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Guanfacine Eases Hyperactivity in Autism; Inflammation Theory Untested

MHD card showing a teal prefrontal dendrite with a magnified membrane of closed HCN channels and an amber microglia cell inside a dashed outline, illustrating that guanfacine eased hyperactivity in autistic children while its anti-inflammatory role remains untested.

Guanfacine, a non-stimulant ADHD medication, reduced hyperactivity in autistic children in a placebo-controlled trial. A 2026 review argues it may also steady prefrontal brain signaling and calm the brain’s immune cells, but that immune effect has never been tested with guanfacine itself.1 Research Highlights Hyperactivity fell in the largest autism trial: in 62 autistic children, …

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SPP1 Marks Cross-Disease Microglial Activation in Neurodegeneration

MHD featured image for SPP1 microglia and neurodegeneration transcriptomics.

A 2026 Glia analysis found a shared microglial transcriptional program across 5 neurodegenerative contexts: ALS, frontotemporal dementia, Alzheimer’s disease, aging, and Parkinson’s disease.1 The standout marker was SPP1, a gene encoding osteopontin, but the finding is a cellular-state signal rather than a ready diagnostic test. Research Highlights Cross-disease microglia converged: the integrated dataset covered ALS, …

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Alzheimer’s Smell Loss Linked to Early Locus Coeruleus Axon Damage

MHD featured image for early locus coeruleus axon loss and Alzheimer's smell dysfunction.

A 2025 Nature Communications study found that Alzheimer’s-like mice lost locus coeruleus noradrenergic axons in the olfactory bulb early: 14% loss by 2 months, 27% by 3 months, and 33% by 6 months, before broader forebrain axon degeneration appeared.1 Early smell loss may reflect a specific brainstem-to-olfactory circuit injury, while smell testing still needs biomarker …

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PTP1B Inhibition Boosted Amyloid Clearance in Alzheimer’s Mice

In APP/PS1 Alzheimer's model mice, deleting PTP1B or treating with the allosteric inhibitor DPM-1003 improved memory behavior, lowered amyloid burden, and pushed microglia toward SYK-driven clearance — a plausible mechanism, not a human treatment result yet.1 Research Highlights PTP1B loss improved behavior in APP/PS1 mice. Genetic deletion and DPM-1003 treatment improved novel object recognition and …

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Chlorpyrifos Exposure Linked to Up to 174% Higher Parkinson’s Risk

MHD featured image for chlorpyrifos exposure, Parkinson's risk, dopaminergic neurons, and autophagy dysfunction.

A human, mouse, and zebrafish study linked long-term chlorpyrifos exposure to Parkinson’s disease risk, with the strongest exposure-duration estimate reaching OR 2.74 for workplace proximity across the 1974-to-index-year window.1 The paper is stronger than a single epidemiology result because animal experiments pointed to dopaminergic neuron loss, microglial activation, pathological α-synuclein, and autophagy dysfunction. Research Highlights …

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P2X7 Receptors in Depression: ATP-Inflammation Target

MHD featured image for P2X7 receptors and depression inflammation pathways.

A 2026 review in Purinergic Signalling argues that P2X7 receptors are one of the clearest molecular bridges between stress, ATP danger signaling, microglial inflammation, NLRP3 inflammasome activation, reduced BDNF, and new antidepressant drug targets.1 Research Highlights P2X7 is the lead receptor: Mattova et al. reviewed 7 ATP-gated P2X receptor subunits, with P2X7 carrying the strongest …

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Depression vs. Schizophrenia: Microglial TSPO and KYNA Signals

MHD featured image for microglial and kynurenine pathway patterns across depression, bipolar disorder, and schizophrenia.

A 2026 systematic review found that microglia-related immune signals do not line up cleanly with psychiatric diagnosis labels: major depression showed frontolimbic TSPO-PET increases, while schizophrenia showed elevated kynurenic acid in cerebrospinal fluid.1 The strongest interpretation is that immune-brain markers may sort subgroups better than DSM categories do. Research Highlights Depression had the clearest TSPO-PET …

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