Pathophysiological Mechanisms Underlying Neurodegenerative Disorders
A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neuropharmacology and Neuropathology".
Deadline for manuscript submissions: closed (5 October 2023) | Viewed by 1941
Special Issue Editor
Interests: neurosciences: epilepsy, Parkinsonism, autism, deep brain stimulation; stem cell research and regenerative medicine; oxidative stress and pathways of oxidant and antioxidant systems such as Nrf2/HO1 pathway; natural plant extracts such as stevia R, palm date fruits and seed extracts
Special Issue Information
Dear Colleagues,
Neurodegenerative disorders (NDD) are a group of diseases characterized by selective dysfunction and progressive loss of neurons, glial cells, and their networks in different parts of the nervous system. Patients with NDD display progressive cognitive loss and/or motor dysfunction as a consequence; for instance, Alzheimer's disease (AD) is characterized by a decrease in cognitive function, whereas amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and Huntington's disease (HD) all exhibit motor deficits (HD). Despite the wide variety of causes of NDD, several research groups have demonstrated that they share common pathways such as the accumulation of insoluble protein aggregates, apoptosis, necrosis, excitotoxicity, and neuroinflammation. Other significant contributors to neurodegeneration include diminished autophagy/lysosomal activity, downstream oxidative stress, and mitochondrial dysfunction. Animal models are effective research tools for figuring out the causes and molecular mechanisms of neurodegenerative diseases as well as discovering new therapeutic agents. This Special Issue aims to present the latest updates on the molecular mechanisms of neurodegenerative diseases in both animal and human studies.
Prof. Dr. Abdelaziz M. Hussein
Guest Editor
Manuscript Submission Information
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Keywords
- neurodegeneration
- neuroinflammation
- excitotoxicity
- neuronal and neuroglial cell deaths
- mitochondrial dysfunctions
- autophagy
