Neuroprotection and Neuroregeneration in Alzheimer's Disease
1Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, 6900 Lake Nona Boulevard, Orlando, FL, USA
2Department of Pharmacology, Ruth and Bruce Rappaport Family Institute for Research in the Medical Sciences, Technion-Israel Institute of Technology, Haifa, Israel
3Department of Neurobiology, Care Sciences and Society, Karolinska Institute, Karolinska University Hospital, Huddinge, Stockholm, Sweden
Neuroprotection and Neuroregeneration in Alzheimer's Disease
Description
Brain aging and age-related neurodegenerative disorders have complex etiology and pathology. The link between healthy aging and age-related disorders is still not clear. Neurodegeneration in Alzheimer's disease (AD) is thought to be initiated by a cascade of neurotoxic events that includes oxidative stress, brain iron dysregulation, glutamate excitotoxicity, nitric oxide, inflammatory process, and neurotoxic processing resulting from misfolding and aggregation of Aβ-peptide, as a possible consequence of the demise of ubiquitin-proteasome system, demonstrated neurochemically and by transcriptomics and proteomic profiling. Although AD patients are benefiting from current symptomatic therapies, they have limitation in their ability to modify the course of the disease. Although many drugs have demonstrated the ability to be neuroprotective in the laboratory, they failed in clinical trials. AD models employed in vitro and in vivo are not a true representation of complex diseases seen in patients. Most efforts have been in the direction of preventing deposition of Aβ-peptide in transgenic mice without pathological process of AD. The complex pathology of AD implies that multiple causes with singular drug treatment may not be sufficient as therapeutic. The new therapeutic strategies for AD should act on multiple neural and biochemical targets involved in the neurodegenerative process.
Current advancement of stem cell research gives hope toward future application to AD therapies. However, without understanding the complex pathological condition of this disease, effective neuroregeneration may not be accomplished.
The present special issue focuses on novel pathways in neurodegeneration and current trends in drug targets and stem cells. Potential topics include, but are not limited to:
- Describing various cellular and animal AD models and discussing pros and cons
- Describing developed drugs which failed or are in the clinic
- Discussing concepts for developing multitarget neuroprotective and/or neuroregenerative drugs
- Describing stem cell therapies as a neuroregenerative approach
- Discussing combined therapeutic approaches of stem cells and drugs
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