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Researchers Reveal Breakthrough in Alzheimer’s Disease and the Shocking Place It Might Originate in Your Body

Although it’s not the first time this was hypothesized, this study is the first time researchers looked at the presence of gingipains within the brains of diseased patients. Even more, the patients themselves were never even diagnosed with Alzheimer’s.

“Our identification of gingipain antigens in the brains of individuals with AD and also with AD pathology but no diagnosis of dementia argues that brain infection with P. gingivalis is not a result of poor dental care following the onset of dementia or a consequence of late-stage disease, but is an early event that can explain the pathology found in middle-aged individuals before cognitive decline,” the authors explained.

While this isn’t a one-size-fits-all answer to what causes Alzheimer’s, it’s a step in the right direction to finding the reasoning behind this life-altering disease.

Researchers map how individual neurons encode behavioral states

National Institutes of Health researchers have mapped how individual neurons in the primary somatosensory cortex receive brain-wide presynaptic inputs that encode behavioral states, refining our understanding of cortical activity.

Neurons in the primary somatosensory cortex process different types of sensory information and exhibit distinct activity patterns, yet the cause of these differences has remained unclear. Previous research emphasized the role of motor cortical regions in movement-related processing, but also recognized that the thalamus plays a role beyond sensory relay.

Using high-resolution single-cell mapping to trace , the team revealed that thalamic input is the primary driver for movement-correlated neurons, while motor cortical input plays a smaller role.

In the body, psilocybin becomes psilocin, which can increase nerve cell communication even in a single dose

A recent study by the Hector Institute for Translational Brain Research (HITBR) at the Central Institute of Mental Health (CIMH) in Mannheim provides the first detailed cellular insights into how psilocin, the active ingredient in magic mushrooms, promotes the growth and networking of human nerve cells.

These findings complement clinical studies on the treatment of mental disorders and could contribute to a better understanding of the neurobiological mechanisms behind the therapeutic effect of psilocybin.

Psilocybin is the well-known in so-called magic mushrooms, which is converted in the body to psilocin—the compound that ultimately unleashes the psychoactive effect. The Mannheim research team worked directly with psilocin to investigate the neurobiological effects.

Study Reveals Critical Age When Your Thinking Begins to Decline

As Shakespeare put it, we all have our entrances and our exits on this grand stage we call life, and now researchers have identified the specific point in middle-age when our brain cells show the first signs of starting down a downward slope.

That age, based on brain scans and tests covering 19,300 individuals, is on average around 44 years. It’s here that degeneration starts to be noticeable, before hitting its most rapid rate at age 67. By the time we reach 90, the speed of brain aging levels off.

According to the team behind the new study, led by researchers from Stony Brook University in the US, the findings could be helpful in figuring out ways to promote better brain health during the later stages of life.

A torpor-like state in mice slows blood epigenetic aging and prolongs healthspan

Dissecting the effects of hypothermic and hypometabolic states on aging processes, the authors show that activation of neurons in the preoptic area induces a torpor-like state in mice that slows epigenetic aging and improves healthspan. These pro-longevity effects are mediated by reduced Tb, reinforcing evidence that Tb is a key mediator of aging processes.

Rosemary Compound Shows Promise for Alzheimer’s Disease

Researchers developed a stable form of carnosic acid, a compound found in rosemary and sage. The compound showed promise for improving learning and memory and reducing signs of Alzheimer’s disease in mouse models. The corresponding study was published in Antioxidants. The researchers hope to test the compound in human trials.

Carnosic acid has both antioxidant and anti-inflammatory properties. While pure carnosic acid is too unstable for medical use, the new compound developed by scientists from Scripps Research fully converts to carnosic acid in the gut before absorption into the bloodstream. They called the compound ‘diAcCA’

As a part of the study, the researchers tested the compound’s efficacy in mouse models for three months. Ultimately, the compound improved learning and memory, and reduced markers of inflammation, formation of amyloid plaques, and phosphorylated tau aggregates.

Excitation-Inhibition Balance Controls Information Encoding in Neural Populations

Understanding how the complex connectivity structure of the brain shapes its information-processing capabilities is a long-standing question. By focusing on a paradigmatic architecture, we study how the neural activity of excitatory and inhibitory populations encodes information on external signals. We show that at long times information is maximized at the edge of stability, where inhibition balances excitation, both in linear and nonlinear regimes. In the presence of multiple external signals, this maximum corresponds to the entropy of the input dynamics. By analyzing the case of a prolonged stimulus, we find that stronger inhibition is instead needed to maximize the instantaneous sensitivity, revealing an intrinsic tradeoff between short-time responses and long-time accuracy.

Why zero could unlock how the brain perceives absence

When I’m birdwatching, I have a particular experience all too frequently. Fellow birders will point to the tree canopy and ask if I can see a bird hidden among the leaves. I scan the treetops with binoculars but, to everyone’s annoyance, I see only the absence of a bird.

Our mental worlds are lively with such experiences of absence, yet it’s a mystery how the mind performs the trick of seeing nothing. How can the brain perceive something when there is no something to perceive?

For a neuroscientist interested in consciousness, this is an alluring question. Studying the neural basis of ‘nothing’ does, however, pose obvious challenges. Fortunately, there are other – more tangible – kinds of absences that help us get a handle on the hazy issue of nothingness in the brain. That’s why I spent much of my PhD studying how we perceive the number zero.

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