
Biomolecules, Год журнала: 2024, Номер 14(11), С. 1389 - 1389
Опубликована: Окт. 31, 2024
The
Язык: Английский
Biomolecules, Год журнала: 2024, Номер 14(11), С. 1389 - 1389
Опубликована: Окт. 31, 2024
The
Язык: Английский
Future Pharmacology, Год журнала: 2024, Номер 4(2), С. 352 - 379
Опубликована: Апрель 30, 2024
Neurodegenerative disorders entail a progressive loss of neurons in cerebral and peripheral tissues, coupled with the aggregation proteins exhibiting altered physicochemical properties. Crucial to these conditions is gradual degradation central nervous system, manifesting as impairments mobility, aberrant behaviors, cognitive deficits. Mechanisms such proteotoxic stress, neuroinflammation, oxidative programmed cell death contribute ongoing dysfunction demise neurons. Presently, neurodegenerative diseases lack definitive cures, available therapies primarily offer palliative relief. The integration nanotechnology into medical practices has significantly augmented both treatment efficacy diagnostic capabilities. Nanoparticles, capable traversing blood–brain barrier, hold considerable potential for diagnosing treating brain pathologies. By combining gene therapy nanotechnology, therapeutic effectiveness against can be substantially enhanced. Recent advancements nano-biomaterial-based methodologies have fortified existing approaches neural stem (NSC) differentiation therapies. NSC-targeting technologies promising, potentially safe method diseases. This review endeavors summarize current insights perspectives on nanotechnology-driven innovations disorders, particular emphasis Alzheimer’s Parkinson’s disease.
Язык: Английский
Процитировано
9Antioxidants, Год журнала: 2024, Номер 13(5), С. 574 - 574
Опубликована: Май 7, 2024
Proteins are essential molecules that play crucial roles in maintaining cellular homeostasis and carrying out biological functions such as catalyzing biochemical reactions, structural proteins, immune response, etc. However, proteins also highly susceptible to damage by reactive oxygen species (ROS) nitrogen (RNS). In this review, we summarize the role of protein oxidation normal aging Alzheimer's disease (AD). The major emphasis review article is on carbonylation nitration AD mild cognitive impairment (MCI). oxidatively modified showed a strong correlation with reported changes brain structure, carbohydrate metabolism, synaptic transmission, energetics, etc., both MCI brains compared controls. Some were found be common targets observed during early stages AD, suggesting those might critical onset symptoms and/or formation pathological hallmarks AD. Further studies required fully elucidate progression pathogenesis
Язык: Английский
Процитировано
6Inflammopharmacology, Год журнала: 2025, Номер unknown
Опубликована: Фев. 27, 2025
Язык: Английский
Процитировано
0Elsevier eBooks, Год журнала: 2025, Номер unknown, С. 519 - 553
Опубликована: Янв. 1, 2025
Язык: Английский
Процитировано
0Biomedical Signal Processing and Control, Год журнала: 2025, Номер 107, С. 107857 - 107857
Опубликована: Март 30, 2025
Язык: Английский
Процитировано
0International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(23), С. 12613 - 12613
Опубликована: Ноя. 24, 2024
Neurodegenerative diseases, such as Alzheimer's, Parkinson's, ALS, and Huntington's, remain formidable challenges in medicine, with their relentless progression limited therapeutic options. These diseases arise from a web of molecular disturbances-misfolded proteins, chronic neuroinflammation, mitochondrial dysfunction, genetic mutations-that slowly dismantle neuronal integrity. Yet, recent scientific breakthroughs are opening new paths to intervene these once-intractable conditions. This review synthesizes the latest insights into underlying dynamics neurodegeneration, revealing how intertwined pathways drive course diseases. With an eye on most promising advances, we explore innovative therapies emerging cutting-edge research: nanotechnology-based drug delivery systems capable navigating blood-brain barrier, gene-editing tools like CRISPR designed correct harmful variants, stem cell strategies that not only replace lost neurons but foster neuroprotective environments. Pharmacogenomics is reshaping treatment personalization, enabling tailored align individual profiles, while diagnostics biomarkers ushering era early, precise disease detection. Furthermore, novel perspectives gut-brain axis sparking interest mounting evidence suggests microbiome modulation may play role reducing neuroinflammatory responses linked neurodegenerative progression. Taken together, advances signal shift toward comprehensive, personalized approach could transform care. By integrating techniques, this offers forward-looking perspective future where treatments aim just manage symptoms fundamentally alter progression, presenting renewed hope for improved patient outcomes.
Язык: Английский
Процитировано
3Antioxidants, Год журнала: 2024, Номер 13(11), С. 1378 - 1378
Опубликована: Ноя. 11, 2024
The major pathological characteristics of Alzheimer's disease (AD) include senile plaques and neurofibrillary tangles (NFTs), which are mainly composed aggregated amyloid-beta (Aβ) peptide hyperphosphorylated tau protein, respectively. excessive production reactive oxygen species (ROS) neuroinflammation crucial contributing factors to the mechanisms AD. Hypoxia-inducible factor-1 (HIF-1) is a transcription factor critical for tissue adaption low-oxygen tension. Growing evidence has suggested HIF-1 as potential therapeutic target AD; conversely, other experimental findings indicate that induction contributes AD pathogenesis. These previous thus point complex, even contradictory, roles in In this review, we first introduce general pathogenic well pathophysiological cancer, immunity, oxidative stress. Based on current literature, then discuss possible beneficial detrimental these sections also summaries multiple chemical reagents proteins have been shown exert effects via either or inhibition HIF-1.
Язык: Английский
Процитировано
2International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(9), С. 4709 - 4709
Опубликована: Апрель 26, 2024
Neurodegenerative disorders (NDs) and the development of various therapeutic strategies to combat them have received increased attention in recent decades [...]
Язык: Английский
Процитировано
0Research Square (Research Square), Год журнала: 2024, Номер unknown
Опубликована: Май 14, 2024
Язык: Английский
Процитировано
0Cells, Год журнала: 2024, Номер 13(19), С. 1600 - 1600
Опубликована: Сен. 24, 2024
Glutamate transporter-1 (GLT-1) dynamics are implicated in excitotoxicity and Alzheimer’s disease (AD) progression. Early stages of AD often marked by hyperactivity increased epileptiform activity preceding cognitive decline. Previously, we identified a direct interaction between GLT-1 Presenilin 1 (PS1) the brain, highlighting as promising target research. This study reports significance this uncovers novel role modulating amyloid-beta (Aβ) production. Overexpression cells reduces levels Aβ40 Aβ42 decreasing γ-secretase pertinent to APP processing induces more “open” PS1 conformation, resulting decreased Aβ42/40 ratio. Inhibition GLT-1/PS1 using cell-permeable peptides produced an opposing effect on Aβ, pivotal regulating Aβ levels. These findings emphasize potential targeting therapeutic strategy for AD.
Язык: Английский
Процитировано
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