Aging, Год журнала: 2024, Номер 16(12), С. 10299 - 10320
Опубликована: Июнь 13, 2024
This study aimed to identify key clock genes closely associated with major depressive disorder (MDD) using bioinformatics and machine learning approaches.
Язык: Английский
Ageing Research Reviews, Год журнала: 2024, Номер 95, С. 102233 - 102233
Опубликована: Фев. 14, 2024
Язык: Английский
Процитировано
17
Neuropsychopharmacology Reports, Год журнала: 2025, Номер 45(1)
Опубликована: Янв. 5, 2025
Alzheimer's disease (AD) is the most common neurodegenerative associated with development of dementia. The hallmarks AD neuropathology are accumulations amyloid peptide (Aβ) and neurofibrillary tangles (NFTs). Aβ derived from processing APP (amyloid beta precursor protein) by BACE1 (beta-secretase 1) γ-secretase through an amyloidogenic pathway. However, ADAM10/α-secretase (ADAM metallopeptidase domain 10) enzymes a non-amyloidogenic pathway produces soluble alpha (sAPPα), which has neuroprotective effect. It been shown that activated platelets implicated in pathogenesis AD, also increases platelet activation. Under physiological conditions, regulate synaptic plasticity increase neuronal differentiation regulation inflammatory response. overactivated contribute to AD. Activated represent main source circulating may be involved neuropathology. Therefore, there close relationship between platelets. This review discusses potential role how targeting reduce
Язык: Английский
Процитировано
3
Signal Transduction and Targeted Therapy, Год журнала: 2025, Номер 10(1)
Опубликована: Фев. 2, 2025
Язык: Английский
Процитировано
3
Frontiers in Medicine, Год журнала: 2025, Номер 12
Опубликована: Фев. 4, 2025
Alzheimer’s disease (AD) is the most common cause of dementia and represents 75% all types. AD neuropathology due to progressive deposition extracellular amyloid-beta (A β ) peptide intracellular hyperphosphorylated tau protein. The accumulated Aβ forms amyloid plaques, while protein neurofibrillary tangles (NFTs). Both plaques NFTs are hallmarks neuropathology. fundamental mechanism involved in pathogenesis still elusive, although more conceivable theory. Aβ-induced neurodegeneration associated neuroinflammation, oxidative stress, endoplasmic reticulum stress (ER), mitochondrial dysfunction contribute development cognitive impairment dementia. Of note, not only originated from brain but also produced peripherally and, via blood–brain barrier (BBB), can accumulate result AD. It has been shown that cardiometabolic conditions such as obesity, type 2 diabetes (T2D), heart failure (HF) regarded possible risk factors for other types dementia, vascular HF-induced chronic cerebral hypoperfusion, inflammation induce progression Interestingly, a systemic causes which turn affects peripheral organs, including heart. through deranged BBB be transported into circulation heart, leading HF. These findings suggest close relationship between However, exact AD-induced HF fully elucidated. Therefore, this review aims discuss link regarding potential role
Язык: Английский
Процитировано
3
Ageing Research Reviews, Год журнала: 2025, Номер unknown, С. 102680 - 102680
Опубликована: Фев. 1, 2025
Язык: Английский
Процитировано
2
Journal of Cellular and Molecular Medicine, Год журнала: 2024, Номер 28(10)
Опубликована: Май 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
Язык: Английский
Процитировано
15
Molecular Neurobiology, Год журнала: 2024, Номер 61(9), С. 7092 - 7108
Опубликована: Фев. 17, 2024
Abstract Parkinson’s disease (PD) is a progressive neurodegenerative of the brain due to degeneration dopaminergic neurons in substantia nigra (SN). Glycogen synthase kinase 3 beta (GSK-3β) implicated pathogenesis PD. Therefore, purpose present review was revise mechanistic role GSK-3β PD neuropathology, and how inhibitors affect neuropathology. GSK-3 conserved threonine/serine protein that intricate regulation cellular anabolic catabolic pathways by modulating glycogen synthase. Over-expression also interconnected with development different diseases. However, underlying mechanism neuropathology not fully clarified. induces triggering mitochondrial dysfunction oxidative stress SN. NF-κB NLRP3 inflammasome are activated response dysregulated leading neuronal injury. Higher expression early stages might contribute reduction neuroprotective brain-derived neurotrophic factor (BDNF). Thus, may be effective reducing inflammatory disorders which associated
Язык: Английский
Процитировано
11
International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(22), С. 11955 - 11955
Опубликована: Ноя. 7, 2024
Alzheimer's disease (AD) and type 2 diabetes mellitus (T2DM) are two prevalent conditions that present considerable public health issue in aging populations worldwide. Recent research has proposed a novel conceptualization of AD as "type 3 diabetes", highlighting the critical roles insulin resistance impaired glucose metabolism pathogenesis disease. This article examines implications this association, exploring potential new avenues for treatment preventive strategies AD. Key evidence linking to emphasizes metabolic processes contribute neurodegeneration, including inflammation, oxidative stress, alterations signaling pathways. By framing within context, we can enhance our understanding its etiology, which turn may influence early diagnosis, plans, measures. Understanding manifestation opens up possibility employing therapeutic incorporate lifestyle modifications use antidiabetic medications mitigate cognitive decline. integrated approach improve patient outcomes deepen comprehension intricate relationship between neurodegenerative diseases disorders.
Язык: Английский
Процитировано
11
Neuropsychopharmacology Reports, Год журнала: 2024, Номер 44(3), С. 639 - 649
Опубликована: Июль 29, 2024
Abstract Neurodegenerative diseases (NDs) such as Alzheimer disease (AD) and Parkinson (PD) are group of affecting the central nervous system (CNS) characterized by progressive neurodegenerations cognitive impairment. Findings from different studies highlighted beneficial detrimental effects serum uric acid on development progression NDs. Therefore, this mini‐review aims to discuss The neuroprotective effect is mainly related antioxidant which alleviates oxidative stress‐induced neurodegeneration in AD PD. However, long‐term hyperuricemia prompts for Hyperuricemia associated with impairment dementia, gout increases dementia risk. In addition, can cause cerebral vascular injury a risk factor Taken together, relationship between NDs remains conflicting. Hence, preclinical clinical indicated regard.
Язык: Английский
Процитировано
7
RSC Advances, Год журнала: 2024, Номер 14(21), С. 14742 - 14757
Опубликована: Янв. 1, 2024
Pregnenolone-based derivatives have been synthesized to inhibit the protofibril formation in order reduce Aβ 1–42 production and prevent its aggregation.
Язык: Английский
Процитировано
6