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These studies show that older adults who frequently pick up a puzzle tended to have the short-term memory capacity of someone eight years their junior and the grammatical reasoning of someone ten years younger.

“We hope this will encourage people to consider how they challenge their brain on a regular basis, and perhaps consider taking up puzzles or evidence-based brain training games as part of a lifestyle approach to keep their brains healthy,” Corbett tells Inverse.

Corbett’s study is one of a few showing that frequent engagement with puzzles has lasting effects on memory and cognitive decline, the slow loss of memory and other problem-solving skills that accompany aging (and is also a feature of brain diseases like Alzheimer’s). Other studies include the Bronx Aging study, which showed that dementia patients who did crossword puzzles started to lose their memory about 2.54 years later than those who didn’t do crosswords.

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A pair of collaborative studies led by Fen-Biao Gao, Ph.D., have identified two potential drug targets for the diseases amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). The studies, which appear in Nature Neuroscience and PNAS, provide a new layer of detail about how hexanucleotide repeat expansions in the C9ORF72 gene, the most common genetic mutation responsible for both ALS and FTD, causes neuron cell death. The Nature Neuroscience study also describes a new mouse model that more closely mimics the gradual build-up of toxins in patients with the diseases.

“Understanding how these mutations lead to motor neuron damage is important to the development of new treatment approaches,” said Dr. Gao, the Governor Paul Cellucci Chair in Neuroscience Research and professor of neurology. “We know that this mutation can cause these diseases. These studies show that both and DNA repair pathways are disrupted when the mutated gene is present in cells. That makes them potentially druggable targets.”

In ALS, a progressive, neurodegenerative disorder affecting the motor neurons in the central nervous system, the C9ORF72 gene accounts for 40 percent of inherited forms of the disease and 6 percent of sporadic cases. As motor neurons die, the brain’s ability to send signals to the body’s muscles is compromised. This leads to loss of voluntary muscle movement, paralysis and eventually death from respiratory failure.

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These days, scientists can collect a few skin or blood cells, wipe out their identities, and reprogram them to become virtually any other kind of cell in the human body, from neurons to heart cells.

The journey from skin cell to another type of functional cell involves converting them into induced (iPSCs), which are similar to the developmentally immature stem cells found in embryos, and then coaxing them to mature into something different.

But the process runs on an invisible clock, one in which scientists are interested in speeding up so adult-like cells are available when needed, whether for testing drugs for precision medicine, transplanting to repair injury or defect, or better understanding basic biology. It involves an FDA-approved compound called polyinosine-polycytidylic acid, or pIC, a double-stranded RNA molecule that activates a cell’s innate defense system. The compound is commonly used to boost vaccines and chemotherapy. The researchers found that when added to induced pluripotent stem cells undergoing the process of transitioning into cardiac muscle cells, pIC accelerated cellular .

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Researchers from the University of Helsinki have discovered a chink in the armour of the tumour cells of glioblastoma, a lethal brain cancer. Alongside the finding, the researchers also came up with a method for attacking this vulnerability. The results gained in experiments conducted with cell cultures and a mouse model are promising.

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A recent article, published in the Oxford journal Brain, categorizes and draws attention to an age-related disease that impacts the brain yet is widely unknown, even among scientists: limbic-predominant age-related TDP-43 encephalopathy (LATE) [1].

The symptoms of this disease are similar to those of Alzheimer’s disease. It causes cognitive impairment and, when presenting alongside Alzheimer’s disease, can lead to even faster degeneration along with heightened agitation and aggression.

This new disease has been found to impact very specific areas of the brain – generally traveling vertically through the brain, it degenerates areas partly responsible for emotions, memory, and language, influencing different areas depending on its stage.

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Elon Musk’s Neuralink startup raises $39 MILLION as it seeks to develop tech that will connect the human brain with computers…


An Elon Musk-backed startup looking to connect human brains to computers has raised most of its $51 million funding target. According to a report Neuralink has raised $39 million.


Scientists might have found an early detection method for some forms of dementia, according to new research by the University of Arizona and the University of Toronto’s Baycrest Health Sciences Centre.

According to the study published in the journal Neuropsychologia last month, patients with a rare neurodegenerative disorder called Primary Progressive Aphasia, or PPA, show abnormalities in in areas that look structurally normal on an MRI scan.

“We wanted to study how degeneration affects function of the brain,” said Aneta Kielar, the study’s lead author and assistant professor in the UA Department of Speech, Language and Hearing Sciences.

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