Titlebook: GeNeDis 2018; Genetics and Neurode Panayiotis Vlamos Conference proceedings 2020 The Editor(s) (if applicable) and The Author(s), under exc

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In Silico and In Vivo Studies on Quercetin as Potential Anti-Parkinson Agent,ently halted the deleterious toxic effects of L-dopa, revealing normalization of catalepsy and rotarod score, in addition to amelioration of neurochemical parameters, indicating benefit of both symptomatic and neuroprotective therapies. In silico molecular docking studies have also shown that querce

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,Treatment Development for Alzheimer’s Disease: How Are We Doing?,essful therapeutically even though they have been associated with reductions in amyloid. Currently, efforts are underway to deliver these therapies to individuals with very early symptoms or at risk for Alzheimer’s dementia by virtue of genetics or a brain amyloid PET scan. Results from these studie

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Microbiome Hijacking Towards an Integrative Pest Management Pipeline,re elucidated in an effort to pave the way for the efficient high-throughput virtual screening of libraries of low molecular weight compounds and thus the discovery of novel modulating agents. Our methodology provides the means to design, test, and identify highly specific pest control substances th

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Regulation and Roles of Autophagy in the Brain,the neural lineage causes uncontrolled increase in autophagy. In turn, increased autophagy mediates the synaptic defects caused by BDNF deficiency. Thus, fasting suppresses autophagy in regions of the mouse forebrain, thereby promoting synaptic remodeling and memory through a BDNF-regulated mechanis

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Human Pluripotent Stem Cells as In Vitro Models of Neurodegenerative Diseases,-like structures (“organoids”) mimicking native brains. Three-dimensional (3D) systems, called cerebral organoids, can recapitulate distinct architectures of the human brain, such as fluid-filled cavities resembling brain ventricles and tissues organized in layers including progenitor ventricular an

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,Alzheimer’s Disease Therapeutic Approaches,changes, including acetylcholine deficiency, glutamate excitotoxicity, extracellular deposition of β-amyloid (Aβ plaques), intracellular neurofibrillary tangles by hyperphosphorylated tau protein deposits, neuroinflammation, and widespread neuronal loss (Godyn et al. Pharmacol Rep 68:127–138, 2016;