International Journal of Biological Macromolecules, Journal Year: 2025, Volume and Issue: 309, P. 142933 - 142933
Published: April 8, 2025
Language: Английский
International Journal of Biological Macromolecules, Journal Year: 2025, Volume and Issue: 309, P. 142933 - 142933
Published: April 8, 2025
Language: Английский
Autophagy, Journal Year: 2023, Volume and Issue: 20(2), P. 259 - 274
Published: Sept. 15, 2023
Multiple sclerosis (MS) is a chronic progressive demyelinating disease of the central nervous system (CNS) due to an increase abnormal peripherally auto-reactive T lymphocytes which elicit autoimmunity. The main pathophysiology MS myelin sheath damage by immune cells and defect in generation oligodendrocytes. Macroautophagy/autophagy critical degradation process that eliminates dysfunctional or superfluous cellular components. Autophagy has property double-edged sword it may have both beneficial detrimental effects on neuropathology. Therefore, this review illustrates protective harmful autophagy with regard disease. prevents progression reducing oxidative stress inflammatory disorders. In contrast, over-activated associated neuropathology case use inhibitors alleviate pathogenesis MS. Furthermore, provokes activation different supporting play intricate role functions modulation regulating cell proliferation related demyelination remyelination. enhances remyelination increasing activity oligodendrocytes, astrocytes. However, induces activating microglia cells. conclusion, specific autophagic activators astrocytes, dendritic (DCs), induce against
Language: Английский
Citations
35Diabetology & Metabolic Syndrome, Journal Year: 2023, Volume and Issue: 15(1)
Published: May 13, 2023
Abstract Human Islet amyloid polypeptide (hIAPP) from pancreatic β cells in the islet of Langerhans has different physiological functions including inhibiting release insulin and glucagon. Type 2 diabetes mellitus (T2DM) is an endocrine disorder due to relative insufficiency resistance (IR) associated with increased circulating hIAPP. Remarkably, hIAPP structural similarity beta (Aβ) can engage pathogenesis T2DM Alzheimer’s disease (AD). Therefore, present review aimed elucidate how acts as a link between AD. IR, aging low cell mass increase expression which binds membrane leading aberrant Ca 2+ activation proteolytic enzymes series events causing loss cells. Peripheral plays major role AD, high level AD risk patients. However, there no hard evidence for brain-derived Nevertheless, oxidative stress, mitochondrial dysfunction, chaperon-mediated autophagy, heparan sulfate proteoglycan (HSPG), immune response, zinc homeostasis could be possible mechanisms induction aggregation risk. In conclusion, increasing levels patients predispose them development progression Dipeptidyl peptidase 4 (DPP4) inhibitors glucagon-like peptide-1 (GLP-1) agonists attenuate by deposition hIAP.
Language: Английский
Citations
33Ageing Research Reviews, Journal Year: 2023, Volume and Issue: 91, P. 102084 - 102084
Published: Oct. 5, 2023
Language: Английский
Citations
32Molecular Medicine, Journal Year: 2023, Volume and Issue: 29(1)
Published: Oct. 25, 2023
Abstract Autophagy is an explicit cellular process to deliver dissimilar cytoplasmic misfolded proteins, lipids and damaged organelles the lysosomes for degradation elimination. The mechanistic target of rapamycin (mTOR) main negative regulator autophagy. mTOR pathway involved in regulating neurogenesis, synaptic plasticity, neuronal development excitability. Exaggerated activity associated with temporal lobe epilepsy, genetic acquired experimental epilepsy. In particular, complex 1 (mTORC1) mainly epileptogenesis. investigation autophagy’s involvement epilepsy has recently been conducted, focusing on critical role rapamycin, autophagy inducer, reducing severity induced seizures animal model studies. induction could be innovative therapeutic strategy managing Despite protective against epileptogenesis its status epilepticus (SE) perplexing might beneficial or detrimental. Therefore, present review aims revise possible
Language: Английский
Citations
29Inflammopharmacology, Journal Year: 2023, Volume and Issue: 31(4), P. 1671 - 1682
Published: May 9, 2023
Language: Английский
Citations
27Cellular and Molecular Neurobiology, Journal Year: 2023, Volume and Issue: 43(7), P. 3405 - 3416
Published: Aug. 4, 2023
Abstract Hypothyroidism (HPT) HPT could be a risk factor for the development and progression of Alzheimer’s disease (AD). In addition, progressive neurodegeneration in AD may affect metabolism thyroid hormones (THs) brain causing local HPT. Hence, present review aimed to clarify potential association between AD. promotes by inducing production amyloid beta (A β ) tau protein phosphorylation with synaptic plasticity memory dysfunction. Besides, THs is dysregulated due accumulation A leading Additionally, can neuropathology through various mechanistic pathways including dysregulation transthyretin, oxidative stress, ER autophagy dysfunction mitochondrial dysfunction, inhibition brain-derived neurotrophic factor. Taken together there link AD, as adversely impacts reverse also true. Graphical
Language: Английский
Citations
26Molecular Neurobiology, Journal Year: 2023, Volume and Issue: 61(5), P. 2469 - 2480
Published: Oct. 28, 2023
Language: Английский
Citations
26Ageing Research Reviews, Journal Year: 2023, Volume and Issue: 92, P. 102119 - 102119
Published: Nov. 4, 2023
Language: Английский
Citations
25Neurochemical Research, Journal Year: 2023, Volume and Issue: 48(11), P. 3255 - 3269
Published: July 13, 2023
Abstract Multiple sclerosis (MS) is an autoimmune demyelinating neurodegenerative disease of the central nervous system (CNS) due to injury myelin sheath by immune cells. The clotting factor fibrinogen involved in pathogenesis MS triggering microglia and progress neuroinflammation. Fibrinogen level correlated with severity; consequently, inhibition cascade may reduce neuropathology. Thus, this review aimed clarify potential role how targeting affects Accumulation CNS occur independently or disruption blood–brain barrier (BBB) integrity MS. acts as transduction increases activation which induces progression inflammation, oxidative stress, neuronal injury. Besides, brain impairs remyelination process inhibiting differentiation oligodendrocyte precursor These findings proposed that associated neuropathology through interruption BBB integrity, induction neuroinflammation, demyelination suppressing oligodendrocytes. Therefore, and/or CD11b/CD18 receptors metformin statins might decrease In conclusion, expression pro-inflammatory effect on
Language: Английский
Citations
24Journal of Cellular and Molecular Medicine, Journal Year: 2024, Volume and Issue: 28(10)
Published: May 1, 2024
Parkinson's disease (PD) is a neurodegenerative disorder of the brain and manifested by motor non-motor symptoms because degenerative changes in dopaminergic neurons substantia nigra. PD neuropathology associated with mitochondrial dysfunction, oxidative damage apoptosis. Thus, modulation apoptosis growth factors could be novel boulevard management PD. Brain-derived neurotrophic factor (BDNF) its receptor tropomyosin kinase type B (TrkB) are chiefly involved neuropathology. BDNF promotes survival nigra enhances functional activity striatal neurons. Deficiency TrkB triggers degeneration accumulation α-Syn As well, BDNF/TrkB signalling reduced early phase Targeting specific activators may attenuate this review aimed to discuss potential role against In conclusion, decreased linked severity long-term complications. Activation
Language: Английский
Citations
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