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Everyday mental quirks like déjà vu might be natural byproducts of a resting mind

A recent study published in Consciousness and Cognition provides evidence that everyday mental quirks like déjà vu or tip of the tongue states are natural byproducts of a resting mind. The findings suggest that when a person’s attention is not fully occupied, a wide variety of spontaneous thoughts and reflective feelings naturally emerge into awareness.

The scientists conducted the research to understand if a broad spectrum of unprompted mental experiences could be systematically captured in a laboratory setting. Past research has mostly focused on involuntary memories, which are recollections of personal events that pop into the mind without warning. The team wanted to know if the same boring, repetitive conditions that produce these memories might also generate other spontaneous phenomena.

They specifically focused on metacognition. Metacognition is a term used to describe the brain’s ability to think about and monitor its own processes. While people sometimes use metacognition deliberately, such as trying to gauge how well they learned a topic for a test, it can also happen without effort.

Do we really control our own decisions?

For decades, neuroscientists have explored a fascinating phenomenon in the human brain known as the split-brain experiment. When the connection between the two hemispheres of the brain — the Corpus Callosum — is surgically cut, something extraordinary happens.

Each hemisphere begins processing information independently.

In groundbreaking research conducted by neuroscientist Michael Gazzaniga, scientists discovered that the speaking side of the brain often creates explanations for actions it did not initiate. This phenomenon is known as the Left-Brain Interpreter.

Instead of admitting uncertainty, the brain rapidly constructs logical stories to explain behavior. These experiments revealed how the human mind continuously builds a coherent narrative about our identity, decisions, and sense of self.

The split-brain studies remain one of the most important discoveries in modern neuroscience, raising profound questions about consciousness, decision-making, and the nature of the human mind.

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Mapping human brain cell type origin and diseases through single-cell transcriptomics

Wang P, Zhao D, Lachman HM, Zheng D. Enriched expression of genes associated with autism spectrum disorders in human inhibitory neurons. Transl Psychiatry. 2018;8:13. https://doi.org/10.1038/S41398-017-0058-6

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Tinnitus Is Somehow Connected to a Crucial Bodily Function

Those who have never endured the relentless ringing of tinnitus can only dream of the torment. In fact, a bad dream may be the closest some get to experiencing anything like it.

The subjective sound, which can also be a hissing, buzzing, or clicking, is heard by no one else, and it may be present constantly, or may come and go.

Neuroscientists at the University of Oxford now suspect that sleep and tinnitus are closely intertwined in the brain.

Brain immune cells may help build Alzheimer’s plaques

A new study led by researchers from VIB and KU Leuven shows that immune cells called microglia can actively promote the formation of plaques in Alzheimer’s disease, challenging the long-standing view that these cells serve only as defenders against plaque buildup. The findings were recently published in the Proceedings of the National Academy of Sciences.

“Most studies suggest that microglia are there to clean up the brain and remove the amyloid plaques. What we discovered is that actually they’re part of the problem. They generate plaques,” says Prof. Joost Schymkowitz, co-senior author of the study at the VIB-KU Leuven Center for Neuroscience. “It was thought that plaques aggregate by themselves. And it seems that the microglia, by trying to deal with the problem, amplify it.”

Alzheimer’s disease affects nearly 55 million people worldwide and is characterized by the accumulation of toxic protein aggregates in the brain known as amyloid plaques. These plaques are associated with neuronal death and progressive dementia. The brain’s microglia have been hailed as protectors against plaque accumulation in the disease, being the focus of several therapies. Nonetheless, the study shows how microglia are active producers of amyloid plaques in the earlier stages of the disease, reconsidering the therapeutic paradigm for Alzheimer’s.

Movies reconstructed purely from mouse brain activity

Scientists have successfully reconstructed videos purely from the brain activity of mice, showing what the mice were seeing, in a new study led by University College London (UCL) researchers. The findings, published in eLife, could help shed light on the intricate workings of how the brain processes visual information and open new avenues for exploring how different species perceive the world.

Over recent years, there has been a growing interest in understanding exactly how the human brain interprets signals from the eye. Images and movies have been played to people in fMRI machines and researchers around the world have tried to decode the brain’s representations of visual information on a pixel level.

TREM2 in neurodegeneration and diseases

Triggering receptor expressed on myeloid cells 2 (TREM2) is a cell surface transmembrane receptor from the TREM receptor family, predominantly expressed on the microglia in the central nervous system (CNS). TREM2-initiated signaling plays a crucial role in regulating neuroinflammation and neurodegeneration, particularly in the context of neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD), through the activation of downstream signaling pathways and transcriptional regulation of relevant genes. In this review, we aim to provide a concise review of the role and mechanistic implications of TREM2 in neurodegeneration and neuroinflammation, with a specific focus on AD and PD. We will discuss the most recent preclinical studies to highlight current advancements in the field. This review is intended to support both basic researchers and clinicians by enhancing their understanding of microglial function in the pathophysiology of AD and PD, as well as its role in neuroinflammation and neurodegeneration. Ultimately, we hope this contribution will pave the way for new discoveries and the development of potential therapeutic interventions.

© 2026. The Author(s).

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Alzheimer’s Disease: From Molecular Mechanisms to Promising Therapeutic Strategies

Brain vasculature in ischemic stroke.

Ischemic stroke induces dynamic cellular structural changes in the neurovascular unit, leading to disrupted structural integrity of the blood–brain barrier, neuronal degeneration, and responsive angiogenesis coordinated by endothelial cells, reactive astrocytes, and pericytes.

After ischemic stroke, the neurovascular coupling function of the neurovascular unit is also disrupted, manifested by the metabolic dysregulation of glucose, lipid/fatty acid, and amino acids.

Neurovascular unit dynamic structural remodeling and metabolic dysfunction following ischemic stroke show cellular states and spatiotemporal heterogeneities, revealing new perspectives on ischemic stroke pathogenesis and future therapeutic strategies.

Multidimensional approach aiming to repair neurovascular unit structural disorganization and restore metabolic homeostasis with cellular and spatiotemporal precision is the optimal therapeutic strategy for ischemic stroke. sciencenewshighlights ScienceMission https://sciencemission.com/neurovascular-unit-in-ischemia


The neurovascular unit (NVU) is a multicellular system functioning to maintain healthy brain homeostasis and regulate the exchange of essential elements between the blood and the brain. Recent studies have shown that, in response to ischemic stroke (IS), the NVU undergoes dynamic structural remodeling and metabolic dysfunction, revealing new features of IS pathogenesis. Recent breakthroughs in single-cell multiomics provide emerging evidence regarding the spatiotemporal heterogeneity of NVU responses to IS. To date, clinical treatments for IS-induced brain injury remain very limited. These new studies have advanced our knowledge of the dynamic cellular and molecular changes of the NVU after IS, paving the way for new therapeutic strategies.

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