Molecular Insights into Tau Pathology in Alzheimer's Disease (AD) and Related Therapeutic Strategies
Alzheimer’s disease (AD) is an age-associated neurodegenerative disease (ND) that impairs memory and cognition, as well as affecting behavioral and social activities. AD is the most common brain disease in humans, with a prevalence of 4-8% in the elderly population worldwide. The global AD population is estimated to increase to 114 million by 2050. Deficiency of the autophagy-lysosomal pathway (ALP) has been shown to play a key role in the pathogenesis of neurodegenerative disorders such as AD, which then manifests as memory loss. Despite a plethora of laboratory and clinical research, there is still no effective treatment for AD. Therefore, considerable challenges remain for researchers in the scientific community and for medical experts to better understand the disease pathogenesis of AD and to develop effective therapeutics. Over the past decades, drug discovery based on the reduction of Aβ plaques has not shown good clinical efficacy. In contrast, the targeting of neurofibrillary tangles (NFTs) appears more likely to be successful. This is because NFTs are comprised of hyperphosphorylated, aggregated and misfolded Tau protein that correlate with cognitive impairment. The development of drugs to prevent the formation of aberrant Tau or to enhance its clearance could therefore be a promising strategy for AD treatment. The promotion of cellular autophagy and ALP using novel phytochemicals from herbal medicines may be an effective AD therapy. One of the most recent and promising strategies for drug discovery in AD is to use traditional herbal medicines to modulate memory improvement and tau degradation.
This Research Topic welcomes contributions in the form of original research articles, reviews and opinions that address/summarize our understanding of Amyloid β and Tau aggregates in the pathogenesis, prognosis, and therapeutics of AD and the challenges remaining.
Dr. Ashok Iyaswamy
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