10 RESULTS
COMMENT The Science article by Clement (Don Cleveland, University of California) and other US and Canadian researchers is a masterpiece in demonstrating the prominent influence of non-neuronal cells on the ALS pathogenesis, which can be extrapolated to other neur
COMMENT Seems interesting. 0 rpochet
COMMENT I would like to stress that already in 1993, Sutherland MK, Wong L, Somerville MJ, Yoong LK, Bergeron C, Parmentier M, McLachlan DR published in Brain Res Mol Brain Res. 1993 Apr;18(1-2):32-42 Reduction of calbindin-28k mRNA levels in Alzheimer as compare
COMMENT Calbindin and parvalbumin were until now both classified as intracellular calcium buffers and therefore no clear physiological distinction were made between them. In this manuscript, Parvizi and Damazio elegantly showed that within the brainstem of the ma
COMMENT The zinc-deficient rat might be useful to study zinc homeostasis within Alzheimer's and ALS rat models. 0 rpochet
COMMENT Adenosine receptors are regulating many "cell behaviors" and deserve much attention by drug discovery people. 0 rpochet
COMMENT The concept of mutated SOD1 aggregate formation was previously evoked, but this article gives experimental evidence supporting this hypothesis. It remains now to explain why not all motoneurons (i.e. oculomotor nucleus) are not impaired. rpochet 0
COMMENT Study of the 3D structure of Cu/Zn SOD1 wild type and its comparison with mutated forms is certainly a strong approach to decipher the causes of motoneuron death. 0 rpochet
COMMENT Drug discovery within the field of neuroinflammation is a research orientation which should be promoted. 0 rpochet
COMMENT This paper should have a broad impact on clinicians and promote neuroimaging. 0 rpochet
