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Category: life extension – Page 12

Can we upload consciousness to computers? | Pigliucci, Yampolskiy, Sandberg, Dijkstra

Massimo Pigliucci, Roman Yampolskiy, Anders Sandberg, and Nadine Dijkstra discuss the latest developments in neuroscience and computer programming.

Can we upload our minds to computers?

With a free trial, you can watch the full debate NOW at https://iai.tv/video/consciousness-in-the-clouds?utm_source=…escription.

The idea of uploading our minds to the digital cloud has not only been taken seriously by Silicon Valley, but turned into a detailed business plan. Elon Musk claims digitising consciousness will revolutionise humanity, and the industry is estimated to be worth $50 billion by 2030. But it’s unknown whether, in principle, we can replicate minds with computer code, or whether we should seek to do so. Critics argue we have no idea how a machine could create consciousness, and neuroscientists have yet to provide an explanation for how the brain does so. A survey of specialists by Nature found the majority thought it unlikely AI would achieve consciousness anytime soon.

Should we see talk of uploading our minds to the cloud as implausible tech marketing nonsense? Should we conclude that if thought and consciousness are unobservable, it will not be possible to replicate the mind with silicon chips? Or is digital immortality such a profound and important sea change in our lives and potential that we should pursue it at all costs?

#consciousness #ai #artificialintelligence #elonmusk #neuralink #neuroscience.

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Plasma proteomics links brain and immune system aging with healthspan and longevity

In a large-scale proteomic study of biological aging of 11 organs from 44,498 individuals in the UK Biobank, the biological ages of the brain and immune system emerged as strong predictors of healthspan and longevity.

Multiomics and cellular senescence profiling of aging human skeletal muscle uncovers Maraviroc as a senotherapeutic approach for sarcopenia

This study leverages single-nucleus multiomics to map cellular senescence atlas in aging human skeletal muscle and uncovers potential targets and senotherapeutics for treating age-associated sarcopenia.

17y Younger Biological Age (Test #4 in 2025): Supplements, Diet

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Role of plasmin in metastatic tumors

FasL is an immune cell membrane protein that triggers a programmed cell death called apoptosis. Activated immune cells, including CAR-T cells made from a patient’s immune system, use apoptosis to kill cancer cells.

The team discovered that in human genes, a single evolutionary amino acid change — serine instead of proline at position 153 — makes FasL more susceptible to being cut and inactivated by plasmin.

Plasmin is a protease enzyme that is often elevated in aggressive solid tumors like triple negative breast cancer, colon cancer and ovarian cancer.

This means that even when human immune cells are activated and ready to attack the tumor cells, one of their key death weapons — FasL — can be neutralized by the tumor environment, reducing the effectiveness of immunotherapies.

The findings may help explain why CAR-T and T-cell-based therapies can be effective in blood cancers but often fall short in solid tumors. Blood cancers often do not rely on plasmin to metastasize, whereas tumors like ovarian cancer rely heavily on plasmin to spread the cancer.

Significantly, the study also showed that blocking plasmin or shielding FasL from cleavage can restore its cancer-killing power. That finding may open new doors for improving cancer immunotherapy.

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DunedinPACNI estimates the longitudinal Pace of Aging from a single brain image to track health and disease

Differences in the Pace of Aging are important for many health outcomes but difficult to measure. Here the authors describe the Dunedin Pace of Aging Calculated from NeuroImaging measure, an approach that uses a single brain image to measure how fast a person is aging and can help predict mortality or the risk of developing chronic disease.

AI-assisted technique can measure and track aging cells

A combination of high-resolution imaging and machine learning, also known as artificial intelligence (AI), can track cells damaged from injury, aging, or disease, and that no longer grow and reproduce normally, a new study shows.

These senescent cells are known to play a key role in wound repair and aging-related diseases, such as cancer and heart disease, so tracking their progress, researchers say, could lead to a better understanding of how tissues gradually lose their ability to regenerate over time or how they fuel disease. The tool could also provide insight into therapies for reversing the damage.

The study included training a computer system to help analyze animal cells damaged by increasing concentrations of chemicals over time to replicate human aging. Cells continuously confronted with environmental or biological stress are known to senesce, meaning they stop reproducing and start to release telltale molecules indicating that they have suffered injury.

Cross-omics risk scores of inflammation markers are associated with all-cause mortality: The Canadian Longitudinal Study on Aging

We developed single-and multi-omics risk scores to assess blood inflammation markers and validated them across three cohorts. Our multi-omics models outperformed blood markers in predicting all-cause mortality, offering a more comprehensive approach to capturing inflammation burden. This may help identify at-risk populations for targeted interventions to reduce inflammation-related mortality.

Abstract: Synaptic plasticity is obstructed by pathogenic tau in the brain

Representing a key mechanism that underlies memory loss in Alzheimer’s disease (AD) and related tauopathies. Here, we found that reduced levels of the memory-associated protein KIdney/BRAin (KIBRA) in the brain and increased KIBRA protein levels in cerebrospinal fluid are associated with cognitive impairment and pathological tau levels in disease. We next defined a mechanism for plasticity repair in vulnerable neurons using the C-terminus of the KIBRA protein (CT-KIBRA). We showed that CT-KIBRA restored plasticity and memory in transgenic mice expressing pathogenic human tau; however, CT-KIBRA did not alter tau levels or prevent tau-induced synapse loss. Instead, we found that CT-KIBRA stabilized the protein kinase Mζ (PKMζ) to maintain synaptic plasticity and memory despite tau-mediated pathogenesis. Thus, our results distinguished KIBRA both as a biomarker of synapse dysfunction and as the foundation for a synapse repair mechanism to reverse cognitive impairment in tauopathy.

1Buck Institute for Research on Aging, Novato, California, USA.

2Memory and Aging Center, Department of Neurology, University of California San Francisco, San Francisco, California, USA.

3Gladstone Institutes, San Francisco, Califoria, USA.

4Weill Institute for Neurosciences, Department of Pathology, University of California San Francisco, San Francisco, California, USA.

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