A new study led by University of Pittsburgh and UPMC Hillman Cancer Center researchers shows that an enzyme called PARP1 is involved in repair of telomeres, the lengths of DNA that protect the tips of chromosomes, and that impairing this process can lead to telomere shortening and genomic instability that can cause cancer.
Researchers have discovered that individuals who live to be 100 years old and remain cognitively healthy possess genetic variations that may protect against Alzheimer’s disease. These “protective alleles” are significantly more prevalent among centenarians compared to Alzheimer’s patients and even middle-aged individuals without the disease. This finding could pave the way for new approaches in preventing and treating Alzheimer’s, particularly by focusing on enhancing these protective genetic mechanisms.
The new findings have been published in the journal Alzheimer’s & Dementia.
Alzheimer’s disease is a progressive neurological disorder that predominantly affects older adults, leading to a decline in cognitive functions such as memory and reasoning. Over time, this can result in a complete loss of independence and eventually death. The risk of developing Alzheimer’s increases significantly with age, and while it is not an inevitable part of aging, it is one of the most common causes of dementia among seniors.
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Achieving Longevity Escape Velocity is likely within the next 10–20 years—why is this happening, and what are the implications?
In Limitless, the film’s protagonist is a struggling writer desperate for success. As luck would have it, he is introduced to an experimental drug that unlocks his full potential.
The film was a box office success, and it is easy to see why.
Nootropics, drugs, and various supplements for memory, focus, and mental agility have been used for millennia. The desire to elevate ourselves is universal, much like the quest for longevity–and, unsurprisingly, the two are intertwined.
The following is a summary of “Emerging therapeutic frontiers in cancer: insights into posttranslational modifications of PD-1/PD-L1 and regulatory pathways,” published in the April 2024 issue of Hematology by Wang et al.
The intricate interplay between programmed cell death ligand 1 (PD-L1), expressed on the surface of tumor cells, and programmed cell death 1 (PD-1), expressed on T cells, constitutes a pivotal mechanism fostering immune evasion by tumor cells through the thwarting of effective tumor antigen-specific T cell activation. The advent of PD-1/PD-L1 blockade has emerged as a transformative strategy in combating tumor immune evasion, garnering substantial interest within the oncology landscape. Clinical investigations have underscored the remarkable efficacy and safety profile of PD-1/PD-L1 blocking antibodies across a spectrum of malignancies, offering a beacon of hope for patients.
Nonetheless, the therapeutic landscape of anti-PD-1/PD-L1 interventions is fraught with challenges, including limited indications and the emergence of drug resistance, necessitating a nuanced approach to therapeutic intervention. Accordingly, unraveling additional regulatory pathways and molecular players associated with PD-1/PD-L1 signaling assumes paramount importance, alongside the strategic implementation of combinational therapeutic modalities, to address the multifaceted dynamics of tumor immune evasion.
Could a future superintelligence bring back the already dead? This discussion has come up a while back (and see the somewhat related); I’d like to resurrect the topic because … it’s potentially quite important.
Algorithmic resurrection is a possibility if we accept the same computational patternist view of identity that suggests cryonics and uploading will work. I see this as the only consistent view of my observations, but if you don’t buy this argument/belief set then the rest may not be relevant.
The general implementation idea is to run a forward simulation over some portion of earth’s history, constrained to enforce compliance with all recovered historical evidence. The historical evidence would consist mainly of all the scanned brains and the future internet.
Harvard researcher Dr. David Sinclair has found himself at the center of controversy within the longevity community.
Sinclair has been a poster child of the longevity movement for years. He’s built several biotechnology companies focused on reversing the effects of aging, won acclaim for his research, and cultivated a loyal base of fans who swear by his lifestyle tips.
He’s also earned his share of critics who say his research isn’t always backed up by sufficient evidence. But over the past months, The Wall Street Journal reported that Sinclair has been battling a new level of backlash from colleagues and researchers who say his claims on curing aging have gone too far.
Instead of creating materials that are made to last, Freeman says their materials are made to task — perform a specific function and then modify themselves to serve a new function.
This achievement holds significant promise for advancements in regenerative medicine, drug delivery methods, and diagnostic technologies.
“With this discovery, we can think of engineering fabrics or tissues that can be sensitive to changes in their environment and behave in dynamic ways,” states Freeman.
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