-month-old APP/PS1 mice. mice (4-month-old males) were randomly assigned to either group or sedentary group, with C57BL/6J control (both sedentary). regimen spanned 8 weeks. Our findings revealed that 8-week reversed impairment step-down fear conditioning Additionally, enhanced basic strength, short-term potentiation (STP), long-term (LTP) hippocampus Moreover, correlated an augmentation synapse numbers, refinement structures, heightened AMPARs. suggest improves behavioral performance facilitates transmission by increasing structural plasticity AMPARs mice, which is involved pre- postsynaptic processes.
Язык: Английский
Процитировано
2
Antioxidants, Год журнала: 2023, Номер 12(12), С. 2087 - 2087
Опубликована: Дек. 7, 2023
Mitochondrial biogenesis and fusion are essential for maintaining healthy mitochondria ATP production. High-intensity interval training (HIIT) can enhance mitochondrial function in mouse hippocampi, but its underlying mechanism is not completely understood. Lactate generated during HIIT may mediate the beneficial effects of on neuroplasticity by activating lactate receptor GPR81. Furthermore, growing evidence shows that contributes to function. Given crucial cerebral physiological processes, current study aimed determine hippocampal In vivo, GPR81 was knocked down hippocampi mice via injection adeno-associated virus (AAV) vectors. The GPR81-knockdown were subjected HIIT. results demonstrated increased numbers, production, oxidative phosphorylation (OXPHOS) mice. addition, induced biogenesis, fusion, synaptic plasticity, ERK1/2 vitro, Neuro-2A cells treated with L-lactate, a agonist, an inhibitor. showed both L-lactate agonist levels, OXPHOS, membrane potential, plasticity. However, inhibition blunted or agonist-induced promotion conclusion, our findings suggest mediates HIIT-induced through GPR81-ERK1/2 pathway.
Язык: Английский
Процитировано
5
Experimental Neurology, Год журнала: 2024, Номер 381, С. 114929 - 114929
Опубликована: Авг. 22, 2024
Язык: Английский
Процитировано
0
International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(19), С. 10244 - 10244
Опубликована: Сен. 24, 2024
Alzheimer’s disease (AD) causes a decline in skeletal muscle function, which can further exacerbate the cognitive dysfunction of patients with AD. It has been widely established that exercise improves AD brain pathology, but role is still poorly understood. In this study, we investigated effects treadmill on ability APP/PS1 transgenic mice and explored potential gene expression changes their muscle. The were subjected to for 12 weeks, followed by Morris water maze open field test. After behavioral experiments, morphology, area, collagen fiber deposition, ultrastructure determined; balance protein synthesis decomposition was analyzed; using RNA-Seq. We found strategy promote learning memory abilities mice, reduce anxiety-like behavior, improve ability, alleviate atrophy, optimize microstructure. also enhance several signaling pathways, such as JAK–STAT, Wnt, NOD-like receptors while decreasing calcium, cAMP, cGMP–PKG, other pathways. Six KEGG enrichment pathways downregulated five upregulated compared wild-type these precisely reversed after exercise. transcription factors Fosb Egr1 decreased, decrease regulated target genes Socs1, Srrm4, Il1b, trend following intervention. exercise, exhibited similar indicating enhanced ability. regulatory related identified study provide valuable insights clinical management treatment
Язык: Английский
Процитировано
0
Journal of Neuroinflammation, Год журнала: 2024, Номер 21(1)
Опубликована: Сен. 28, 2024
Язык: Английский
Процитировано
0