
Biophysical Chemistry, Journal Year: 2021, Volume and Issue: 281, P. 106735 - 106735
Published: Nov. 30, 2021
Language: Английский
Biophysical Chemistry, Journal Year: 2021, Volume and Issue: 281, P. 106735 - 106735
Published: Nov. 30, 2021
Language: Английский
Antioxidants, Journal Year: 2024, Volume and Issue: 13(7), P. 862 - 862
Published: July 18, 2024
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that comprises amyloid-beta protein (Aβ) as main component of neuritic plaques. Its deposition considered trigger for AD pathogenesis, progression, and the clinical symptoms cognitive impairment. Some distinct pathological features include phosphorylation tau protein, oxidative stress, mitochondrial dysfunction. These consequences tend to produce reactive oxygen species (ROS), resulting in dysregulation various signaling pathways neuroinflammation neurodegeneration. The relationship between Aβ cascade stress pathogenesis like “chicken egg” story, with etiology regarding these two factors remaining question “which comes first.” However, this review, we have tried our best clarify interconnection mechanisms show precise cause-and-effect relationship. Based on above hallmarks AD, several therapeutic strategies using natural antioxidants, monoclonal antibodies, vaccines are employed anti-Aβ therapy decrease ROS, burden, chronic neuroinflammation, synaptic failure. antioxidants immunotherapeutics demonstrated significant neuroprotective effects symptomatic relief vitro vivo models, well trials AD. none them received final approval enter drug market mitigating In extensively elaborate pitfalls, assurances, important crosstalk concerning current therapy. Additionally, discuss future development more Aβ-targeted approaches optimization treatment mitigation.
Language: Английский
Citations
9Chemical Science, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 1, 2025
This review highlights the potential of multi-target-directed strategies that address amyloid-β aggregation, metal ion dyshomeostasis, and enzyme dysfunction, offering a comprehensive effective approach to treating Alzheimer's disease.
Language: Английский
Citations
1Neurotoxicity Research, Journal Year: 2025, Volume and Issue: 43(1)
Published: Jan. 8, 2025
Language: Английский
Citations
1BMC Neuroscience, Journal Year: 2025, Volume and Issue: 26(1)
Published: March 3, 2025
This systematic review sought to assess the impact of nicotinamide adenine dinucleotide (NAD+) precursors on cognitive impairments in several diseases rat/mouse models. Accumulating evidence suggests that inflammation, apoptosis, oxidative stress responses, and mitochondrial dysfunction are potential factors deficits aging, Alzheimer's disease (AD), diabetes, traumatic brain injury (TBI), vascular dementia (VAD), schizophrenia. NAD+ have received increased interest due their unique molecular structure targets antioxidant inflammatory pathways function. The PubMed, Scopus, Google Scholar, Embase, Web Science databases were searched through May 30, 2024. Studies investigating effect rodent models included. Two reviewers independently extracted evaluated data. PRISMA guidelines for reporting reviews followed. Thirty preclinical studies included review. revealed treatment with rescues by inhibiting stress, apoptosis improving Preclinical has demonstrated may be more effective learning memory recovery AD, TBI, VAD, outcomes this investigation lead additional use treating human decline.
Language: Английский
Citations
1Biophysical Chemistry, Journal Year: 2021, Volume and Issue: 281, P. 106735 - 106735
Published: Nov. 30, 2021
Language: Английский
Citations
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