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Category: neuroscience

Summary: Researchers explore the close relationship between depression and pain. For some people, unexplained symptoms of pain, such as back or headaches, could be an early indicator of depression before mood changes occur.

Source: Mayo Clinic

Pain and depression are closely related. Depression can cause pain – and pain can cause depression. Sometimes pain and depression create a vicious cycle in which pain worsens symptoms of depression, and then the resulting depression worsens feelings of pain.

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Anacardic acid, a compound found in cashew nuts, promoted myelin regeneration and eased neuronal damage and disability in two mouse models of multiple sclerosis (MS).

These protective effects were associated with maturation of myelin-producing cells and production of IL-33, an immune-related molecule with a neuroreparative role in the central nervous system (CNS, the brain and spinal cord).

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How we adapt to aging late in life may be genetically influenced, according to a study led by a psychologist at the University of California, Riverside.

The research, published in Aging Cell, has implications for how relate to aging. Epigenesis is a process in which chemicals attached to DNA control its activity. Epigenetic changes, which can be passed on to offspring, may be critical to accelerated aging as well as declines in cognitive and physical functioning that often accompany aging. Epigenetic modifications resulting in altered may occur due to a number of biological processes, including one the researchers focused on: DNA methylation.

In DNA methylation, groups are added to the DNA molecule. DNA has four different types of nucleotides: A, T, G, and C. DNA methylation occurs at the C bases of eukaryotic DNA. Changes in DNA methylation correlate strongly with aging.

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Summary: Researchers identified a group of closely related genes that capture molecular links between Alzheimer’s and LATE, a common brain disorder that mimics Alzheimer’s symptoms.

Source: Brigham and Women’s Hospital

Alzheimer’s disease is one of the most common causes of dementia, and while most people might know someone who is affected by it, the genetic factors behind the disease are less known. A new study by investigators from Brigham and Women’s Hospital uncovered a group of closely related genes that may capture molecular links between Alzheimer’s disease and Limbic-predominant Age-related TDP-43 Encephalopathy, or LATE, a recently recognized common brain disorder that can mimic Alzheimer’s symptoms. LATE is often combined with Alzheimer’s disease to cause a more rapid cognitive decline. The study’s results are published in Neuron.

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A leading expert in socially responsible technology innovation Dr Andrew Maynard told us “I think Musk’s overreaching and he probably knows it.

”That said, Elon Musk has got a track record of doing things that other people said can’t be done. So I think that this is going to be an interesting space because of that… [But] I think we’re a long way from understanding how this works.

”Even with Elon Musk’s system you have around ten thousand electrodes. There are billions of neurons in your brain. It’s a needle in a haystack”.

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Scientists investigating Alzheimer’s treatments at the Salk Institute have uncovered some key mechanisms that enable an experimental drug to reverse memory loss in mouse models of the disease. The discovery not only bodes well for the possibility of clinical trials, but provides researchers with a new target to consider in the wider development of compounds to counter the degenerative effects of the condition.

The research centers on a drug called CMS121, which is a synthetic version of a chemical called fisetin that occurs naturally in fruits and vegetables. The Salk team’s previous studies concerning CMS121 have produced some very promising results, with one paper published last year describing how the drug influences age-related metabolic pathways in the brain, protecting against the type of degeneration associated with Alzheimer’s. This followed earlier studies demonstrating how fisetin can prevent memory loss in mice engineered to develop Alzheimer’s.

Work continues at Salk to understand how exactly fisetin and the synthetic variant CMS121 produces these anti-aging effects on the brain. In their latest study, the researchers again turned to mice engineered to develop Alzheimer’s, which were administered daily doses of CMS121 from the age of nine months. This is the equivalent to middle age in humans, with the mice already exhibiting learning and memory problems before the treatment began.

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Newswise — Most of modern medicine has physical tests or objective techniques to define much of what ails us. Yet, there is currently no blood or genetic test, or impartial procedure that can definitively diagnose a mental illness, and certainly none to distinguish between different psychiatric disorders with similar symptoms. Experts at the University of Tokyo are combining machine learning with brain imaging tools to redefine the standard for diagnosing mental illnesses.

“Psychiatrists, including me, often talk about symptoms and behaviors with patients and their teachers, friends and parents. We only meet patients in the hospital or clinic, not out in their daily lives. We have to make medical conclusions using subjective, secondhand information,” explained Dr. Shinsuke Koike, M.D., Ph.D., an associate professor at the University of Tokyo and a senior author of the study recently published in Translational Psychiatry.

“Frankly, we need objective measures,” said Koike.

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“How would you like to be known as the neurosurgeon who cured Parkinson’s disease?”

A month before the scheduled surgery, the four researchers were ready to chaperone the brain cells on their 190-mile journey. They never anticipated they were in for “The Amazing Race”-meets-“ER.”

It was after midnight on a late summer night in 2017, and they had less than eight hours to get the cells by ambulance, private plane, and another ambulance from Dana-Farber Cancer Institute in Boston to Weill Cornell Medical Center in Manhattan. If it took longer, the cells would almost certainly be DOA, and so might the researchers’ plan to carry out an experimental transplant surgery unprecedented in the annals of medicine: replacing the dysfunctional brain cells of a Parkinson’s disease patient with the progeny of an extraordinary type of stem cell. Created in the lab from a patch of the patient’s own skin, these cells, it was hoped, would settle into the brain like they belonged there and permanently restore the patient’s ability to walk and move normally.

If successful, the surgery could forever change Parkinson’s disease, from an inexorable, cruel, and sometimes fatal decline to — for at least some patients — a condition that can be successfully treated.

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