Of the 100 year old who died and their brain were later on examined to have Alzheimer’s, 25% of them has but did not exhibit signs of Alzheimer’s.

Why?

They are not stressed, they get massage, take a walk and are surrounded by family and support of the community.

I train my caregivers to comfort our seniors with massage, music, walk in the sun, and happy conversations with loving spirit.

Connie

 

Reducing the RNA binding protein TIA1 protects against tau-mediated neurodegeneration in vivo

Emerging studies suggest a role for tau in regulating the biology of RNA binding proteins (RBPs). We now show that reducing the RBP T-cell intracellular antigen 1 (TIA1) in vivo protects against neurodegeneration and prolongs survival in transgenic P301S Tau mice. Biochemical fractionation shows co-enrichment and co-localization of tau oligomers and RBPs in transgenic P301S Tau mice. Reducing TIA1 decreased the number and size of granules co-localizing with stress granule markers. Decreasing TIA1 also inhibited the accumulation of tau oligomers at the expense of increasing neurofibrillary tangles. Despite the increase in neurofibrillary tangles, TIA1 reduction increased neuronal survival and rescued behavioral deficits and lifespan. These data provide in vivo evidence that TIA1 plays a key role in mediating toxicity and further suggest that RBPs direct the pathway of tau aggregation and the resulting neurodegeneration. We propose a model in which dysfunction of the translational stress response leads to tau-mediated pathology.

“Reducing the RNA binding protein TIA1 protects against tau-mediated neurodegeneration in vivo” by Daniel J. Apicco, Peter E. A. Ash, Brandon Maziuk, Chelsey LeBlang, Maria Medalla, Ali Al Abdullatif, Antonio Ferragud, Emily Botelho, Heather I. Ballance, Uma Dhawan, Samantha Boudeau, Anna Lourdes Cruz, Daniel Kashy, Aria Wong, Lisa R. Goldberg, Neema Yazdani, Cheng Zhang, Choong Y. Ung, Yorghos Tripodis, Nicholas M. Kanaan, Tsuneya Ikezu, Pietro Cottone, John Leszyk, Hu Li, Jennifer Luebke, Camron D. Bryant & Benjamin Wolozin in Nature Neuroscience. Published online November 20 2017 doi:10.1038/s41593-017-0022-z

 

TIA1 is a 3’UTR mRNA binding protein that can bind the 5’TOP sequence of 5’TOP mRNAs. It is associated with programmed cell death (apoptosis) and regulates alternative splicing of the gene encoding the Fas receptor, an apoptosis-promoting protein.[1] Under stress conditions, TIA1 localizes to cellular RNA-protein conglomerations called stress granules.[2]

Mutations in the TIA1 gene have been associated with amyotrophic lateral sclerosis, frontotemporal dementia, and Welander distal myopathy.[3][4][5]