Neurotoxicity Research, Journal Year: 2020, Volume and Issue: 38(4), P. 833 - 849
Published: June 18, 2020
Language: Английский
Neurotoxicity Research, Journal Year: 2020, Volume and Issue: 38(4), P. 833 - 849
Published: June 18, 2020
Language: Английский
Molecules, Journal Year: 2020, Volume and Issue: 25(24), P. 5789 - 5789
Published: Dec. 8, 2020
Alzheimer’s disease (AD) is a disorder that causes degeneration of the cells in brain and it main cause dementia, which characterized by decline thinking independence personal daily activities. AD considered multifactorial disease: two hypotheses were proposed as for AD, cholinergic amyloid hypotheses. Additionally, several risk factors such increasing age, genetic factors, head injuries, vascular diseases, infections, environmental play role disease. Currently, there are only classes approved drugs to treat including inhibitors cholinesterase enzyme antagonists N-methyl d-aspartate (NMDA), effective treating symptoms but do not cure or prevent Nowadays, research focusing on understanding pathology targeting mechanisms, abnormal tau protein metabolism, β-amyloid, inflammatory response, free radical damage, aiming develop successful treatments capable stopping modifying course AD. This review discusses currently available future theories development new therapies disease-modifying therapeutics (DMT), chaperones, natural compounds.
Language: Английский
Citations
1898The Lancet Neurology, Journal Year: 2021, Volume and Issue: 20(6), P. 484 - 496
Published: April 30, 2021
Language: Английский
Citations
722Frontiers in Aging Neuroscience, Journal Year: 2021, Volume and Issue: 13
Published: July 23, 2021
The ability to investigate therapeutic interventions in animal models of neurodegenerative diseases depends on extensive characterization the model(s) being used. There are numerous that have been generated study Alzheimer's disease (AD) and underlying pathogenesis disease. While transgenic instrumental understanding AD mechanisms risk factors, they limited degree characteristics displayed comparison with humans, full spectrum effects has yet be recapitulated a single mouse model. Model Organism Development Evaluation for Late-Onset Disease (MODEL-AD) consortium was assembled by National Institute Aging (NIA) develop more robust increased relevance human disease, standardize models, improve preclinical testing animals, establish clinically relevant biomarkers, among other aims toward enhancing translational value clinical drug design treatment development. Here we conducted detailed 5XFAD mouse, including transcriptomics, electroencephalogram, vivo imaging, biochemical characterization, behavioral assessments. data from this is publicly available through Knowledge Portal.
Language: Английский
Citations
234Cells, Journal Year: 2022, Volume and Issue: 11(16), P. 2607 - 2607
Published: Aug. 21, 2022
Nearly half a century has passed since the discovery of cytoplasmic inheritance human chloramphenicol resistance. The was then revealed to take place maternally by mitochondrial DNA (mtDNA). Later, number mutations in mtDNA were identified as cause severe inheritable metabolic diseases with neurological manifestation, and impairment functions been probed pathogenesis wide range illnesses including neurodegenerative diseases. Recently, growing preclinical studies have that animal behaviors are influenced possibly loss stress resilience. Indeed, high 54% patients one most common primary diseases, encephalomyopathy lactic acidosis stroke-like episodes (MELAS) syndrome, present psychiatric symptoms cognitive impairment, mood disorder, anxiety, psychosis. Mitochondria multifunctional organelles which produce cellular energy play major role other homeostasis, signaling, gene expression, among others. Mitochondrial observed be compromised become less resilient under continuous stress. Meanwhile, inflammation linked activation tryptophan (Trp)-kynurenine (KYN) system, observably contributes development pathological conditions disorders. This review discusses mitochondria Trp-KYN interaction system mitochondria, current understanding involvement clinical
Language: Английский
Citations
133Nutrients, Journal Year: 2021, Volume and Issue: 14(1), P. 20 - 20
Published: Dec. 22, 2021
Alzheimer’s disease (AD) is the most common form of neurodegenerative disorders affecting mostly elderly. It characterized by presence Aβ and neurofibrillary tangles (NFT), resulting in cognitive memory impairment. Research shows that alteration gut microbial diversity defects brain axis are linked to AD. Probiotics known be one best preventative measures against decline Numerous vivo trials recent clinical have proven effectiveness selected bacterial strains slowing down progression probiotics modulate inflammatory process, counteract with oxidative stress, modify microbiota. Thus, this review summarizes current evidence, strains, AD, harmful for mechanism action preventing A literature search on databases such as PubMed, Semantic Scholar, Nature, Springer link identified potentially relevant articles topic. However, upon consideration inclusion criteria limitation publication year, only 22 been further reviewed. The query includes few sets keywords follows. (1) OR microbiome microbes AND (2) Alzheimer aging dementia (3) trial animal study. results evidenced study help clearly illustrate relationship between probiotic supplementation systematic will identify novel therapeutic strategies future free from triggering any adverse effects human body.
Language: Английский
Citations
117International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(7), P. 3995 - 3995
Published: April 3, 2024
Neurodegenerative disorders (NDs) have become increasingly common during the past three decades. Approximately 15% of total population world is affected by some form NDs, resulting in physical and cognitive disability. The most NDs include Alzheimer’s disease, Parkinson’s amyotrophic lateral sclerosis, Huntington’s disease. Although are caused a complex interaction genetic, environmental, lifestyle variables, neuroinflammation known to be associated with all often leading permanent damage neurons central nervous system. Furthermore, numerous emerging pieces evidence demonstrated that inflammation not only supports progression but can also serve as an initiator. Hence, various medicines capable preventing or reducing been investigated ND treatments. While anti-inflammatory medicine has shown promising benefits several preclinical models, clinical outcomes questionable. In this review, we discuss their current treatment strategies, role pathophysiology use agents potential therapeutic option.
Language: Английский
Citations
37Ageing Research Reviews, Journal Year: 2025, Volume and Issue: unknown, P. 102660 - 102660
Published: Jan. 1, 2025
Language: Английский
Citations
4Pharmacology & Therapeutics, Journal Year: 2019, Volume and Issue: 199, P. 173 - 187
Published: March 12, 2019
Language: Английский
Citations
125Environmental Science and Pollution Research, Journal Year: 2020, Volume and Issue: 27(36), P. 44659 - 44672
Published: March 23, 2020
Language: Английский
Citations
91Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring, Journal Year: 2021, Volume and Issue: 13(1)
Published: Jan. 1, 2021
Abstract Early‐onset Alzheimer's disease (EOAD) is generally known as a dominant due to highly penetrant pathogenic mutations in the amyloid precursor protein, presenilin 1 and 2. However, they explain only fraction of EOAD patients (5% 10%). Furthermore, 10% 15% families present with clear autosomal inheritance. Studies showed that 35% 60% have at least one affected first‐degree relative. Parent–offspring concordance was estimated be <10%, indicating full alleles are not sole players EOAD. We aim summarize current knowledge rare variants underlying familial seemingly sporadic (AD) patients. Genetic findings indicate addition beta pathway, other pathways importance AD pathophysiology. discuss difficulties interpreting influence on onset we underline value carefully selected ethnicity‐matched cohorts genetic research.
Language: Английский
Citations
73