John Q. Trojanowski

TL;DR: The unexpected lack of neuropathological findings to explain the cognitive deterioration in this group of elderly patients with schizophrenia prompts speculation about alternative etiologies.

TL;DR: It is found that MED283-TrkA cells expressing a dominant negative Ras inhibitor (N17Ras) failed to undergo ERK activation and apoptosis following NGF treatment, whereas the ERK kinase (mitogen-activated protein kinase kinase) inhibitors PD98059 and U0126 eliminated ERKactivation but had no effect on apoptosis.

TL;DR: The accumulation of -synuclein into filamentous inclusions appears to play a mechanistic role in the pathogenesis of several progressive neurological disorders including PD, dementia with LBs, Down’s syndrome, FAD, LB variant of AD, sporadic AD, multiple system atrophy, and other synucleinopathies.

TL;DR: The hypotheses that antemortem cerebrospinal fluid tau levels correlate with postmortem tau pathology in frontotemporal lobar degeneration (FTLD) and tauopathy patients have higher phosphorylated‐tau levels compared to transactivation response element DNA‐binding protein 43 (TDP‐43) proteinopathy patients while accounting for Alzheimer's disease (AD) copathology are tested.

TL;DR: Clinical features in sporadic nfVPPA caused by FTLD subtypes relate to neurodegeneration of GM and WM in frontal motor speech and language networks and it is proposed that early WM atrophy in nfvPPA is suggestive of FTLD-tau pathology while early selective GM loss might be indicative of FT LD-TDP.