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NMDAR/TRPM4 Death Complex Blocker Preserved Memory in Alzheimer’s Mice

MHD featured image for the NMDAR/TRPM4 death complex, FP802, and Alzheimer's mouse-model memory protection.

A 2026 Molecular Psychiatry study found that oral FP802 disrupted the NMDAR/TRPM4 death complex and preserved memory-task performance in 5xFAD Alzheimer’s mice treated for 3 months.1 The finding is mechanistically sharper than a generic anti-amyloid claim: FP802 targeted a glutamate-toxicity complex downstream of amyloid stress. Research Highlights Complex formation was blocked: 5xFAD mice had increased …

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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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Multiple Sclerosis Personalized Therapy: 70% Delphi Consensus

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An Italian multiple sclerosis Delphi panel reached consensus on 116 of 166 votes, meaning 70% of expert votes aligned and 30% still exposed disagreement about personalized therapy, patient involvement, and treatment sequencing.1 The result supports individualized MS treatment planning, but it is consensus evidence rather than proof that one disease-modifying therapy fits every high-risk patient. …

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Microplastics and Parkinson’s Disease: 6 Plausible Brain-Risk Pathways

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A 2026 mechanistic review linked microplastics to 6 proposed Alzheimer’s disease pathways and 6 proposed Parkinson’s disease pathways.1 The calibrated interpretation is that microplastics are biologically plausible brain stressors, but the human evidence does not yet prove that they cause Parkinson’s disease or Alzheimer’s disease. Research Highlights Exposure is widespread: the review cited an estimate …

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Parkinson’s Balance Study Finds Cortical-Latency Muscle Control at 215 ms

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A 36-person Parkinson’s disease balance study found that perturbation-evoked muscle activity could be split into brainstem-latency LLR1 responses around 116-119 ms, cortical-latency LLR2 responses around 200-215 ms, and an antagonist destabilizing component around 173-181 ms.1 Parkinson’s disease lowered clinical balance scores, but the broad claim that Parkinson’s patients had higher cortical-latency LLR2 responses than older …

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TMEV Viral Parkinson’s Mouse Model Caused 20-Week Dopamine-Lesion Behaviors

MHD featured image for a viral Parkinson's mouse model using Theiler's murine encephalomyelitis virus.

A 2026 mouse study found that Theiler’s murine encephalomyelitis virus (TMEV) injected into the substantia nigra produced persistent Parkinson’s-like motor signals through 20 weeks, including apomorphine-induced rotations at every measured post-injection timepoint.1 The finding makes TMEV a useful viral-neuroinflammation model of dopamine-neuron injury, but it does not show that Theiler’s virus causes human Parkinson’s disease. …

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Parkinson’s Diabetes Oxidative Stress: 8-OHdG Rose, F2-Isoprostanes Did Not

MHD featured image for Parkinson's disease, diabetes, oxidative stress, 8-OHdG, and F2-isoprostanes.

A 2026 meta-analysis of 54 human studies found that 8-hydroxy-2′-deoxyguanosine rose in Parkinson’s disease, while F2-isoprostanes did not show a statistically confirmed Parkinson’s signal; type 2 diabetes showed much larger peripheral oxidative-stress elevations than Parkinson’s disease for both biomarkers. Research Highlights Parkinson’s DNA-oxidation signal was moderate: Msigwa et al. pooled 5 Parkinson’s disease studies with …

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