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Microglia

All articles tagged with #microglia

Midlife brain remodeling: immune cell shifts and genome architecture decline
science24 days ago

Midlife brain remodeling: immune cell shifts and genome architecture decline

Researchers report a major midlife brain remodeling between about ages 50 and 75, including a sharp decline of embryonically derived microglia that are increasingly replaced by inflammatory, blood-derived cells, a weakening of cells maintaining the blood-brain barrier, and widespread deterioration of the genome's three-dimensional organization. The findings suggest aging involves coordinated remodeling across immune, vascular, and neuronal systems and may help explain why age is the strongest risk factor for Alzheimer’s and other neurodegenerative diseases, highlighting new potential therapeutic targets; the work is part of the NIH’s 4D Nucleome program and builds on single-cell analyses of the hippocampus.

via Science Daily|
#alzheimers-disease#blood-brain-barrier#brain-aging
Atlas of brain microproteins links tiny MKKS peptide to microglial energy in Alzheimer's
science24 days ago

Atlas of brain microproteins links tiny MKKS peptide to microglial energy in Alzheimer's

Researchers built a frontal cortex microprotein atlas by integrating transcriptomics, mass spectrometry, and deep-learning predicted spectra across 600+ postmortem brains with and without Alzheimer’s disease, identifying 1,067 MPs not present in UniProt and showing that several are differentially expressed in AD. A key finding is the MKKS-derived 63–aa micropeptide micro-MKKS63, which is the predominant translation product, downregulated in AD, and whose loss impairs microglial mitochondrial respiration, implicating MPs in microglial bioenergetics. The atlas expands the brain proteome, reveals decoupling of smORF/MORF expression at some loci, and provides an open-access resource (spectra, sequences, and a browsable app) for studying MPs in aging and neurodegeneration.

via nature.com|
#alzheimers-disease#microglia#microproteins
Indole Metabolites and AhR Signaling Offer New Route to Combat Adolescent Depression
science29 days ago

Indole Metabolites and AhR Signaling Offer New Route to Combat Adolescent Depression

Study links reduced microbiota-derived indole metabolites in unmedicated depressed adolescents and CRS-stressed mice to depressive behaviors; supplementing tryptophan or indole derivatives activates AhR signaling, balancing anti- and pro-inflammatory factors, normalizing microglial activation, and promoting hippocampal neurogenesis, thereby alleviating depression-like symptoms. AhR is essential for these effects, suggesting indole-AhR axis as a potential therapeutic target for adolescent depression.

via Nature|
#aryl-hydrocarbon-receptor#gut-microbiota#indole-derivatives
Connecticut Teen Scientist Co-Authors Yale Neuroscience Paper on Kv1.3 and Neurodegeneration
science1 month ago

Connecticut Teen Scientist Co-Authors Yale Neuroscience Paper on Kv1.3 and Neurodegeneration

Connecticut high-school student Lilah Mehta entered a Yale biomedical research lab at 16 and co-authored a peer‑reviewed neuroscience study on Kv1.3 channels in microglia and T cells, with implications for neurodegeneration. She navigated lab setbacks, used databases like PubMed and ScienceDirect to learn, and earned regional recognition through CT science fairs and the ASPIRE program, while aiming for a future in medicine and environmental science.

via The Times of India|
#kv13#lilahmehta#microglia
Human-specific SRGAP2 gene may slow microglial maturation to bolster cognition
science1 month ago

Human-specific SRGAP2 gene may slow microglial maturation to bolster cognition

Researchers at Columbia's Zuckerman Institute found that human-specific copies of SRGAP2 are much more abundant in microglia than in neurons and slow microglial maturation to about four to eight years (versus roughly three weeks in mice). This coordinated, neotenic timing between microglia and neurons may help explain the human brain's developmental pace and its advanced cognitive abilities, with implications for understanding brain development and disease.

via Science Daily|
#brain-development#human-evolution#microglia
Midlife brain-immune shift linked to dementia risk
health1 month ago

