A possible mechanism for controlling processive transport by microtubule-associated proteins.

Molecular mechanisms of axonal transport have been evaluated by several investigators. It seems that microtubules (MTs) act as a track for the transport and microtubule-associated proteins (MAPs) seem to play as a regulating factor in it. In order to transport MTs must move in the radial direction to make room for a vesicle and when the cargo passes, return to the previous position for the maintenance of neuronal structure. An inhibitor factor against the radial movement is the steric constraints resulted from presence of MAPs. In fact, inter-microtubular spaces (IMS) in the neuronal processes are resulted from the space-making role of the MAPs. Since the IMS must be locally altered to make enough room for a vesicle, it seems relevant to imagine some mechanisms that control the steric constraints for an efficient vesicular transport. Here we juxtapose the older findings and the recent ones to investigate the possible effects of MAPs on the processive transport.

Complex I deficiency in Persian multiple sclerosis patients.

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system characterized by the morphological hallmarks of inflammation, demyelination and axonal loss. Until now, little attention has been paid to the contribution of mitochondrial respiratory chain enzyme activities to MS. In this study, kinetic analysis of mitochondrial respiratory chain complex I enzyme (measured as NADH-ferricyanide reductase) was performed on intact mitochondria isolated from fresh skeletal muscle in MS patients (n = 10) and control subjects (n = 11). Mitochondrial DNA common deletion and deletions were also tested in MS patients. Our findings showed that complex I activities were significantly reduced (P = 0.007) in patients compared with control. However, we could not find deletion in mtDNA of patients with MS. The presupposition of relationship between MS and mitochondrial disorders is due to predominant maternal transmission of MS in affected parent-child pairs, pathoaetiological role of respiratory chain dysfunction in multisystem disorders and important role of it in neurodegenerative disorders, a number of patients such as LHON or other mtDNA abnormality with developed neurological symptoms indistinguishable from MS and similarity of clinical symptoms in mitochondrial disorders to those of MS. This study suggested that a biochemical defect in complex I activity may be involved in pathogenesis of MS.