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Category: neuroscience – Page 26

Boosting good gut bacteria population through targeted interventions may slow cognitive decline

The origin of neurodegenerative diseases like Alzheimer’s or dementia isn’t limited to the brain. The state of your gut can quietly set off a cycle of chronic, system-wide inflammation that nudges the brain toward cognitive decline. But how does the pathogenesis of a disease that seems purely brain-based begin in the gut—an organ that is mostly busy producing chemicals for digesting food?

It turns out these two entities are linked by the gut-brain axis, a two-way communication superhighway that constantly sends signals between the digestive tract and the central nervous system. It runs on chemical messengers like neurotransmitters and fatty acids, sharing information that shapes our memory, mood, and inflammation triggers.

An analysis of 15 studies involving more than 4,200 participants found that the gut-brain highway can be put to work as a drug-free route to support cognitive health. Tuning the gut microbiota through diet, supplements, or medical interventions such as fecal microbiota transplantation (FMT) can help improve memory, executive function, and overall cognitive performance, particularly in early or mild cases of cognitive impairment.

Frontiers: Year 2020 this gene therapy in mice shows promise for als gene therapy in humans

Gene therapy is an emerging and powerful therapeutic tool to deliver functional genetic material to cells in order to correct a defective gene. During the past decades, several studies have demonstrated the potential of AAV-based gene therapies for the treatment of neurodegenerative diseases. While some clinical studies have failed to demonstrate therapeutic efficacy, the use of AAV as a delivery tool has demonstrated to be safe. Here, we discuss the past, current and future perspectives of gene therapies for neurodegenerative diseases. We also discuss the current advances on the newly emerging RNAi-based gene therapies which has been widely studied in preclinical model and recently also made it to the clinic.

Gene therapy is an emerging therapeutic tool used to deliver functional genetic material to cells in order to correct a defective gene. By delivering a copy of a therapeutic gene to affected cells, the product encoded by that gene [i.e., its messenger RNA (mRNA) and/or proteins] will be continuously synthesized within the cell, utilizing the cell’s own transcriptional and translational machinery (Porada et al., 2013). The main advantage of this technology is that it offers a potentially life-long therapeutic effect without the need for repeated administration. Gene therapy can be used to correct defective genes by introducing a functional copy of the gene, by silencing a mutant allele using RNA interference (RNAi), by introducing a disease-modifying gene, or by using gene-editing technology (Grimm and Kay, 2007; Dow et al., 2015; Saraiva et al., 2016).

Gene therapy vectors can be either viral or non-viral. Different physical and chemical systems can be applied to deliver therapeutic genes to cells without the need of a viral vector. Non-viral vectors have no size limitation for the therapeutic gene, generally have a low immunogenicity risk, and can be produced at relatively low costs (Nayerossadat et al., 2012). However, due to the fact that high therapeutic doses are required when using non-viral technologies, and the resulting gene expression is generally transient, most gene therapies now rely on viral vectors. Numerous viral vector types have been tested in clinic, including vaccinia, measles, vesicular stomatitis virus (VSV), polio, reovirus, adenovirus, lentivirus, γ-retrovirus, herpes simplex virus (HSV) and adeno-associated virus (AAV) (Lundstrom, 2018).

Gene therapy for deafness approved

The world’s first gene therapy for deafness received approval from the U.S. Food and Drug Administration today. The treatment, from biotech company Regeneron, targets hearing loss caused by inherited mutations in the OTOF gene, which encodes otoferlin, a protein that allows the inner ear’s hair cells to sense and transmit sound to the brain. Patients receive a one-time ear injection containing viral vectors that carry a working copy of the OTOF gene into their cells. In a clinical trial, nine of 12 deaf children who initially received the Regeneron therapy gained enough hearing to stop using cochlear implants; three within that group ended up having normal hearing. Although many gene therapies cost $1 million or more, Regeneron said its treatment, called Otarmeni, will be free in the United States.

Eli Lilly & Co. and researchers in China are also developing gene therapies for OTOF mutations, which account for up to 3% of cases of inherited deafness. One U.S.-Chinese team reported in Nature this week that among 24 patients, including some adults, hearing improvements have lasted more than 2 years in some cases, NPR reports. Researchers eventually hope to treat other types of genetic deafness as well, but those attempts face more challenges. For example, for some disorders, it may be necessary to regenerate lost hair cells. In others, targeting the wrong cell type could damage hearing.

Label-free optical imaging enables automated measurement of human white matter microstructure

White matter pathways allow distant parts of the brain to communicate, supporting memory, emotion, and language. One such pathway, the uncinate fasciculus, connects the front of the temporal lobe with regions of the frontal cortex involved in decision-making and social behavior. Despite its importance, little is known about the microscopic structure of this tract in the human brain.

Traditional techniques such as electron microscopy can reveal fine details, but they often fail when applied to postmortem human tissue, which is frequently degraded.

In a study published in Biophotonics Discovery, researchers report a new way to examine white matter structure in postmortem human brains.

Recent Scientific Evidence that Supports Nichols’s Lost Primal Eye Theory of Mind I. Core Premise: The Evolutionary Shift

The Phantom Organ and The “Hard Problem” — I apply MVT to solve David Chalmers’s “Hard Problem” of consciousness-the question of why physical brain processes are accompanied by subjective feelings (qualia).

