Towards Advanced iPSC-based Drug Development for Neurodegenerative Disease DOI
Svetlana Pasteuning-Vuhman, Rianne de Jongh,

Annabel Timmers

et al.

Trends in Molecular Medicine, Journal Year: 2020, Volume and Issue: 27(3), P. 263 - 279

Published: Oct. 26, 2020

Language: Английский

Beneficial Role of Phytochemicals on Oxidative Stress and Age-Related Diseases DOI Open Access
Cinzia Forni, Francesco Facchiano, Manuela Bartoli

et al.

BioMed Research International, Journal Year: 2019, Volume and Issue: 2019, P. 1 - 16

Published: April 7, 2019

Aging is related to a number of functional and morphological changes leading progressive decline the biological functions an organism. Reactive Oxygen Species (ROS), released by several endogenous exogenous processes, may cause important oxidative damage DNA, proteins, lipids, cellular dysfunctions. The imbalance between ROS production antioxidant defenses brings stress conditions and, accumulation ROS, aging-associated diseases. purpose this review provide overview most relevant data reported in literature on natural compounds, mainly phytochemicals, with activity their potential protective effects age-related diseases such as metabolic syndrome, diabetes, cardiovascular disease, cancer, neurodegenerative chronic inflammation, possibly lower side effects, when compared other drugs.

Language: Английский

Citations

446

Modeling Alzheimer’s disease with iPSC-derived brain cells DOI Creative Commons

Jay Penney,

William T. Ralvenius, Li‐Huei Tsai

et al.

Molecular Psychiatry, Journal Year: 2019, Volume and Issue: 25(1), P. 148 - 167

Published: Aug. 7, 2019

Alzheimer’s disease is a devastating neurodegenerative disorder with no cure. Countless promising therapeutics have shown efficacy in rodent models yet failed to benefit human patients. While hope remains that earlier intervention existing will improve outcomes, it becoming increasingly clear new approaches understand and combat the pathophysiology of are needed. Human induced pluripotent stem cell (iPSC) technologies changed face preclinical research iPSC-derived types being utilized study an array conditions, including disease. All major brain can now be differentiated from iPSCs, while complex co-culture systems developed facilitate neuroscience research. Many cellular functions perturbed recapitulated using cells vitro, platforms beginning yield insights into interactions occur between during neurodegeneration. Further, iPSC-based genome editing tools critical understanding roles numerous genes mutations found modify risk past decade. still their relative infancy, these developing hold considerable promise push forward efforts other disorders.

Language: Английский

Citations

368

Synaptic basis of Alzheimer’s disease: Focus on synaptic amyloid beta, P-tau and mitochondria DOI
Albin John, P. Hemachandra Reddy

Ageing Research Reviews, Journal Year: 2020, Volume and Issue: 65, P. 101208 - 101208

Published: Nov. 4, 2020

Language: Английский

Citations

263

The Microbiota–Gut–Brain Axis and Alzheimer’s Disease: Neuroinflammation Is to Blame? DOI Open Access
Ashwinipriyadarshini Megur, Daiva Baltriukienė, Virginija Bukelskienė

et al.

Nutrients, Journal Year: 2020, Volume and Issue: 13(1), P. 37 - 37

Published: Dec. 24, 2020

For years, it has been reported that Alzheimer’s disease (AD) is the most common cause of dementia. Various external and internal factors may contribute to early onset AD. This review highlights a contribution disturbances in microbiota–gut–brain (MGB) axis development Alteration gut microbiota composition determined by increase permeability barrier immune cell activation, leading impairment blood–brain function promotes neuroinflammation, neuronal loss, neural injury, ultimately Numerous studies have shown plays crucial role brain changes behavior individuals formation bacterial amyloids. Lipopolysaccharides amyloids synthesized can trigger cells residing activate response neuroinflammation. Growing experimental clinical data indicate prominent dysbiosis microbiota–host interactions Modulation with antibiotics or probiotic supplementation create new preventive therapeutic options Accumulating evidences affirm research on MGB involvement AD necessary for treatment targets therapies

Language: Английский

Citations

233

The neuroprotective role of melatonin in neurological disorders DOI Creative Commons
Badrah S. Alghamdi

Journal of Neuroscience Research, Journal Year: 2018, Volume and Issue: 96(7), P. 1136 - 1149

