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Alzheimer’s Disease: Have We Been Focusing on the Wrong Proteins?
| Content Provider | Semantic Scholar |
|---|---|
| Author | Gotesman, Ryan |
| Copyright Year | 2017 |
| Abstract | Alzheimer’s disease (AD) is a neurodegenerative disorder and the most common form of dementia, characterized by neuronal atrophy in the cerebral cortex and hippocampus1. The disease commonly affects those over the age of 65, clinically manifesting as loss of memory and cognitive decline2. The neuropathological origins of AD have been classically attributed to misfolded proteins, specifically plaques composed of the amyloid-β (Aβ) peptide and neurofibrillary tangles (NFTs) consisting of aggregates of hyper-phosphorylated tau. Currently no disease-modifying drugs capable of stopping or slowing the progression of the disease exist and only symptomatic treatments are available. As 1 in 85 people worldwide are projected to suffer from AD by 2050, an improved understanding of the disease and the development of novel therapies will become more pressing with each passing year3. |
| File Format | PDF HTM / HTML |
| Volume Number | 2 |
| Alternate Webpage(s) | https://journals.mcmaster.ca/catalyst/article/download/1303/1179 |
| Alternate Webpage(s) | https://journals.mcmaster.ca/catalyst/article/download/1303/1423 |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |