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Papers by Robert Weissert

Frontiers in Physiology, Dec 19, 2017

Journal für Neurologie, Neurochirurgie und Psychiatrie, Dec 9, 2014

Frontiers in Immunology, Oct 8, 2020

Arthritis Research & Therapy, 2012

Frontiers in Neurology, Jun 6, 2019

Journal of Neuroinflammation, Sep 17, 2015

European Neurology, Dec 27, 2004

Short Reports 9 Greenan JT, Grossmann RI, Goldberg HI: Cerebral vasculitis: MR imaging and angiog... more Short Reports 9 Greenan JT, Grossmann RI, Goldberg HI: Cerebral vasculitis: MR imaging and angiographic correlation. Radiology 1992;182:65–72. 10 Diener H-C, Bogousslavsky J, Brass LM, Cimminiello C, Csiba L, Kaste M, Leys D, Matias-Guiu J, Rupprecht H-J, on behalf of the MATCH Investigators: Management of atherothrombosis with clopidogrel in high-risk patients with recent transient ischaemic attack or ischaemic stroke (MATCH): Study design and baseline data. Cerebrovasc Dis 2004;17:253– 261.

American Journal of Pathology, Mar 1, 2007

The Journal of Neuroscience, Aug 6, 2003

Journal of the Neurological Sciences, Oct 1, 2009

Journal of Biological Chemistry, May 1, 2012

Journal of Neurology, Apr 20, 2007

To study the safety and efficacy of treosulfan, a cytotoxic alkylating agent, in patients with ac... more To study the safety and efficacy of treosulfan, a cytotoxic alkylating agent, in patients with active secondary progressive multiple sclerosis. Treosulfan (L-threitol-1,4-bis(methanesulfonate)) is a bifunctional alkylating agent with a favorable profile of side effects, approved for the treatment of ovarian cancer. Treosulfan has previously been shown to reduce the severity of experimental allergic encephalomyelitis under pre-therapeutic and therapeutic conditions. In human peripheral blood mononuclear cells, treosulfan reduces proliferative capacity and increases apoptosis. This is a nonrandomized, open label study conducted in two centers. Eleven patients with active secondary progressive MS that failed to or did not qualify for approved disease modifying drugs were treated with treosulfan for 1 year. Patients received intravenous infusions of 7 g/m(2) every 4 weeks for 3 months (cycles 1-4, induction phase) with a predefined one-step dose escalation, thereafter every 3 months for the following 9 months (cyles 5-7, maintainance phase). Cranial MRI was performed every 3 months, EDSS and MSFC as well as physical examination were assessed at each clinical visit. Treatment with treosulfan was safe and well tolerated. Nine of 11 patients remained on study drug over the complete treatment period and showed clinical stabilisation or improvement as determined by EDSS and MSFC. Two patients discontinued study drug because of leukocytopenia and withdrawal of consent, respectively. No clinical relapses were observed during the treatment period. Thus, the median number of relapses per year was reduced signifi- cantly by 1.5 (range -3 to 0), p &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.016, compared to prestudy. Therapy with treosulfan lead to a clear reduction of MRI activity as revealed by a reduced number of Gd + enhancing lesions on T1 weighted images. The mean number and volume of T2 lesions remained unchanged over 1 year. Four out of 9 patients under treosulfan showed no detectable disease activity (no Gd enhancing lesions, no new or newly enlarging T2 lesions). Application of treosulfan in MS was safe and well tolerated. Further studies are warranted to evaluate the efficacy of this treatment in secondary progressive MS.

Journal of Neuroimmune Pharmacology, May 10, 2013

Multiple sclerosis is an autoimmune disease of the central nervous system (CNS) that leads to cha... more Multiple sclerosis is an autoimmune disease of the central nervous system (CNS) that leads to changes of nerve conduction due to damage of CNS- resident cells, primarily oligodendrocytes and neurons. CD4+ T cells are of primary importance in the immune cascades leading to tissue damage, but also CD8+ T cells, NK cells and B cells and antibodies contribute to tissue damage. In addition, the innate immune response and mainly microglial cells participate in the events leading to lesions. There are different types of MS and possibly this is due to different underlying immune mechanisms. The current treatment options mainly affect the immune response but have not much influence on secondary signaling changes in astrocytes and neurons which contribute to constant disease progression. The immune response in MS must be seen in the systemic context and there are strong indications that the gut and lung immunity affect MS disease precipitation. The strongest genetic influence in MS is mediated by the HLA class II genes and in Western Europeans and North Americans the disease is associated with HLA-DR2b. Possibly this is due to presentation of a set of specific antigens in context of this HLA allele. Novel data indicates that the immune response in MS is not only focused on certain myelin proteins like myelin basic protein (MBP) but to additional astrocytic and neuronal proteins, which is also mirrored in the pathology. While in the past the disease has been considered as mainly a white matter disease, nowadays it is clear that also grey matter is affected by the aberrant immune response. Still much needs to be learned regarding the underlying events in MS. This expanded knowledge is important to finally discover curative therapies.