Multi-strain probiotics ameliorate Alzheimer’s-like cognitive impairment and pathological changes through the AKT/GSK-3β pathway in senescence-accelerated mouse prone 8 mice

Brain Behavior and Immunity, Journal Year: 2024, Volume and Issue: 119, P. 14 - 27

Published: March 26, 2024

Language: Английский

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Exploring the molecular mechanisms of MSC-derived exosomes in Alzheimer's disease: Autophagy, insulin and the PI3K/Akt/mTOR signaling pathway

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 176, P. 116836 - 116836

Published: June 7, 2024

Alzheimer's disease (AD) is a devastating neurological condition characterized by cognitive decline, motor coordination impairment, and amyloid plaque accumulation.The underlying molecular mechanisms involve oxidative stress, inflammation, neuronal degeneration.This study aimed to investigate the therapeutic

Language: Английский

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Protective Effects of Bifidobacterium Breve MCC1274 as a Novel Therapy for Alzheimer’s Disease

Nutrients, Journal Year: 2025, Volume and Issue: 17(3), P. 558 - 558

Published: Jan. 31, 2025

Alzheimer’s disease (AD) is the most common form of dementia and characterized by memory impairment that significantly interferes with daily life. Therapeutic options for AD substantively modify progression remain a critical unmet need. In this regard, gut microbiota crucial in maintaining human health regulating metabolism immune responses, increasing evidence suggests probiotics, particularly beneficial bacteria, can enhance cognitive functions. Recent studies have highlighted positive effects Bifidobacterium breve MCC1274 (B. MCC1274) on individuals mild (MCI) schizophrenia. Additionally, oral supplementation B. has been shown to effectively prevent decline AppNL–G–F mice. relation pathology, found reduce amyloid-β (Aβ) accumulation tau phosphorylation both wild-type (WT) It also decreases microglial activation increases levels synaptic proteins. review, we examine AD, exploring potential mechanisms action how probiotic strain may aid preventing or treating disease. Furthermore, discuss broader implications improving overall host provide insights into future research directions promising therapy.

Language: Английский

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Aβ-Induced Drp1 phosphorylation through Akt activation promotes excessive mitochondrial fission leading to neuronal apoptosis

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, Journal Year: 2016, Volume and Issue: 1863(11), P. 2820 - 2834

Published: Sept. 9, 2016

Language: Английский

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Sulforaphene Ameliorates Neuroinflammation and Hyperphosphorylated Tau Protein via Regulating the PI3K/Akt/GSK-3βPathway in Experimental Models of Alzheimer’s Disease

Oxidative Medicine and Cellular Longevity, Journal Year: 2020, Volume and Issue: 2020, P. 1 - 17

Published: Sept. 11, 2020

Alzheimer’s disease (AD) is the most common form of dementia characterized by progressive loss cognitive functions due to neuronal death mainly in hippocampal and cortical brain. Sulforaphene (SF) one main isothiocyanates isolated from a Chinese herb Raphani Semen. In this study, we aimed investigate neuroprotective effects SF using vitro vivo models AD. Streptozotocin (STZ) was intracranially injected into rats; then, (25 50 mg/kg) given orally once day for 6 consecutive weeks. After drug treatment, were assessed Morris Water Maze Test (MWMT). MWMT, rats euthanized brain tissues collected. test, BV-2 microglia pretreated with (1 2 μ M) 1 h then stimulated lipopolysaccharide (LPS) another 23 h. Both molecular histological methods used unravel action mechanisms elucidate signaling pathway. The MWMT results showed that treatment significantly improved STZ-induced deficits rats. markedly suppressed production tumor necrosis factor- α (TNF- ) interleukin-6 (IL-6) but increased release IL-10 STZ-treated addition, inhibited phosphorylation tau protein at Thr205, Ser396, Ser404 sites, while enhancing ratios p-Akt (Ser473)/Akt p-GSK-3 β (Ser9)/GSK-3 hippocampus On other hand, also attenuated cytotoxicity induced LPS cells. obviously releases nitric oxide (NO), TNF- , IL-6 LPS-stimulated Moreover, mitigated nuclear translocation p-NF- κ B p65 ratio Taken together, possessed against LPS-induced neuroinflammation cells via modulation PI3K/Akt/GSK-3 pathway inhibition NF- activation, suggesting promising agent worthy further development AD treatment.

