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Drug Development.
Alzheimers Dement
December 2024
University of California San Diego, La Jolla, CA, USA.
Background: Our lab has developed a CRISPR-based, gene-editing strategy that targets the extreme C-terminus (C-term) of APP (amyloid precursor protein) - a gene with a central and indisputable role in AD. We have reported previously that APP C-terminus CRISPRs effectively attenuate APP β-cleavage and Alzheimer's pathology in vivo. Here, we present new data demonstrating the feasibility and efficacy of a clinically-viable, "all-in-one" therapeutic vector that has all the components needed for APP C-terminus editing (Cas enzyme / gRNAs / regulatory elements) packaged into a single AAV.
View Article and Find Full Text PDFDrug Development.
Alzheimers Dement
December 2024
ICMR - National Institute of Nutrition, Hyderabad, Telangana, India.
Background: Traditionally associated with recreational and spiritual uses, psychedelics have gained attention in psychotherapy for their therapeutic potential. Functioning as potent 5-hydroxytryptamine (5HT) agonists, these compounds have demonstrated the ability to enhance neural plasticity by activating serotoninergic and glutamatergic systems. Despite these recognized effects, their role in treating neurodegenerative disorders, particularly dementia, remains relatively unexplored.
View Article and Find Full Text PDFBackground: Alzheimer's disease (AD) remains a formidable neurodegenerative challenge, characterized by profound cognitive decline. Despite decades of research, effective disease-modifying therapies are elusive. Recent advances in molecular neuropharmacology have unveiled potential therapeutic targets for AD, offering renewed hope.
View Article and Find Full Text PDFDementia Care Research and Psychosocial Factors.
Alzheimers Dement
December 2024
National Center for Geriatrics and Gerontology, Obu, Aichi, Japan.
Background: The effectiveness of multimodal lifestyle interventions to prevent dementia is being validated. Since a relatively long period (∼2 years) is required for manifesting an impact on cognitive function, the exploration of an alternative marker that exhibits changes within a comparatively brief duration, thereby prognosticating future alterations in cognitive function, is needed. The decline in gait function is associated with cognitive impairment and is also a predictor of future cognitive decline.
View Article and Find Full Text PDFBackground: Lecanemab is a humanized IgG1 monoclonal antibody binding with high affinity to protofibrils of amyloid-beta (Aβ) protein. In clinical studies, lecanemab has been shown to reduce markers of amyloid in early symptomatic Alzheimer's disease (AD) and slow decline on clinical endpoints of cognition and function. Herein, a modeling approach was used to correlate amyloid reduction with change in rate of AD progression.
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