Beyond Wolfram Syndrome 1: The WFS1 Gene’s Role in Alzheimer’s Disease and Sleep Disorders DOI Creative Commons
Valerio Caruso, Luciana Rigoli

Biomolecules, Год журнала: 2024, Номер 14(11), С. 1389 - 1389

Опубликована: Окт. 31, 2024

The

Язык: Английский

Nanotechnology-Driven Therapeutic Innovations in Neurodegenerative Disorders: A Focus on Alzheimer’s and Parkinson’s Disease DOI Creative Commons

Antea Kršek,

Lara Batičić

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

9

Protein Oxidation in Aging and Alzheimer’s Disease Brain DOI Creative Commons
Rukhsana Sultana, D. Allan Butterfield

Antioxidants, 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

6

Anti-inflammatory and antioxidant effects of baicalein: targeting Nrf2, and NFĸB in neurodegenerative disease DOI

Omkar Kumar Kuwar,

Neena Kalia

Inflammopharmacology, Год журнала: 2025, Номер unknown

Опубликована: Фев. 27, 2025

Язык: Английский

Процитировано

0

CRISPR/Cas9 gene editing for treating gene and protein disorders DOI
Chukwuebuka Emmanuel Umeyor, Preeya Negi,

R. Agarwal

и другие.

Elsevier eBooks, Год журнала: 2025, Номер unknown, С. 519 - 553

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

0

MFIFN: A multimodal feature interaction fusion network-based model for Alzheimer’s disease classification DOI

Yibo Huang,

Jie Liu, Zhiyong Li

и другие.

Biomedical Signal Processing and Control, Год журнала: 2025, Номер 107, С. 107857 - 107857

Опубликована: Март 30, 2025

Язык: Английский

Процитировано

0

Decoding Neurodegeneration: A Review of Molecular Mechanisms and Therapeutic Advances in Alzheimer’s, Parkinson’s, and ALS DOI Open Access
Corneliu Toader,

Călin Petru Tătaru,

Octavian Munteanu

и другие.

International 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

3

Potential Roles of Hypoxia-Inducible Factor-1 in Alzheimer’s Disease: Beneficial or Detrimental? DOI Creative Commons
Tsu‐Kung Lin,

Chi-Ren Huang,

Kai-Jung Lin

и другие.

Antioxidants, 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

2

Special Issue ‘Advances in Neurodegenerative Diseases Research and Therapy 2.0’ DOI Open Access
Sumonto Mitra

International 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

0

Alzheimer's Disease Investigated via Gene-Environment Interactions, Biochemical Pathways, Cellular Processes, and Disease Phenotype Variability DOI Creative Commons
Viqas Shafi,

Ifrah Siddiqui

Research Square (Research Square), Год журнала: 2024, Номер unknown

Опубликована: Май 14, 2024

Abstract Background: Alzheimer's disease (AD) is a neurodegenerative disorder influenced by genetic and environmental factors. APOE, APP, PSEN1, PSEN2, CLU, SORL1, BIN1, CR1, PICALM, TREM2, ABCA7, CD33 play key roles in AD pathogenesis, affecting biochemical pathways cellular processes. However, the interaction between predisposition factors, as well reasons for variability phenotype, remain poorly understood. This study aims to investigate these interactions improve our understanding of etiology inform personalized interventions. Methods: A comprehensive search encompassing databases such PubMed, MEDLINE, Google Scholar, open access/subscription-based journals was conducted retrieve relevant articles investigation genes involved including CD33. Articles were searched without any date restrictions. Utilizing criteria delineated methodology section, studies systematically reviewed elucidate how factors genetics influence onset, progression, symptom severity, progression rates. adheres PRISMA guidelines (Preferred Reporting Items Systematic Reviews Meta-Analyses). Results: Our revealed complicated predisposition, pathways, processes pathogenesis. amyloid-beta production, tau pathology, lipid metabolism, inflammation AD. These interact with diet, pollutants, head trauma, lifestyle, modulating risk progression. Additionally, we found phenotype among individuals carrying similar mutations, modifiers, cognitive reserve, neurobiological differences. Conclusion: multifactorial critical pathogenesis inflammation. further Understanding essential developing interventions delay reduce slow

Язык: Английский

Процитировано

0

Glutamate Transporter 1 as a Novel Negative Regulator of Amyloid β DOI Creative Commons
Priyanka Sinha,

Yuliia Turchyna,

Shane Mitchell

и другие.

Cells, 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

0