Lifeboat Foundation

Today, we will be taking a look at a new study showing that an NAD+ precursor was able to improve mitochondrial function in cells and flies with a model of Parkinson’s disease.

Summary

While mitochondrial dysfunction is emerging as key in Parkinson’s disease (PD), a central question remains whether mitochondria are actual disease drivers and whether boosting mitochondrial biogenesis and function ameliorates pathology. We address these questions using patient-derived induced pluripotent stem cells and Drosophila models of GBA-related PD (GBA-PD), the most common PD genetic risk. Patient neurons display stress responses, mitochondrial demise, and changes in NAD+ metabolism. NAD+ precursors have been proposed to ameliorate agerelated metabolic decline and disease. We report that increasing NAD+ via the NAD+ precursor nicotinamide riboside (NR) significantly ameliorates mitochondrial function in patient neurons. Human neurons require nicotinamide phosphoribosyltransferase (NAMPT) to maintain the NAD+ pool and utilize NRK1 to synthesize NAD+ from NAD+ precursors. Remarkably, NR prevents the age-related dopaminergic neuronal loss and motor decline in fly models of GBA-PD.

Continue reading “NAD+ Precursor Has Therapeutic Potential Against Parkinsons Disease” »

Great news.

Fresh or frozen human blood samples can be directly transformed into patient-specific neurons to study disorders such as schizophrenia and autism, Stanford researchers find.

Johnson and Johnson recently announced that it was halting a clinical trial for a new Alzheimer’s drug after safety issues emerged. This latest failure adds to the dozens of large, costly clinical trials that have shown no effect in treating this devastating disease.

The growing list of failures should give us pause for thought – have we got the causes of Alzheimer’s all wrong?

In the first analysis of the disease, the German physician, Alois Alzheimer, noted odd changes in the brain of a patient who died of the condition. Alzheimer identified two kinds of protein aggregates that are not found in younger brains: plaques that are found between brain cells and tangles that are found inside brain cells.

Continue reading “Why Insulin Is a New Suspect in Alzheimer’s Disease” »

Very promising since “Identifying what changes are happening in the brain when interventions successfully reduce depressive symptoms could allow us to create more effective, pharmaceutical-free approaches to help alleviate depression in people who experience chronic traumatic brain injury symptoms,” said study author Dr. Sandra Bond Chapman, founder and chief director of the Center for BrainHealth.

Images show prefrontal connectivity patterns after cognitive training in individuals who suffered traumatic brain injury. Kihwan Han et al (2018) _____ Cognitive training reduces depression, rebuilds injured brain structure & connectivity after traumatic brain injury (UT-Dallas release): “New research from the Center.

MIT researchers, working with scientists from Brigham and Women’s Hospital, have developed a new way to power and communicate with devices implanted deep within the human body. Such devices could be used to deliver drugs, monitor conditions inside the body, or treat disease by stimulating the brain with electricity or light.

The implants are powered by radio frequency waves, which can safely pass through human tissues. In tests in animals, the researchers showed that the waves can power devices located 10 centimeters deep in tissue, from a distance of 1 meter.

Continue reading “Wireless System Can Power Smart Devices Inside the Body” »

New research on brain ageing and mitochondria from Salk Institute.

Thanks to a new technique, researchers from the Salk Institute’s Gage laboratory have shown that impaired energy production might be a reason why human brains are susceptible to age-related diseases in the first place [1].

In particular, Salk scientists observed that induced neurons (iNs) obtained from fibroblasts of older individuals had dysfunctional mitochondria and therefore decreased energy levels compared to younger neurons. Out-of-shape mitochondria have previously been implicated in degenerative brain diseases, such as Alzheimer’s and Parkinson’s, and this finding might help reveal more about the connection between these diseases and this particular hallmark of aging.

Continue reading “Mitochondrial dysfunction in aged brain cells” »

http://www.thepathmag.com/can-you-actually-hack-your-dna-to-slow-down-aging/

Many technologies / interventions progressing down the development pathways in the coming years — but there are a lot of free, common sense adjustments you can make today:

http://www.blogtalkradio.com/entrepreneursempower/2018/06/03…ira-pastor

I t’s an odd thing for someone to say about neurons: “Let’s see if anyone is awake.” And it’s an even odder thing to hear in a cavernous, half-furnished office suite where one whole room is occupied only by copy machines and a lonely foosball table.

Not far from that foosball table, Oshiorenoya Agabi and Benjamin Sadrian are sitting in a lab at their startup, Koniku, in Berkeley, California. Agabi founded the company, and Sadrian is a senior neuroscientist. They are toggling between a microscope and a screen full of blue graphs, looking for signs of activity in a cluster of neurons. Sadrian pauses as he scrolls through slightly fuzzy readouts on the screen, reminiscent of stock charts with buzz cuts. “I wish you’d come later, even tomorrow,” he sighs.

These readouts measure signals inside cells, and Agabi and Sadrian are looking for spikes that would show Koniku’s neurons reacting to a chemical Sadrian exposed them to moments ago. When we examined them under the microscope, they glowed a faint neon green, which indicates they’re starting to mature. A few tentative dendrites reached out into the void, the neurons just beginning to form connections with one another. But the telltale spikes don’t materialize on the screen. At just six days old, these neurons are still too young to do the jobs they’ve been engineered to do.

Continue reading “The Birth of Wetware” »