Rakez Kayed

This study shows that soluble pathogenic tau aggregates are transmitted to astrocytes, causing mitochondrial dysfunction, senescence, and neurovascular uncoupling in a tauopathy model.

The paper identifies disease-specific tau polymorphs and their unique protein interaction networks in Alzheimer's, PSP, and DLB, revealing distinct molecular signatures and therapeutic targets.

The paper detects an unfolded p53 conformation (U-p53AZ) in Alzheimer's disease brain samples, showing colocalization with pTau in neurofibrillary tangles.

This study shows that pathological tau isoforms in retinal ganglion cells (RGCs) are linked to RGC degeneration in Alzheimer's disease, with significant correlations between tau levels and disease severity.

This study quantifies retinal tau isoforms in early and advanced AD and links them to brain pathology and cognitive status.

This study investigates how WT and P301L tau proteins modulate transcription and alternative polyadenylation profiles in neuronal cells, revealing distinct gene expression changes related to chromatin remodeling and splicing.

This study shows that caspase inhibition reduces tau cleavage and neurotoxicity in iPSC-derived neurons with the V337M MAPT mutation.

This paper identifies a complex involving HNRNPA2B1, N6-methyladenosine modified transcripts, and toxic tau oligomers that mediates neurodegeneration.

This study shows that intracellular Aβ oligomers increase neuronal hyperexcitability through synaptic mechanisms, spreading excitability across neural networks.

This study investigates how Alzheimer's disease-derived extracellular vesicles propagate tau pathology and affect GABAergic neuronal transmission.

The paper develops molecular models of amyloid beta 42 oligomers, annular protofibrils, and transmembrane channels based on electron microscopy observations.