68 RESULTS
COMMENT What a stunning turnaround in a field wherein people thought as late as 1997, and some even thereafter, that genetics were irrelevant to PD and it was all about environment! In the light of the MPTP story, obviously also an important advance, the field la
COMMENT This is a very interesting paper that adds to our understanding of the in-vivo biology of plaques, and it would be interesting to add further nuances to these insights by comparing the effects of diffuse versus neuritic plaques on the integrity of dendrit
COMMENT Mechanisms leading to the formation of α-synuclein inclusions in Parkinson's disease (PD) and related α-synucleinopathies characterized predominantly by abundant fibrillary intracellular α-synuclein inclusions in neurons and their processes as well a
COMMENT The paper from the LaFerla lab is most interesting, and extremely well done, which I have mentioned in recent interviews to other news outlets. However, I do not think the data in this paper resolve controversies about the validity of the amyloid cascade
COMMENT This work is interesting, but highly speculative since the linkage between BMAA or other cycad components or cycads themselves remains tenuous, and earlier data over a decade ago to suggest that cycads or BMAA induced a progressive neurological disease in
COMMENT These two reports from Scott Brady’s and Larry Goldstein’s laboratories are highly significant because they extend the concept that neurodegenerative disease is caused by impaired axonal transport, beyond more common disorders like Alzheimer's, to al
COMMENT Many neurodegenerative diseases share an enigmatic symmetry, i.e. missense mutations in the gene encoding the disease protein cause a familial variant of the disorder as well as its hallmark brain lesions, but the same brain lesions also form from the cor
COMMENT Considerable progress is being made towards the development of novel and more effective therapeutic approaches for the treatment of Alzheimer's disease (AD) based on a design strategy to prevent or eliminate Aβ- deposits in fibrillar and non-fibrilla
