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Researchers Simulate Alzheimer’s Progression Across the Entire Brain

This hypothesis has led to a new “whole-brain” mathematical and computational model developed at the MOX Laboratory of the Department of Mathematics of Politecnico di Milano. The model is designed to describe in an integrated way the interaction between the spread of amyloid beta and the functioning of the cerebral vascular network. The aim is to provide a tool capable of simulating, on the scale of the whole organ, how small biological or vascular alterations can evolve over time and contribute to neurodegeneration. The model and the accompanying scientific study have been published in the prestigious scientific journal Computer Methods in Applied Mechanics and Engineering.

The model integrates two scales of analysis. On the one hand, it describes the dynamics of the production, transformation, diffusion and elimination of the healthy and pathological forms of amyloid beta. On the other, it describes blood flow through a “macroscopic” description of arteries, capillaries and veins, treating brain tissue as a porous medium perfused by blood vessels, through a macroscopic compartmental model. The two components are then connected to represent the possible mechanism of mutual reinforcement between protein accumulation and vascular dysfunction.

The simulations show a particularly relevant result: the brain can evolve into different states depending on the initial conditions. Small localised amounts of amyloid beta can be eliminated, allowing the system to return to a healthy state. Conversely, larger amounts can trigger a self-sustained spread of the pathology at brain scale.

Brain Dramatically Remodels Its Cellular Composition, Starting in Midlife

The aging human brain is fascinating, because in some ways, it improves with age – but we generally hear more about how it declines. That’s understandable!

After all, there are a host of neurodegenerative diseases that none of us want to end up with.

Previous research has shown that some of the seemingly inevitable declines in brain health, often seen in 70-and 80-year old brains, start in midlife.

Genetic deletions may help explain differences in schizophrenia severity

Schizophrenia affects approximately 23 million people worldwide, with onset usually occurring during a person’s late adolescence or 20s. Impairments associated with schizophrenia include hallucinations, delusions, and disorganized thinking and behavior.

Now, researchers at the University of Washington are investigating how genetic changes affect the severity of schizophrenia symptoms. A new study, published in the American Journal of Psychiatry, supports the idea that deletions in genes that regulate early brain and neuron development are associated with more severe features of schizophrenia spectrum disorders, particularly lower cognitive abilities.

Gastrointestinal symptoms correlate with core clinical features and systemic inflammation in myalgic encephalomyelitis/chronic fatigue syndrome

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating multisystem illness marked by fatigue, cognitive impairment, and post-exertional malaise. Gastrointestinal (GI) symptoms are frequently reported, yet their relationship to central features of the illness and biological correlates remains poorly understood.

We aimed to characterize GI symptom burden in ME/CFS and evaluate its associations with core clinical features and specific immune and inflammatory markers, with attention to potential gut-related contributions to disease expression.

GI symptoms and 49 additional symptoms across nine domains were assessed in 116 ME/CFS patients and 80 matched controls. Plasma C-reactive protein (CRP) and antibodies against dietary and microbial antigens were measured as indicators of systemic inflammation and putative gut-derived antigen exposure.

Defining Endogenous DMT Brain Biotypes: A Multi-Modal Neuroimaging Study

Could Your Brain Have Its Own “DMT Signature”? A New Research Proposal Aims to Find Out.

A new neuroscience research proposal is exploring a fascinating question: Do people naturally differ in their levels or activity of endogenous DMT, and could those differences be reflected in distinct brain “biotypes”?

Rather than administering DMT, the researchers propose analyzing an existing dataset of approximately 1,100 participants using multiple complementary measures, including:

PET imaging to examine serotonin receptor systems.

Structural and functional MRI to assess brain anatomy and connectivity.

Diffusion MRI to evaluate white matter microstructure.

Blood biomarkers.

Mind-wandering mechanisms change depending on eye state

A type of brain activity linked to arousal and attention can track mind wandering. But research conflicts on whether this activity promotes or hinders mind wandering. Esther Thielking of Barnard College and colleagues explored whether having the eyes open or closed changes the relationship between this brain activity and mind wandering.

Said Thielking, “We predicted that eye state might explain these conflicts because closing the eyes strengthens [this brain activity] and reverses its relationship with sleepiness, which is itself closely tied to mind wandering.”

As reported in their JNeurosci paper, the researchers recorded brain activity in adults with their eyes open or closed as they performed a task involving paying attention to sounds or letting their minds wander.

The calcium pump ATP2B1/PMCA1 regulates CNS vascular development by facilitating Norrin Frizzled4 signaling

Jo et al. identify the plasma membrane Ca2+−pump ATP2B1/PMCA1 as a regulator of endothelial Norrin/Frizzled4 and Wnt signaling in the CNS vasculature. Loss of ATP2B1 elevates intracellular Ca2+ and activates NFAT, suppressing β-catenin signaling and linking Ca2+ homeostasis to angiogenesis and blood-brain barrier integrity.

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