Keeping a regular daily schedule may help reduce pain and depression, especially among older adults with insomnia. Researchers found that consistent times for waking, eating, socializing, and sleeping were linked to better well-being regardless of sleep quality. These routines may strengthen the body’s internal clock and limit the disruptive effects of “social jet lag.”
A team of CNRS scientists has pinpointed the brain mechanisms behind the famous “Proust’s madeleine” phenomenon, in which smells bring back vivid, emotional memories.
This work, published in PLOS Biology on July 14, 2026, shows that early-life olfactory experiences leave a lasting impression on the brain, capable of reactivating the context and emotions associated with that memory throughout our lives.
The neuroscientists revealed the central role played by neurons in the olfactory bulb, an area of the brain that continues to develop during childhood. When these neurons are reactivated in adulthood by odors we experienced in childhood, they activate cerebral circuits involved in both memory and reward.
Glioblastoma multiforme (GBM) is the most aggressive and lethal type of brain tumor. Both therapeutic resistance and restricted permeation of drugs across the blood–brain barrier (BBB) play a major role in the poor prognosis of GBM patients. Accumulated evidence suggests that in many human cancers, including GBM, therapeutic resistance can be attributed to a small fraction of cancer cells known as cancer stem cells (CSCs). CSCs have been shown to have stem cell-like properties that enable them to evade traditional cytotoxic therapies, and so new CSC-directed anti-cancer therapies are needed. Nanoparticles have been designed to selectively deliver payloads to relevant target cells in the body, and there is considerable interest in the use of nanoparticles for CSC-directed anti-cancer therapies.
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.
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.
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.
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.
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.
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.