Nichols’s theory posits that self-referential consciousness and abstract thought in many modern animals are the evolutionary result of the loss of a physical sensory organ: the parietal/pineal eye (the “primal eye”). Nichols maps this transition across three brain states in vertebrate evolution: The E2 State (Finite-State): Early fish, amphibians, and ancestral reptiles (as well as modern “living fossils” like the Tuatara) possessed a functional, light-sensitive median eye on top of their skulls, connected to the pineal gland. This organ directly controlled thermoregulation, circadian rhythms, and basic predator detection in coldblooded (ectothermic) animals. Their brains were “hard-wired,” responding directly to environmental stimuli. The E1 State (Infinite-State): As mammals and birds evolved warmbloodedness (endothermy), external temperature sensing became redundant, and advanced lateral eyes took over visual duties. The primal eye atrophied, leaving behind only the internal pineal gland. Freed from the direct “lock-step” control of the sun, the brain became plastic and self-organising (infinite-state). The E0 State: Some lineages, like certain dinosaurs and modern crocodilians, lost both the median eye and the pineal gland entirely. II. The Phantom Organ and The “Hard Problem” Nichols applies MVT to solve David Chalmers’s “Hard Problem” of consciousness-the question of why physical brain processes are accompanied by subjective feelings (qualia). The Virtual Sensor: Just as an amputee can experience a “phantom limb” because the neural matrix still expects the arm, the E1 mammalian brain experiences a “phantom eye”. The brain was built over millions of years to process a central stream of generic sensory data from the primal eye. Centrally Evoked Mentation: When the physical eye retreated, it left an internal sensory void. The brain compensated by simulating the presence of this lost hub to unscramble data from the other senses. This virtual simulation is the seat of the subjective “I”. III. The Origins of REM Sleep and Dreaming Nichols heavily critiques philosophers like Owen Flanagan, who argue that dreams are useless evolutionary “spandrels” (biological noise). Baseline Architecture: In MVT, Rapid Eye Movement (REM) sleep is the baseline functional state of the new E1 architecture. Because the physical tether to sunlight was severed, the brain uses this “phantom” space to generate internal models.

For the first time, scientists pinpoint the brain cells behind depression

Scientists have identified two specific types of brain cells that behave differently in people with depression, offering a clearer picture of what is happening inside the brain. By analyzing donated brain tissue with advanced genetic tools, the researchers found changes in neurons linked to mood and stress, as well as in immune-related microglia cells. These differences point to disruptions in key brain systems and reinforce that depression is rooted in biology, not just emotions.

Autoantibody map uncovers body-wide immune attacks across Alzheimer’s, Parkinson’s and MS

Researchers at the University of São Paulo (USP) in Brazil discovered that neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, and multiple sclerosis, are more complex than previously thought. Their analysis of nearly 600 blood samples from patients with and without these diseases revealed that neurodegenerative processes extend beyond the central nervous system, affecting various targets throughout the body.

“We conducted a systemic analysis based on autoantibodies—defense proteins [immunoglobulins] that mistakenly attack the body’s healthy cells, tissues, or organs instead of external pathogens. In this study, we saw that, contrary to what was previously thought, these diseases don’t involve an antibody attacking only a specific region of the connection between neurons [synapse], like a thief breaking in through a door. It’s a systemic attack, like machine-gunning an entire house,” explains Júlia Nakanishi Usuda, first author of the study.

The study, published in the journal iScience, identified more than 9,000 autoantibodies from public databases. Based on the results, the researchers suggest that, rather than focusing on isolated molecular targets, treatment strategies for these diseases should focus on blocking the autoimmune response systemically. While the data science study still needs to be confirmed through in vitro and in vivo testing, it reinforces a new paradigm for treating neurodegenerative diseases.

Gene-screen strategy separates Parkinson’s promoters from protectors, revealing new drug targets

A novel strategy that combines computational and experimental approaches has allowed researchers at Baylor College of Medicine and the Duncan Neurological Research Institute (Duncan NRI) at Texas Children’s Hospital to distinguish alterations in gene function that contribute to Parkinson’s disease from those that protect from the condition. The study, published in Neurobiology of Disease, revealed novel risk factors and previously unrecognized therapeutic targets, offering hope for a future in which effective therapies will be available to prevent, slow down or stop this devastating disease.

“Parkinson’s disease is the most common neurodegenerative movement disorder—it affects more than 10 million people worldwide,” said corresponding author Dr. Juan Botas, professor of molecular and human genetics and molecular and cellular biology at Baylor. Botas also is a member of the Duncan NRI and director of the High Throughput Behavioral Screening Core at Texas Children’s.

“People with the condition have tremors, muscle stiffness and balance problems. They move slowly with a shuffling gait; their symptoms often start gradually and worsen over the years. Current therapies only relieve symptoms but do not prevent the gradual loss of brain cells called neurons that cause the disease,” said Dr. Botas.

Researchers use statistics and math to understand how the brain works

Nothing rivals the human brain’s complexity. Its 86 billion neurons and 85 billion other cells make an estimated 100 trillion connections. If the brain were a computer, it would perform an exaflop (a billion-billion) mathematical calculations every second and use the equivalent of only 20 watts of power. As impressive as the brain is, neurologists can’t fully explain how neurons work together.

To help find answers, researchers at the Institute for Neuroscience, Neurotechnology, and Society (INNS) at Georgia Tech are using math, data, and AI to unlock the secrets of thought. Together they are helping turn the brain’s raw electrical “noise” into real insights about how people think, move, and perceive the world.

Fair warning: Prepare your neurons for the complexity of this brain research ahead.

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