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1. TIA1 regulates the generation and response to toxic tau oligomers Abstract RNA binding proteins (RBPs) are strongly linked to the pathophysiology of motor neuron diseases. Recent studies show that RBPs, such as TIA1, also contribute to the pathophysiology of tauopathy. RBPs co-localize with tau pathology, and reduction of TIA1 protects against tau-mediated neurodegeneration. The mechanism through which TIA1 reduction protects...
2. Prion-like propagation of β-amyloid aggregates in the absence of APP overexpression The amyloid cascade hypothesis posits that the initiating event in Alzheimer’s disease (AD) is the aggregation and deposition of the β-amyloid (Aβ) peptide, which is a proteolytic cleavage product of the amylo… Read More......
3. Induction of calcitonin gene-related peptide expression in rats by cortical spreading depression Cephalalgia, Ahead of Print. Read More...Read More......
4. Alzheimer’s disease pathology propagation by exosomes containing toxic amyloid-beta oligomers Abstract The gradual deterioration of cognitive functions in Alzheimer’s disease is paralleled by a hierarchical progression of amyloid-beta and tau brain pathology. Recent findings indicate that toxic oligomers of amyloid-beta may cause propagation of pathology in a prion-like manner, although the underlying mechanisms are incompletely understood. Here we show that...