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Researchers at The University of Texas MD Anderson Cancer Center have shown that therapeutically restoring ‘youthful’ levels of a specific subunit of the telomerase enzyme can significantly reduce the signs and symptoms of aging in preclinical models. If these findings are validated in clinical trials, they could have important therapeutic implications for age-related diseases such as Alzheimer’s, Parkinson’s, heart disease, and cancer.

The study, published in Cell, identified a small molecule compound that restores physiological levels of telomerase reverse transcriptase (TERT), which normally is repressed with the onset of aging. Maintenance of TERT levels in aged lab models reduced cellular senescence and tissue inflammation, spurred new neuron formation with improved memory, and enhanced neuromuscular function, which increased strength and coordination.

The researchers show that TERT functions not only to extend telomeres, but also acts as a transcription factor to affect the expression of many genes directing neurogenesis, learning and memory, cellular senescence, and inflammation.

Neurons in the brain are like vast networks, receiving thousands of signals from other neurons through tiny structures called synapses.


Researchers from Bonn and Japan have clarified how neighboring synapses coordinate their response to plasticity signals: Nerve cells in the brain receive thousands of synaptic signals via their “antenna,” the so-called dendritic branch. Permanent changes in synaptic strength correlate with changes in the size of dendritic spines. However, it was previously unclear how the neurons implement these changes in strength across several synapses that are close to each other and active at the same time.

The researchers—from the University Hospital Bonn (UKB), the University of Bonn, the Okinawa Institute of Science and Technology Graduate University (OIST) and the RIKEN Center for Brain Science (CBS)—assume that the competition between for molecular resources and the spatial distance between simultaneously stimulated spines affect their resulting dynamics. The results of the study have now been published in the journal Nature Communications.

Neurons are the computing units of the brain. They receive thousands of synaptic signals via their dendrites, with individual synapses undergoing activity-dependent plasticity. This is the mechanism underlying our memory and thinking and reflects long-lasting changes in synaptic strength.

A nanoparticle formulation, using oligonucleotide chemistry, able to release a gene editing system with single cell resolution after near infrared laser activation. The full potential of the formulation was demonstrated in the brain after intracerebral and intranasal administrations. The spot of the laser defined the region of gene editing.

Understanding cellular architectures and their connectivity is essential for interrogating system function and dysfunction. However, we lack technologies for mapping the multiscale details of individual cells and their connectivity in the human organ–scale system. We developed a platform that simultaneously extracts spatial, molecular, morphological, and connectivity information of individual cells from the same human brain. The platform includes three core elements: a vibrating microtome for ultraprecision slicing of large-scale tissues without losing cellular connectivity (MEGAtome), a polymer hydrogel–based tissue processing technology for multiplexed multiscale imaging of human organ–scale tissues (mELAST), and a computational pipeline for reconstructing three-dimensional connectivity across multiple brain slabs (UNSLICE).

WEHI researchers have found a specific immunotherapy could hold promise for treating gliomas, an aggressive form of brain cancer with limited treatment options.

The new study shows that CAR T cell therapy not…


Researchers at WEHI have identified a promising new two-in-one treatment that not only targets and destroys an aggressive form of brain cancer, but also helps the immune system develop a lasting defence against it.

This dual-action approach uses a specific immunotherapy known as CAR T cell therapy to treat gliomas, an incurable brain cancer with few treatment options.

Will artificial intelligence save us or kill us all? In Japan, AI-driven technology promises better lives for an aging population. But researchers in Silicon Valley are warning of untamable forces being unleashed– and even human extinction.

Will artificial intelligence make life better for humans or lead to our downfall? As developers race toward implementing AI in every aspect of our lives, it is already showing promise in areas like medicine. But what if it is used for nefarious purposes?

In Japan, the inventor and scientist behind the firm Cyberdyne is working to make life better for the sick and elderly. Professor Yoshiyuki Sankai’s robot suits are AI-driven exoskeletons used in rehabilitative medicine to help stroke victims and others learn to walk again. But he doesn’t see the benefits of AI ending there; he predicts a future world where AIs will live in harmony with humans as a new, benevolent species.

Yet in Silicon Valley, the cradle of AI development, there is an unsettling contradiction: a deep uncertainty among many developers about the untamable forces they are unleashing. Gabriel Mukobi is a computer science graduate student at Stanford who is sounding the alarm that AI could push us toward disaster– and even human extinction. He’s at the forefront of a tiny field of researchers swimming against the current to make sure AI is safe and beneficial for everyone.

Scraps of DNA discarded by our neurons’ power units are being absorbed into our nuclear genome far more frequently than assumed, potentially putting our brains at greater risk of developing life-threatening conditions.

An investigation by a team of researchers led by Columbia University in the US has found individuals with higher numbers of nuclear mitochondrial insertions – or NUMTs (pronounced new-mites) – in their brain cells are more likely to die earlier than those with fewer DNA transfers.

Mitochondria serve as our cells’ batteries, churning out energy in a form of chemical currency that suits most of our body’s metabolic needs. Once a discrete microbial organism in its own right, these tiny powerhouses were co-opted by our unicellular ancestors billions of years in the past, genes and all.