Language: Английский

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Inverse relationship between Alzheimer’s disease and cancer, and other factors contributing to Alzheimer’s disease: a systematic review

BMC Neurology, Journal Year: 2016, Volume and Issue: 16(1)

Published: Nov. 22, 2016

The AD etiology is yet not properly known. Interactions among environmental factors, multiple susceptibility genes and aging, contribute to AD. This study investigates the factors that play role in causing how changes cellular pathways PUBMED database, MEDLINE database Google Scholar were searched with no date restrictions for published articles involving roles cancers, cell survival, growth, proliferation, development, also contributing Alzheimer’s disease. research explores inverse relationship between cancer, other behind using several already literature find of Cancer disease have many aspects such as P53, estrogen, neurotrophins growth cAMP, EGFR, Bcl-2, apoptosis pathways, IGF-1, HSV, TDP-43, APOE variants, notch signals presenilins, NCAM, TNF alpha, PI3K/AKT/MTOR pathway, telomerase, ROS, ACE levels. occurs when brain neurons weakened survival responses, maintenance mechanisms, anti-stress responses Vimentin, Carbonic anhydrases, HSPs, SAPK. In these are upregulated maintained. Evolutionarily conserved mechanisms FOXO impaired Countermeasures or compensatory by affected Tau, Beta Amyloid, S100, last attempts which may be protective certain time, can speed up microenvironment via C-ABL activation, GSK3, neuro-inflammation. relationship; any cancer sustain downregulated neuro-degeneration. When aged genetically susceptible age related gene expression changes, altered regulation death they Amyloid Plaques, NFTs, this provides neuroprotection time ultimately become pathological developing new potential diagnostic tests, interventions treatments.

Language: Английский

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Stimulation of ACE2/ANG(1–7)/Mas Axis by Diminazene Ameliorates Alzheimer’s Disease in the D-Galactose-Ovariectomized Rat Model: Role of PI3K/Akt Pathway

Molecular Neurobiology, Journal Year: 2018, Volume and Issue: 55(10), P. 8188 - 8202

Published: March 7, 2018

Language: Английский

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Attenuation of Aluminum Chloride-Induced Neuroinflammation and Caspase Activation Through the AKT/GSK-3β Pathway by Hesperidin in Wistar Rats

Neurotoxicity Research, Journal Year: 2018, Volume and Issue: 34(3), P. 463 - 476

Published: April 23, 2018

Language: Английский

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Role of transient receptor potential ankyrin 1 channels in Alzheimer’s disease

Journal of Neuroinflammation, Journal Year: 2016, Volume and Issue: 13(1)

Published: April 27, 2016

Transient receptor potential ankyrin 1 (TRPA1) channel plays an important role in pain and inflammation. However, little is known about the significance of TRPA1 pathophysiology Alzheimer's disease (AD).Wild-type (WT), TRPA1(-/-), amyloid precursor protein (APP)/presenilin (PS1) transgenic (APP/PS1 Tg) mice, mouse model AD, APP/PS1 Tg/TRPA1(-/-) mice were used to examine pathogenesis AD. Western blot was for expression; immunohistochemistry histological examination. The behaviors evaluated by locomotion, nesting building, Y-maze Morris water maze tests; levels interleukin (IL)-1β, IL-4, IL-6 IL-10 activities phosphatase 2B (PP2B), NF-κB nuclear factor activated T cells (NFAT) measured conventional assay kits; Fluo-8 NW calcium (Ca(2+)) kit measurement intracellular Ca(2+) level primary astrocytes HEK293 cells.The expression channels higher brains, mainly hippocampus, from Tg than WT mice. Ablation TRPA1-channel function alleviated behavioral dysfunction, Aβ plaque deposition pro-inflammatory cytokine production but increased astrogliosis brain lesions. influx elicited both TRPA1-transfected treated with fibrilized Aβ1-42; these abrogated pharmacological inhibition activity, disruption or removal extracellular Ca(2+). Inhibition activity exacerbated Aβ1-42-induced inhibited Aβ1-42-increased PP2B activation, cytokines transcriptional factors NFAT Pharmacological diminished cytokines, activation astrocytes.TRPA1 - signaling may play a crucial regulating astrocyte-derived inflammation

Language: Английский

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Astaxanthin targets PI3K/Akt signaling pathway toward potential therapeutic applications

Food and Chemical Toxicology, Journal Year: 2020, Volume and Issue: 145, P. 111714 - 111714

Published: Aug. 30, 2020

Language: Английский

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