The five main string-theory candidates may all just be pieces of a larger, cohesive whole — and M-theory could bring them together.
We will be issuing ticket refunds to attendees, who cannot attend the new date.
Berlin / Mountain View, March 12, 2020.
Forever Healthy Foundation and SENS Research Foundation have decided to reschedule Undoing Aging 2020 to October, 21–23. Following the WHO’s declaration of COVID-19 as a pandemic, we will do our share to prevent it from spreading further. We will be issuing ticket refunds to attendees, who cannot attend the new date.
The Undoing Aging Conference in October will be focused on the cellular and molecular repair of age-related damage as the basis of therapies to bring aging under full medical control and will bring together scientists and startups from around the globe, all pioneers in their respective fields, who are leading the charge in maintaining and restoring full health in old age.
J Gen Psychol. 2009 Jan;136:21–39. doi: 10.3200/GENP.136.1.21–40.
The authors examined the role of cognitive operations in discriminations between externally and internally generated events (e.g., reality monitoring) in healthy and pathological aging. The authors used 2 reality-monitoring distinctions to manipulate the quantity and quality of necessary cognitive operations: discriminating between I performed versus I imagined performing and between I watched another perform versus I imagined another performing. Older adults had more difficulty than did younger adults when discriminating between memories in both versions of the task. In addition, older adults with Alzheimer’s-type dementia showed marked difficulties when attributing a source to imagined actions. The authors interpret these findings in terms of an age difficulty or the failure to use cognitive operations as useful cues during source monitoring.
A new study shows that the effects of aging appear in the brain can appear in your 40s. Cutting carbohydrates may protect you, though.
Circa 2018 we need crispr pills for this.
The steady march of aging might not have to be so steady, according to a growing body of research. Now a team from the University at Buffalo has isolated a single gene that controls senescence, the process that stops cells from dividing and contributes to aging symptoms. Ramping it up, they found how easily the effect can spread among neighboring cells. That makes the gene a crucial target for future work into anti-aging and cancer therapies.
Living cells have a natural limit to the amount of times they can divide, before they stop and become what are known as senescent cells. The problem is, over time these senescent cells build up in the body, eventually contributing to the physical symptoms we associate with aging, such as increased risk of diabetes, heart disease, arthritis and cataracts. On the other hand though, completely halting senescence can lead to cancer, as the cells continue to divide unchecked.
Realizing this mechanism, scientists have been developing ways to clear out these senescent cells, including a new class of drugs known as senolytics. In tests, these drugs have been found to extend the lifespan of mice by up to an impressive 35 percent, and keep them in better health for longer.