A Cell Press publication in December 2009 included details regarding a new study carried out on mice, which indicated that the fountain of youth might still be within reach – with new treatments being developed to prolong youthfulness whilst also stating that these might also help delay the development of Alzheimer’s disease.
Andrew Dillin, The Salk Institute for Biological Studies said, “There’s something about being youthful that protects us from Alzheimer’s disease. People say that if you live long enough, you get Alzheimer’s. But if that were true, mice that live longer should get the disease at the same rate. That’s not what we found.”
The research shows that mice which carried human genes that caused the development of Alzheimer’s could be steered clear of the disease by lessening the ‘insulin/IGF signalling’ pathway peppered with amyloid plaques.
“We expected to see less plaque in the protected mice. Instead we saw the same number of plaques, but there was a qualitative difference in how they looked. They were condensed so that they took up less area in the brain,” said Dillin.
He also said they were yet to fully comprehend how exactly the diminished IGF signal prevented the mice from developing Alzheimer’s – but said the pathway was recognized as one that negatively controls transcription factors that have control over other genes that encode molecular chaperones. They protect all the proteins in a cell.
Dillin said, “To maintain youth, you have to protect the proteome, not just the genome.” This could ring true with regards to cells known to not divide and replace easily and often, such as neurons, heart and muscle. Those prone to develop Alzheimer’s due to hereditary reasons carry it with them their entire lives and only develop it when they reach their 50’s.
Plans to also test similar factors could be beneficial towards other neurodegenerative diseases like Parkinson’s and Huntington’s diseases.