Lifeboat Foundation

Summary: A “flicker treatment” that uses flickering lights and sounds has been shown to be tolerable, safe, and effective in treating adults with mild cognitive impairment.

Source: Georgia Tech.

For the past few years, Annabelle Singer and her collaborators have been using flickering lights and sound to treat mouse models of Alzheimer’s disease, and they’ve seen some dramatic results.

Summary: The reactivation of learned material during slow oscillation/sleep spindle complexes, and the precision of SO-spindle coupling predicts how strong a memory will be reactivated in the brain.

Source: University of Birmingham.

While we sleep, the brain produces particular activation patterns. When two of these patterns – slow oscillations and sleep spindles – gear into each other, previous experiences are reactivated. The stronger the reactivation, the clearer will be our recall of past events, a new study reveals.

Summary: A new algorithm that uses data from memory tests and blood samples is able to accurately predict an individual’s risk for developing Alzheimer’s disease.

Source: Lund University.

Researchers at Lund University in Sweden have developed an algorithm that combines data from a simple blood test and brief memory tests, to predict with great accuracy who will develop Alzheimer’s disease in the future.

Senior director, milken institute center for the future of aging, milken institute; executive director, alliance to improve dementia care.

Nora Super is the Senior Director of the Milken Institute Center for the Future of Aging (CFA) (https://milkeninstitute.org/centers/center-for-the-future-of-aging) and the Executive Director of the Milken Institute Alliance to Improve Dementia Care (https://milkeninstitute.org/centers/center-for-the-future-of…tia-care).

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Researchers identify a mechanism that could lead to new treatments for brain injuries caused by oxygen deprivation.

In a surprising discovery, researchers at Massachusetts General Hospital (MGH) identified a mechanism that protects the brain from the effects of hypoxia, a potentially lethal deprivation of oxygen. This serendipitous finding, which they report in Nature Communications, could aid in the development of therapies for strokes, as well as brain injury that can result from cardiac arrest, among other conditions.

However, this study began with a very different objective, explains senior author Fumito Ichinose, MD, PhD, an attending physician in the Department of Anesthesia, Critical Care and Pain Medicine at MGH, and principal investigator in the Anesthesia Center for Critical Care Research. One area of focus for Ichinose and his team is developing techniques for inducing suspended animation, that is, putting a human’s vital functions on temporary hold, with the ability to “reawaken” them later. This state of being would be similar to what bears and other animals experience during hibernation. Ichinose believes that the ability to safely induce suspended animation could have valuable medical applications, such as pausing the life processes of a patient with an incurable disease until an effective therapy is found. It could also allow humans to travel long distances in space (which has frequently been depicted in science fiction).

Might interest some.

A new study from the Institute of Psychiatry, Psychology and Neuroscience (IoPPN) at King’s College London has established that Intermittent Fasting (IF) is an effective means of improving long term memory retention and generating new adult hippocampal neurons in mice, in what the researchers hope has the potential to slow the advance of cognitive decline in older people.

The study, published today in Molecular Biology, found that a calorie restricted diet via every other day fasting was an effective means of promoting Klotho gene expression in mice. Klotho, which is often referred to as the “longevity gene” has now been shown in this study to play a central role in the production of hippocampal adult-born new neurons or neurogenesis.

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Is this the reason why the general public view the emerging field of regenerative medicine with such scepticism? Has a combined cultural history of being bombarded with empty promises of longevity made us numb to such a prospect? Possibly, although I believe it might go deeper than old fashioned scepticism. After all, our species is hardly a stranger to believing something if we desire for it to be true, regardless of how much evidence is presented to us.

Maybe we are simply experiencing just another example of humans finding dramatic change to our way of life hard to comprehend and accept. After all, practically every major change in our recent history was largely believed to be an impossibility by the general public, right up until the point that it became the norm. Everything from the aeroplane to the internet was seen as science fiction, but yet today they are integral parts of our lives. Now, this is not to say that everything the general public is sceptical of will inevitably turn out to prove them wrong, but lessons from our history do show that when it comes to scientific progress, the public will not believe it until they can see it.

Some would believe that scepticism towards regenerative medicine strikes at something much deeper in our psych, as it threatened to fundamentally change our entire outlook on the world. For our entire lives, we have been taught by our interactions with others exactly how life is supposed to progress. You are supposed to suffer a gradual decay of mental and physical abilities, until eventually you die. That is just how it is, and if that were to ever change then we would all have to change how we think about the world. The concept of a 125 year old with the appearance of a 25 year old seems bizarre to us right now, and to many the idea of ever lasting health just goes against their fundamental beliefs of how the world functions to such an extent that they cannot comprehend anything different. Some would even go far as to defend the ageing process as being an integral part of life, displaying what can only be described as ‘Stockholm syndrome with extra steps’.

3D printing, also called additive manufacturing, has become widespread in recent years. By building successive layers of raw material such as metals, plastics, and ceramics, it has the key advantage of being able to produce very complex shapes or geometries that would be nearly impossible to construct through more traditional methods such as carving, grinding, or molding.

The technology offers huge potential in the health care sector. For example, doctors can use it to make products to match a patient’s anatomy: a radiologist could create an exact replica of a patient’s spine to help plan surgery; a dentist could scan a patient’s broken tooth to make a perfectly fitting crown reproduction. But what if we took a step further and apply 3D printing techniques to neuroscience?

Stems cells are essentially the body’s raw materials; they are pluripotent elements from which all other cells with specialized functions are generated. The development of methods to isolate and generate human stem cells, has excited many with the promise of improved human cell function understanding, ultimately utilizing them for regeneration in disease and trauma. However, the traditional two-dimensional growth of derived neurones–using flat petri dishes–presents itself as a major confounding factor as it does not adequately mimic in vivo three-dimensional interactions, nor the myriad developmental cues present in real living organisms.

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Mutations in the RAB39B gene cause X-linked intellectual disability (XLID), comorbid with autism spectrum disorders or early Parkinson’s disease. One of the functions of the neuronal small GTPase RAB39B is to drive GluA2/GluA3 α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) maturation and trafficking, determining AMPAR subunit composition at glutamatergic postsynaptic neuronal terminals. Taking advantage of the Rab39b knockout murine model, we show that a lack of RAB39B affects neuronal dendritic spine refinement, prompting a more Ca2+-permeable and excitable synaptic network, which correlates with an immature spine arrangement and behavioural and cognitive alterations in adult mice. The persistence of immature circuits is triggered by increased hypermobility of the spine, which is restored by the Ca2+-permeable AMPAR antagonist NASPM.