Tomas Deierborg

This study shows that Galectin-3 promotes tau pathology, neuroinflammation, white matter degeneration, and proteomic dysregulation, and that its deletion reduces these effects.

This paper identifies shared metabolic and kinase signaling disruptions in Parkinson's disease and multiple system atrophy using patient-derived models and postmortem tissue.

This study demonstrates that NosaPlugs nasal inserts can deliver memantine to the brain in mice, providing a proof-of-concept for nose-to-brain drug delivery.

This study shows that Aβ antibodies target not only amyloid plaques but also neurons, glial cells, and blood vessels in AD mouse models.

This paper identifies Galectin-3 as a key regulator of amyloid-beta aggregation and microglial dysfunction in Alzheimer's disease, showing its role in neurotoxicity and potential as a therapeutic target.

This study shows that early-life immune activation in 5xFAD mice alters microglial responses and reduces Aβ pathology, with effects on cytokine levels and memory deficits.

This study shows that palmitate exposure causes microglia to change their metabolism and release EVs that affect behavior and metabolism in mice.

This study shows that APP and Aβ increase neuronal hyperexcitability and impair homeostatic synaptic and intrinsic plasticity in Alzheimer's disease models.

This study shows that inflammatory bowel disease (IBD) leads to α-synuclein aggregation in the gut and brain, supporting Braak's hypothesis of Parkinson's disease origin in the enteric nervous system.

This study identifies galectin-3 as a novel endogenous TREM2 ligand that regulates microglial activation and Aβ fibrillation in Alzheimer’s disease.