11617 RESULTS
COMMENT While overt efforts to create models of human disease in lower systems represent a relatively new area of investigation, in fact, this work has been going on in another guise for a very long time. Much of this work can be described as genetic analysis, or
COMMENT This is a report to support neurogenesis in the adult human brain. Transplanted cells (Hoehn, 2002; Zung, 2003) and endogenous stem cells localized in the subventricular zone (Parent, 2002) are reported to migrate through white matter of the adult brain.
COMMENT This seems to be a careful attempt to understand how alpha-synuclein and lipid vesicles interact to generate toxic products. 0 vincent.marchesi
COMMENT It is well established that chaperone proteins are involved in assisting all but the smallest proteins to fold properly during protein biosynthesis. It is not unreasonable to suspect that abnormal chaperone functions might also play a role in diseases inv
COMMENT Not enough attention is paid to normal mechanisms of protein turnover as a contributing factor in neurodegenerative diseases. Mutations involving ubiquitin ligases are the first of many proteins that are likely to be invoved in ubiuquitin-mediated degrada
COMMENT By showing that knockout of the Drosophila homologue of parkin produces a substantial phenotype, Greene et al. provide an important in-vivo model for this genetic form of PD. The phenotype is clearly related to mitochondrial triggering of apoptosis, echoi
COMMENT These elegant experiments by Meyer-Luehmann and colleagues demonstrate that the proteopathic corruption of tissue can be more strongly influenced by the environment in which the tissue develops than by the lineage of the tissue itself (I will forego the o
COMMENT This is a complicated story in which peptides known to form fibrillar aggregates are found to increase the levels of APP and APLP2 in primary cultures of astrocytes and neurons. The increase in APP and APLP2 only in cultures exposed to fibrillar peptides
COMMENT These are difficult experiments to evaluate. One wonders how intracerebral injections of small peptides can act on specific targets inside CNS cells. Although often used, this approach needs many functional correlations to be interpretable. One would like
COMMENT The article by Martinez and colleagues identifies the calcium-binding protein calmodulin as a new binding partner for α-synuclein. This intriguing observation adds to the growing list of proteins that bind α-synuclein. This list includes phospholipase D,
COMMENT The findings by Staropoli and colleagues (2003) provide strong evidence that an altered cell cycle machinery plays a crucial role in the pathogenesis of Parkinson’s disease (PD), especially the autosomal recessive, early onset form of PD (ARPD). However,
COMMENT Having proof that established prion replication in the living situation can be controlled, there is no reason why these mouse monoclonal antibodies should not be humanized and infused into the brains of patients with human prion diseases. a.attwood 0
COMMENT We are pleased that White and colleagues confirm our recent findings that anti-prion antibodies have the potential to be used as prophylaxes following scrapie exposure (Sigurdsson et al., 2002; Sigurdsson et al., 2003). We were surprised that they did not
COMMENT This is a very exciting development for a rapidly fatal disease, for which there is no known therapy. Particularly important is that the passive immunotherapy can be started relatively late in the replication phase of the disease. While not identical, bot
COMMENT This is a great paper and an important step forward in two regards. Firstly, it makes all of us working on parkin reevaluate an important but unstated assumption, namely, that parkin acts as a single protein enzyme. The paper clearly shows that parkin can
