Abstract
Updates in Solving the Mystery of Alzheimer's Disease Pathology
Highlights
Studies at Children's Hospital in Boston, Massachusetts have recently discovered that there are two types of Tau proteins, soluble tau and insoluble tau. The significant of both has not been determined, yet one can guess that the soluble tau gets cleared and the insoluble tau probably induces the formation of insoluble neurofibrillary tangles (NFTs) which in turn lead to nerve cell death
The pathology of the brain is very complex, and it is only after decades of research and the invention of advanced imaging equipment and other scientific tools have researchers begun to unravel the mystery of the brain
It is a consensus that both Aβ and tau proteins play an important role in the pathology Alzheimer’s disease (AD), but the debate remains on whether reducing the aggregation of both insoluble Aβ and tau proteins, halts or reduces the progression of AD or whether there is a threshold of tau opathy and Aβ opathy that sets off a cascade of events that is irreversible and independent to the amount of aggregation of Aβ and tau
Summary
Dead and dying nerve cells (black triangle figures) contain tangles, which are made up of twisted strands of a protein called Tau. For years, investigators have believed that the pathology of Alzheimer’s disease (AD) was driven by the production and deposition of the β-amyloid peptide (Aβ). It is believed that there are two hallmark pathologies required for a diagnosis of Alzheimer’s disease (AD): (1) extracellular plaque deposits of the β-amyloid peptide (Aβ); and (2) flame-shaped neurofibrillary tangles (NFTs) of the microtubule binding protein tau[1]. Onset forms of AD are associated with genetic markers or mutations in either the precursor protein for Aβ (the β-amyloid precursor protein, APP) or in presenilin-1 (PS1) or presenilin-2 (PS2) Despite this genetic evidence and the involvement of Aβ in inducing synaptic dysfunction, disrupting neural connectivity, the amounts and distribution of Aβ deposition have shown only a weak correlation to progressive and gradual decline in cognitive function. Phase 3: Tau clearance and tau-mediated neuronal injury and dysfunction
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: International Journal of Clinical Pharmacology & Pharmacotherapy
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
