Gizmag is reporting that a scientific journal article published on 12 November 2015 demonstrates that a new Alzheimer's drug reverses ageing. The authors of the article hypothesized that since Alzheimer's was caused by ageing symptoms, then reversing those symptoms would prevent or treat Alzheimer's.
Gizmag:
The Salk research is looking to tackle the disease from a new angle. It expands upon a
previous study conducted back in 2013, working with a potent memory-enhancing and
neurotrophic drug called J147.
Unlike most medicines designed to combat the disease, J147 was synthesized after looking at age-associated brain toxicities, and looks to tackle the major risk factor for the disease – old age itself.
The older research looked at the effect of J147 on mice with an inherited form of Alzheimer's, finding that it was able to prevent and even reverse memory loss in subjects. While that was promising, inherited Alzheimer's is far less common than cases of the disease triggered by old age.
The new study looked to discover whether the experimental drug is as effective at fighting Alzheimer's caused by old age, which is responsible for 99 percent of cases. Once the results were in, things were looking very positive, with the researchers surprised by how effective it had proved.
"We did not predict we'd see this sort of anti-aging effect," says lead author Antonio Currais. "But J147 made old mice look like they were young, based upon a number of physiological parameters."
Salk Institute for Biological Studies: Press Release, 12 November 2015.
Research report: "A comprehensive multiomics approach toward understanding the
relationship between aging and dementia" in
Aging, vol. 7/11 (November 2015), pp. 1-19.
Abstract: Because age is the greatest risk factor for sporadic Alzheimer’s disease (AD), phenotypic screens based upon
old age‐associated brain toxicities were used to develop the potent neurotrophic drug J147. Since certain aspects of aging
may be primary cause of AD, we hypothesized that J147 would be effective against AD‐associated pathology in rapidly
aging SAMP8 mice and could be used to identify some of the molecular contributions of aging to AD. An inclusive and
integrative multiomics approach was used to investigate protein and gene expression, metabolite levels, and cognition in
old and young SAMP8 mice. J147 reduced cognitive deficits in old SAMP8 mice, while restoring multiple molecular markers
associated with human AD, vascular pathology, impaired synaptic function, and inflammation to those approaching the
young phenotype. The extensive assays used in this study identified a subset of molecular changes associated with aging
that may be necessary for the development of AD.
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