Summary: Lower cholesterol levels may put people with schizophrenia at higher risk for violent behaviors, including self-harm and suicide. Researchers say lower cholesterol levels make brain cells less sensitive to serotonin, increasing symptoms of depression, impulsivity, and aggression.
Source: Brunel University.
Linked to lower risk of heart attacks and strokes, low cholesterol may also be a sign people with schizophrenia are at high risk of self-harm, suicide and violence.
The mechanism by which sleep disruption impedes neurodevelopment, however, is still not well understood. It may be that increased wakefulness due to sleep disruption increases glutamate circulation in the brain, affecting glutamatergic structures. Alternatively, decreased REM sleep may reduce “pruning”, an essential developmental process in which superfluous synapses are removed to improve signaling and organization.
The period of neurodevelopment extending from birth to roughly two years of age is one of frenetic, constant change. Neurons and synapses form, are organized, and are pruned. It is well known that sleep plays a fundamental role in these processes, and disruptions to sleep at this stage can be devastating to neurodevelopment and may be the cause of disorders like autism spectrum disorder (ASD).
Understanding the relation between sleep and neurodevelopment in early life is thus essential to understanding (and perhaps preventing) developmental disorders. Building on previous work with prairie voles—a highly social animal with neurodevelopmental similarities to humans—researchers from Portland and California recently published a paper in Current Research in Neurobiology examining the effects of early life sleep disruptions (ELSD) on the prefrontal cortex (PFC).
The prefrontal cortex plays an important role in higher-order social learning, executive function, and cognitive flexibility. It’s also one of the last brain structures to mature, and is thus particularly sensitive to disruptions in development.
Nad plus works for alzheimers.
In June of 2,018 the World Health Organization (WHO) released the 11th edition of its International Classification of Diseases, and for the first time added aging.1 The classification of aging as a disease paves the way for new research into novel therapeutics to delay or reverse age-related illnesses such as cancer, cardiovascular and metabolic disease, and neurodegeneration.2,3 Nutrient sensing systems have been an intense focus of investigation, including mTOR (the mammalian target of rapamycin) for regulating protein synthesis and cell growth; AMPK (activated protein kinase) for sensing low energy states; and sirtuins, a family of seven proteins critical to DNA expression and aging, which can only function in conjunction with NAD+ (nicotinamide adenine dinucleotide), a coenzyme present in all living cells.4
Across the kingdom of life, an increase in intracellular levels of NAD+ triggers shifts that enhance survival, including boosting energy production and upregulating cellular repair.5 In fact, the slow, ineluctable process of aging has been described as a “cascade of robustness breakdown triggered by a decrease in systemic NAD+ biosynthesis and the resultant functional defects in susceptible organs and tissues.”6 Aging is marked by epigenetic shifts, genomic instability, altered nutrient sensing ability, telomere attrition, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and dysregulated intercellular communication.7,8
By middle age, our NAD+ levels have plummeted to half that of our youth.9 Numerous studies have demonstrated that boosting NAD+ levels increases insulin sensitivity, reverses mitochondrial dysfunction, and extends lifespan.10,11 NAD+ levels can be increased by activating enzymes that stimulate synthesis of NAD+, by inhibiting an enzyme (CD38) that degrades NAD+, and by supplementing with NAD precursors, including nicotinamide riboside(NR) and nicotinamide mononucleotide (NMN).12,13 A conceptual framework called NAD World, formulated over the last decade by developmental biologist Shin-ichiro Imai, MD, PhD, of Washington University School of Medicine, posits NMN as a critical, systemic signaling molecule that maintains biological robustness of the communication network supporting NAD+.6.
Because we can’t possibly absorb every single stimulus, our brain lets some of these signals filter through to our consciousness while others don’t.
But where specifically in the brain does that filtering take place? If somewhere in the brain exists the gateway to consciousness, which part of the brain functions as the gatekeeper?
Researchers at the University of Michigan Medical School set out to answer this question. Their study, published Tuesday in Cell Reports, suggests they’ve found the answer.
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Papers referenced in the video:
Human microbiome: an academic update on human body site specific surveillance and its possible role.
https://pubmed.ncbi.nlm.nih.gov/32524177/
Taxonomic signatures of cause-specific mortality risk in human gut microbiome.
https://pubmed.ncbi.nlm.nih.gov/33976176/
The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication.
https://pubmed.ncbi.nlm.nih.gov/32082260/
Inhibiting antibiotic-resistant Enterobacteriaceae by microbiota-mediated intracellular acidification.
https://pubmed.ncbi.nlm.nih.gov/30563917/
Short chain fatty acids in human large intestine, portal, hepatic and venous blood.
Because the brain responses in children with different forms of autism overlapped, future therapies that are effective for Phelan-McDermid syndrome could potentially help other autistic children with similar neural patterns, Siper says.
Brain responses to visual stimuli are smaller and weaker in children with Phelan-McDermid syndrome, an autism-linked genetic condition, than in non-autistic children, according to a new study. The difference in response is greater in children with larger genetic mutations.
Mutations or deletions in SHANK3, one of the genes most strongly linked to autism, cause Phelan-McDermid syndrome. More than 80 percent of people with the condition have autism; they also often have intellectual disability, developmental delays and other medical issues, though these traits and their severity can vary widely.
The new study is the first to use electroencephalography (EEG) to measure visual evoked potentials — brain responses that occur shortly after a person views a visual stimulus — in people with Phelan-McDermid syndrome. The team previously identified differences in these responses in people with ‘idiopathic’ autism, or autism with no known genetic cause. Other researchers have linked atypical visual evoked potentials to other single-gene causes of autism, such as Rett syndrome.
What is your mind? It’s a strange question, perhaps, but if pressed, you might describe it as the part of yourself that makes you who you are—your consciousness, dreams, emotions, and memories. Scientists believed for a long time that such aspects of the mind had specific brain locations, like a circuit for fear, a region for memory, and so on.
But in recent years we’ve learned that the human brain is actually a master of deception, and your experiences and actions do not reveal its inner workings. Your mind is in fact an ongoing construction of your brain, your body, and the surrounding world.
About 11.1 million Americans are living with long COVID-19, according to new estimates from The American Academy of Physical Medicine and Rehabilitation.
Long COVID-19, or persistent symptoms up to six months after being cleared of the illness, affects around 30 percent of individuals who had COVID-19, according to two recent publications from the Journal of the American Medical Association. Symptoms of long COVID-19 are varied and may include neurological challenges, cognitive problems, shortness of breath, fatigue, pain and mobility issues.
The AAPM&R has developed a dashboard estimating long COVID-19 infections. The model assumes that 30 percent of people who recover from acute COVID-19 develop long COVID-19, but users can adjust estimates based on higher or lower percentages. U.S. case data is pulled from Baltimore-based Johns Hopkins University COVID-19 data. U.S. census data uses2019estimates.