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Researchers at Brown University have discovered a way to stimulate cellular autophagy, which is a natural recycling system built into every cell in the body. This has the potential to combat many age-related neurodegenerative diseases.

What is autophagy?

Autophagy means “eating of self” (from Ancient Greek “auto” = self, “phagein” = to devour). Autophagy is how cells break down broken or dysfunctional organelles and proteins in the cell [1,2]. This essentially means that autophagy can consume organelles, such as mitochondria, peroxisomes, and the endoplasmic reticulum, as part of this process. There is also evidence to support that high levels of autophagy are linked to longevity.

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Physical exercise is a key piece of the brain health puzzle, but certainly not a magic pill.


___ Exercise ‘doesn’t slow’ progression of dementia (NHS Choices): A trial in which people with dementia took part in a moderately intense exercise programme for 4 months found their mental decline did not slow and may even have worsened faster than in people who did not take part in the programme…While the exercise.

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A chance lab discovery is opening up the possibility for wide-scale improvements in drug screening, application of selective painkillers, and selectively nuking cancer cells. The mystery material? Graphene, a semi-metal that’s composed of a single layer of carbon atoms. It’s already being used to make flexible OLED displays and reduce the energy costs of desalination, but its potential benefits for the medical field look promising too.

It began with a theory — scientists at the University of California knew graphene could convert light into electricity, and wondered whether that electricity had the capacity to stimulate human cells. Graphene is extremely sensitive to light (1,000 times more than traditional digital cameras and smartphones) and after experimenting with different light intensities, Alex Savchenko and his team discovered that cells could indeed be stimulated via optical graphene stimulation.

“I was looking at the microscope’s computer screen and I’m turning the knob for light intensity and I see the cells start beating faster,” he said. “I showed that to our grad students and they were yelling and jumping and asking if they could turn the knob. We had never seen this possibility of controlling cell contraction.”

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Nicotinamide adenine dinucleotide (NAD+), a nucleotide, is critical for life to exist. From the most simple bacteria to complex multicellular organisms such as humans, NAD is a vital component of cellular function and thus life.

An increased level of NAD+ appears to convey health and longevity, and a decrease is associated with aging and disease. Today, we are going to look at NAD+, why it declines with age, and what science might do about it.

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Aurora Flight Services’ Autonomous Aerial Cargo Utility System (AACUS) took another step forward as an AACUS-enabled UH-1H helicopter autonomously delivered 520 lb (236 kg) of water, gasoline, MREs, communications gear, and a cooler capable of carrying urgent supplies such as blood to US Marines in the field.

Last week’s demonstration at the Marine Corps Air Ground Combat Center Twentynine Palms in California was the first ever autonomous point-to-point cargo resupply mission to Marines and was carried out as part of an Integrated Training Exercise. The completion of what has been billed as the system’s first closed-loop mission involved the modified helicopter carrying out a full cargo resupply operation that included takeoff and landing with minimal human intervention.

Developed as part of a US$98-million project by the US Office of Naval Research (ONR), AACUS is an autonomous flight system that can be retrofitted to existing helicopters to make them pilot optional. The purpose of AACUS is to provide the US armed forces with logistical support in the field with a minimum of hazard to human crews.

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At the cellular level, aging and cancer are two sides of the same coin. The mechanism that limits a cell’s lifespan can be slowed down, but that can turn them cancerous, as they divide unchecked. Now, scientists at EPFL have found a way to manipulate that mechanism to effectively turn off cancer’s immortality, letting it die slowly and naturally.

Every time a cell divides, it consults the blueprints contained in the chromosomes, but some genetic information is lost with every division. To protect the important bits, the tips of the chromosomes are covered with repeating sequences of “junk” DNA known as telomeres. Eventually even they erode away, leaving the cell vulnerable to damage – which we recognize as wrinkles, grey hairs, decreased metabolism, and higher chances of disease. In that way, telomere length is inextricably linked to aging.

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