Gunnar K. Gouras

Errors in peptide synthesis are a source of discrepancies in Aβ42 studies

This study shows that sequence imperfections in synthetic Aβ42 peptides cause differences in aggregation behavior compared to recombinant Aβ42.

Neuronal age drives β-sheet accumulation and, together with ApoE4, enhances synaptic Aβ localization in APPNL-F neurons

The paper shows that neuronal age and ApoE4 genotype increase synaptic Aβ accumulation and alter its structural form in APPNL-F neurons.

Aβ Antibodies Target Not Only Amyloid Plaques But Also Distinct Brain Cells And Vessels

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

Galectin-3 drives neuroinflammatory amyloid remodeling by stabilizing intermediate Aβ species and altering lysosomal processing

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.

Proteomic analysis across patient iPSC-based models and human post-mortem hippocampal tissue reveals early cellular dysfunction, progression, and prion-like spread of Alzheimer s disease pathogenesis

The paper uses proteomic analysis of patient iPSC-derived brain cells and post-mortem hippocampal tissue to study early AD pathogenesis and prion-like spread.

Apolipoprotein E intersects with amyloid-β within neurons

The paper shows that ApoE4 increases Aβ42 levels in neurons and demonstrates intracellular intersection of ApoE with APP/Aβ in AD transgenic neurons.

Aβ/APP-induced hyperexcitability and dysregulation of homeostatic synaptic plasticity in models of Alzheimer's disease

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

APOE4 affects basal and NMDAR mediated protein synthesis in neurons by perturbing calcium homeostasis

This study shows APOE4 disrupts calcium homeostasis in neurons, leading to sustained translation inhibition and impaired NMDAR signaling, while APOE3 causes a transient calcium response with recovery.

FRET-based screening in HEK293T identifies p38 MAPK and PKC inhibition as therapeutic targets for α-synuclein aggregation