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Alzheimers Dement
December 2024
Indiana University School of Medicine, Indianapolis, IN, USA.
Background: The TaRget Enablement to Accelerate Therapy Development of Alzheimer's Disease (TREAT-AD) Centers are dedicated to identifying and validating targets from the NIH Accelerating Medicines Partnership for Alzheimer's Disease (AMP-AD). The centers develop Target Enabling Packages (TEPs) to explore new therapeutic target hypotheses, moving beyond the traditional focus on amyloid or tau pathologies. In accordance with open science principles, data, methods, and tools are freely shared with the research community via an open-access platform, the AD Knowledge Portal.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Indiana University School of Medicine, Indianapolis, IN, USA.
Background: The goal of the TREAT-AD Center is to enable drug discovery by developing assays and providing tool compounds for novel and emerging targets. The role of microglia in neuroinflammation has been implicated in the pathogenesis of Alzheimer's disease (AD). Genome-wide association studies, whole genome sequencing, and gene-expression network analyses comparing normal to AD brain have identified risk and protective variants in genes essential to microglial function.
View Article and Find Full Text PDFBackground: SUVN-I7016031 is a novel and selective positive allosteric modulator (PAM) of the M1 subtype of the muscarinic acetylcholine receptors (mAChRs). The proposed primary indication for SUVN-I7016031 is in the treatment of dementia such as Alzheimer's disease dementia (ADD) and Parkinson's disease dementia (PDD). In the current research, the pharmacological properties of SUVN-I7016031 in various types of dementia were investigated.
View Article and Find Full Text PDFBackground: There are no cures for Alzheimer's disease (AD), a progressive neurodegenerative disorder characterized by elevation of beta-amyloid and tau proteins besides neuronal death and causing cognitive impairment. Phosphodiesterase 5 (PDE5) is a cyclic guanosine monophosphate-degrading enzyme involved in numerous biological pathways including those relevant to memory formation. PDE5 inhibition offers the potential to attenuate AD progression by acting at the downstream level of beta-amyloid and tau elevation.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Federal University of Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease and the most common form of dementia. Although AD is characterized by the accumulation of amyloid beta (Aβ) plaques and neurofibrillary tangles (NFTs), it's estimated that nearly half of AD cases might be attributed to modifiable risk factors and lifestyle-based interventions may offer promising preventative strategies to delay disease onset and progression. Polyphenolic derivatives easily found in foods like luteolin and curcumin have shown beneficial effects to counteract cognitive decline.
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