Midlife brain-immune shift linked to dementia risk

New research finds that around age 50 the brain’s protective microglia decline and are replaced by inflammatory cells from the blood, a shift that may raise dementia risk, including Alzheimer’s, and is accompanied by deterioration of the blood–brain barrier and widespread DNA/gene changes. The study analyzed postmortem hippocampal tissue from 40 adults across ages 20–95, a small, early-stage look that cannot prove causation but suggests a possible mechanism and potential for blood-derived immune cells to be targeted for future therapies. The work, funded by NIH and published in Science, highlights variability in brain aging and the need for further research into triggers and modifiers of this immune-cell replacement.

via Fox News|
#alzheimers#blood-brain-barrier#brain-aging
science1 month ago

Youthful TIMP2 Revives Brain Microglia Function in Mice

A youth-associated protein TIMP2 helps brain-resident immune cells (microglia) maintain debris-clearing function and limit inflammatory aging. In aging mice, removing TIMP2 causes microglia to adopt aging-like traits and higher inflammatory signals; conversely, systemic TIMP2 administration improves debris clearance and reduces inflammatory markers, suggesting youth factors can influence brain aging and may inform strategies for neurodegenerative diseases, though human relevance remains to be tested.

via SciTechDaily|
#aging#brain-health#microglia
Aging erodes microglial chromatin, unleashing retroelements to fuel inflammation and senescence
neuroscience1 month ago

Aging erodes microglial chromatin, unleashing retroelements to fuel inflammation and senescence

Aging reduces chromatin compaction and downregulates the histone chaperone DAXX in microglia, enabling derepression of endogenous retroelements and shifting microglia from a homeostatic to a reactive, inflammatory state. Loss of DAXX drives chromatin decompaction at LTR-RTEs, loss of homeostatic markers, cell-cycle re-entry and DNA damage, followed by microglial depletion and replacement by DAXX-deficient, ApoE-high microglia exhibiting senescence features. Sustained senescence relies on PML and interferon targets, underscoring chromatin maintenance as key to microglial identity, brain homeostasis and aging-related behavioral changes.

via Nature|
#aging#cellular-senescence#daxx
Alzheimer’s Sleep Breakthrough: Blocking Brain Immune Cells Reverses Sleep Loss in Mice
health1 month ago

Alzheimer’s Sleep Breakthrough: Blocking Brain Immune Cells Reverses Sleep Loss in Mice

UK researchers found microglia drive sleep loss in an Alzheimer's mouse model; temporarily removing these brain immune cells with the drug PLX3397 for 14 days restored more than two hours of restorative sleep, without reducing amyloid plaques, suggesting inflammation—not plaques alone—drives sleep disruption and offering a new target for therapies and potential EEG-based biomarkers.

via Good News Network|
#alzheimers#brain#health
Protective Brain Microglia Rise with Alzheimer's Progression, Study Finds
science1 month ago

Protective Brain Microglia Rise with Alzheimer's Progression, Study Finds

An unprecedented analysis of over 830,000 brain immune cells from 1,607 donors identified a disease-associated microglia subtype that expands as Alzheimer's progresses and relies on the TREM2-MITF-GPNMB pathway to clear harmful material, suggesting therapies should bolster the brain’s natural immune defenses rather than focus solely on amyloid plaques.

via Neuroscience News|
#alzheimers-disease#brain-immunity#microglia
Blocking Brain Immune Cells Restores Sleep in Alzheimer’s-Model Mice
science2 months ago

Blocking Brain Immune Cells Restores Sleep in Alzheimer’s-Model Mice

Researchers at the University of Kentucky found that sleep disruption in Alzheimer’s-model mice is driven by microglia-driven inflammation rather than amyloid plaques. When microglial activity was blocked, the mice gained about two extra hours of restorative sleep per night, although plaque levels did not change. This suggests that calming microglia could improve sleep and potentially slow disease progression, but the findings are currently limited to animal models.

via ScienceAlert|
#alzheimers-disease#amyloid-beta#microglia