Published: March 1, 2018

Melatonin is a neurohormone secreted from the pineal gland and has wide-ranging regulatory neuroprotective role. It been reported that melatonin level disturbed in some neurological conditions such as stroke, Alzheimer's disease, Parkinson's which indicates its involvement pathophysiology of these diseases. Its properties qualify it to be promising potential therapeutic agent, with no side effects, for disorders. This review discusses localizes effect

Language: Английский

Citations

200

Melatonin: Clinical Perspectives in Neurodegeneration DOI Creative Commons

Daniel P. Cardinali

Frontiers in Endocrinology, Journal Year: 2019, Volume and Issue: 10

Published: July 16, 2019

Neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's (PD) are important health problems there is a growing recognition that both governmental non-governmental organizations must make efforts to prevent, in addition treat, them. In this context, the pineal product melatonin has promising significance. Melatonin, an unusual phylogenetically conserved molecule present all known aerobic organisms, effective chronobiotic cytoprotective. As chronobiotic, afternoon increase "opens doors of sleep" every night therapeutic use been demonstrated preserve slow wave sleep effectively. cytoprotective molecule, reverses low degree inflammatory damage seen neurodegenerative disorders ageing. One characteristics advancing age gradual decrease circulating levels melatonin. Both vitro vivo, prevented neurodegeneration observed experimental models AD PD. Melatonin also increased removal toxic proteins by brain glymphatic system. A limited number clinical trials have indicated potential value neuroprotective drug treatment AD, particularly at early stage cognitive impairment, From animal studies effects need high doses become apparent (i.e. 40-100 mg/day range). The off-label discussed.

Language: Английский

Citations

166

Melatonin and Health: Insights of Melatonin Action, Biological Functions, and Associated Disorders DOI Open Access
Sheikh Bilal Ahmad, Aarif Ali, Midhat Bilal

et al.

Cellular and Molecular Neurobiology, Journal Year: 2023, Volume and Issue: 43(6), P. 2437 - 2458

Published: Feb. 8, 2023

Language: Английский

Citations

134

Persistent remodeling and neurodegeneration in late-stage retinal degeneration DOI
Rebecca L. Pfeiffer, Robert E. Marc, Bryan W. Jones

et al.

Progress in Retinal and Eye Research, Journal Year: 2019, Volume and Issue: 74, P. 100771 - 100771

Published: July 26, 2019

Language: Английский

Citations

144

Melatonin: A review of its potential functions and effects on neurological diseases DOI
Mehmet Günata, Hakan Parlakpınar, Ahmet Acet

et al.

Revue Neurologique, Journal Year: 2019, Volume and Issue: 176(3), P. 148 - 165

Published: Nov. 11, 2019

Language: Английский

Citations

135

Understanding the Amyloid Hypothesis in Alzheimer’s Disease DOI
Giulia Paroni, Paola Bisceglia, Davide Seripa

et al.

Journal of Alzheimer s Disease, Journal Year: 2019, Volume and Issue: 68(2), P. 493 - 510

Published: March 12, 2019

The amyloid hypothesis (AH) is still the most accepted model to explain pathogenesis of inherited Alzheimer's disease (IAD). However, despite neuropathological overlapping with non-inherited form (NIAD), AH waver in explaining NIAD. Thus, 30 years after its first statement several questions are open, mainly regarding role plaques (AP) and apolipoprotein E (APOE). Accordingly, a pathogenetic including AP APOE unifying IAD NIAD missing. In present understanding AH, we suggested that amyloid-β (Aβ) peptides production formation physiological aging process resulting from systemic age-related decrease efficiency proteins catabolism/clearance machinery. this Aβ act as neurotoxic molecules, but only above critical concentration [Aβ]c. A threshold mechanism triggers IAD/NIAD onset when [Aβ]≥[Aβ]c. process, modifies [Aβ]c an isoform-specific way. Consequently, all factors influencing anabolism, such beta precursor protein (APP), presenilin 1 (PSEN1), 2 (PSEN2) gene mutations, and/or could contribute exceed [Aβ]c, being characteristic each individual. model, does not depend on interpretation theories for NIAD, will why APOE4 may be observed healthy they cause AD. It clear further studies needed confirm our model. Nevertheless, suggestion useful better understand

Language: Английский

Citations

131