Gunnar Brinkmalm

This study uses mouse models with tau mutations to show two distinct pathogenic mechanisms in tauopathies, with different progression patterns and responses to amyloid.

This study uses mass spectrometry to analyze retinal and hippocampal tau phosphorylation in Alzheimer's disease and multiple sclerosis, finding significant differences in p-tau peptides between diagnoses and Braak stages.

The paper identifies novel APP transcripts that generate Aβ independently of β-secretase, showing their expression and presence in CSF.

This paper introduces a new mouse model, NLFTaum/h, that shows ageing and amyloid-β can initiate tau pathology without MAPT mutations, revealing interactions between age, Aβ, and human tau.

This study identifies chromosome 21 genes other than APP that modulate amyloid-β accumulation in Down syndrome mouse models.

This study shows that mutations in the juxtamembrane cholesterol-binding site of APP reduce production of toxic Aβ40 and Aβ42 peptides and increase shorter, less toxic Aβ peptides.

The paper shows that trisomy 21 cerebral organoids exhibit AD-like pathology, which can be suppressed by BACE2 trisomy and inhibited by BACE1 inhibitors, suggesting BACE2 as an AD-suppressor gene.