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 …
A 2025 Nature Aging study found that hippocampal ferritin light chain 1 (FTL1) rose with age in mouse neurons, tracked poorer cognition, and became experimentally reversible in old mice. This is an animal-mechanism result, not a human anti-aging treatment.1 Research Highlights FTL1 rose in aged hippocampus: Western blot data showed higher hippocampal FTL1 in aged …
A Cell Reports study tied C9orf72-related ALS/FTD inflammation to a gut-bacterial product: inflammatory microbial glycogen appeared in 15 of 22 ALS fecal samples, 1 of 1 C9orf72-frontotemporal dementia sample, and 4 of 12 healthy controls.1 The result supports a narrower gene-by-microbial-product mechanism that makes C9orf72 loss of function more inflammatory. Research Highlights Human samples carried …
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 …
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 …
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. …
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 …