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As implanted devices and commercial headsets advance, what will the real-world impacts be?

Scientists from Centogene, a company focused on rare and neurodegenerative diseases, along with their collaborators at University College London and elsewhere have published a study that links the Acyl-CoA Binding Domain Containing 6 (ACBD6) gene to new forms of early-onset dystonia and parkinsonism. The study is published in Brain in a paper titled, “Bi-allelic ACBD6 variants lead to a neurodevelopmental syndrome with progressive and complex movement disorders.”

Using whole exome sequencing data from 45 patients—23 males and 22 females between the ages of 1 and 50 years old—the researchers identified several novel and ultra-rare bi-allelic predicted loss-of-function variants in ACBD6, which are linked to a unique neurodevelopmental syndrome. The condition is accompanied by complex and progressive cognitive and movement disorders such as dystonia in 94% of cases and parkinsonism in older patients or about 32% of cases.

To test the association between ACBD6 and the syndrome, the researchers used zebrafish and frog knockouts. According to tests described in the paper, they observed similar phenotypes to those of affected individuals such as movement disorders, seizures, and facial dysmorphology in the zebrafish models. Their observations of the effects in zebrafish suggest “a combination of muscle and neuronal degeneration leading to movement abnormalities” resulting from the loss of the gene. When they assessed the effects of inactivating the gene in frogs, they observed reported failures in cell movement during gastrulation as a result of the gene’s loss.

Summary: Researchers made a breakthrough in memory research by genetically modifying the LIMK1 protein, crucial for memory, to be controlled by the drug rapamycin.

This study demonstrates the ability to enhance memory functions by manipulating synaptic plasticity in the brain.

The engineered protein showed significant memory improvement in animal models with age-related cognitive decline, offering potential for innovative treatments for neuropsychiatric diseases like dementia. This ‘chemogenetic’ approach, blending genetics and chemistry, opens new avenues in neurological research and therapy.

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Summary: Researchers developed an experimental computing system, resembling a biological brain, that successfully identified handwritten numbers with a 93.4% accuracy rate.

This breakthrough was achieved using a novel training algorithm providing continuous real-time feedback, outperforming traditional batch data processing methods which yielded 91.4% accuracy.

The system’s design features a self-organizing network of nanowires on electrodes, with memory and processing capabilities interwoven, unlike conventional computers with separate modules.

Back in 2021, a test of cephalopod smarts reinforced how important it is for us humans to not underestimate animal intelligence.

Cuttlefish were given a new version of the marshmallow test, and the results may demonstrate that there’s more going on in their strange little brains than we knew.

Their ability to learn and adapt, the researchers said, could have evolved to give cuttlefish an edge in the cutthroat eat-or-be-eaten marine world they live in.

A pair of studies from the laboratory of Evangelos Kiskinis, Ph.D., associate professor in the Ken and Ruth Davee Department of Neurology’s Division of Neuromuscular Disease and of Neuroscience, have uncovered novel cellular mechanisms that are involved in two types of genetic amyotrophic lateral sclerosis, or ALS.

The findings, published in Science Advances and Cell Reports, improve the understanding of ALS, a progressive neurodegenerative disease that attacks motor neurons in the brain and spinal cord, and provides support for the future development of targeted therapies.

An estimated 32,000 individuals are currently living with ALS in the U.S., according to the Les Turner ALS Foundation. There are two types of ALS: sporadic (non-genetic), which makes up more than 90% of all ALS cases, and familial (genetic).

Having healthy mitochondria, the organelles that produce energy in all our cells, usually portends a long healthy life whether in humans or in C. elegans, a tiny, short-lived nematode worm often used to study the aging process.

Researchers at the Buck Institute have identified a new drug-like molecule that keeps mitochondria healthy via mitophagy, a process that removes and recycles damaged mitochondria in multicellular organisms. The compound, dubbed MIC, is a natural compound that extended lifespan in C. elegans, ameliorated pathology in neurodegenerative disease models of C. elegans, and improved mitochondrial function in mouse muscle cells. Results are published in the November 13, 2023, edition of Nature Aging.

Defective mitophagy is implicated in many age-related diseases. It’s tied to neurodegenerative disorders such as Parkinson’s and Alzheimer’s; it plays a role in cardiovascular diseases including heart failure; it influences metabolic disorders including obesity and type 2 diabetes; it is implicated in muscle wasting and sarcopenia and has a complex relationship with cancer progression.

Scientists from the Shenzhen Institute of Advanced Technology (SIAT) within the Chinese Academy of Sciences (CAS), along with their partners, have designed a targeted gene therapy approach to mitigate the primary motor symptoms of Parkinson’s disease in both rodents and nonhuman primates.

The study was recently published in the journal Cell.

Parkinson’s disease, characterized by the loss of midbrain dopaminergic neurons, is one of the most common neurodegenerative diseases in the elderly population, affecting more than 6 million people worldwide.