Why is it that you can remember the name of your childhood best friend that you haven’t seen in years yet easily forget the name of a person you just met a moment ago? In other words, why are some memories stable over decades, while others fade within minutes?
Using mouse models, Caltech investigators have now ascertained that powerful, stable memories are cyphered by “groups” of neurons all firing in synchronicity, giving repetitiveness that modify these memories to prevail over time. The research has deductions for apprehension how memory might be moved after brain damage, such as by strokes or Alzheimer’s malady.
Now, Salk Institute researchers have formed a new tool — dubbed SATI — to edit the mouse genome, enabling the team to aim a wide range of mutations and types of cells.
The new genome-editing technology, described in Cell Research, could be expanded for use in a broad range of gene mutation conditions such as Huntington’s disease and the rare premature aging syndrome, progeria. “This study has shown that SATI is a powerful tool for genome editing,” says Juan Carlos Izpisua Belmonte, a professor in Salk’s Gene Expression Laboratory and senior author of the paper. “It could prove instrumental in developing effective strategies for target-gene replacement of many different types of mutations, and opens the door for using genome-editing tools to possibly cure a broad range of genetic diseases.”
Source: A novel technology for genome-editing a broad range of mutations in live organisms: Scientists develop a new gene-editing tool that could help treat many disorders caused by gene mutations — ScienceDaily
New research from the USC Viterbi School of Engineering could be critical to our comprehension of how the aging procedure functions. The discoveries conceivably make ready for better cancer drugs and progressive new medications that could tremendously improve human health in the twilight years.
The work, from Assistant Professor of Chemical Engineering and Materials Science Nick Graham and his group as a team with Scott Fraser, Provost Professor of Biological Sciences and Biomedical Engineering, and Pin Wang, Zohrab A. Kaprielian Fellow in Engineering, was as of late distributed in the Journal of Biological Chemistry.
“To drink from the fountain of youth, you need to make sense of where the fountain of youth is, and comprehend what the fountain of youth is doing,” Graham said. “We’re doing the inverse; we’re attempting to examine the reasons cells age, with the goal that we may almost certainly plan medicines for better aging.”
What makes cells age?
To accomplish this, lead author Alireza Delfarah, a graduate student in the Graham lab, concentrated on senescence, a characteristic procedure wherein cells for all time quit making new cells. This procedure is one of the key reasons for age-related deterioration, showing in diseases, for example, joint inflammation, osteoporosis and coronary disease.
“Senescent cells are viably something contrary to stem cells, which have a boundless potential for self-reestablishment or division,” Delfarah said. “Senescent cells can never isolate again. It’s an irreversible condition of cell cycle arrest.”
The study group found that the aging, senescent cells quit delivering a class of synthetics called nucleotides, which are the building blocks of DNA. When they took young cells and constrained them to quit delivering nucleotides, they ended up senescent, or aged.
“This implies the generation of nucleotides is fundamental to keep cells young,” Delfarah said. “It likewise implies that on the off chance that we could keep cells from losing nucleotide production, the cells may age all the more gradually.”
Alireza Delfarah, Sydney Parrish, Jason A. Junge, Jesse Yang, Frances Seo, Si Li, John Mac, Pin Wang, Scott E. Fraser, Nicholas A. Graham. Inhibition of nucleotide synthesis promotes replicative senescence of human mammary epithelial cells. Journal of Biological Chemistry, 2019; 294 (27): 10564 DOI: 10.1074/jbc.RA118.005806