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New Molecular Insights into Disease Exacerbation in Multiple Sclerosis

New Molecular Insights into Disease Exacerbation in Multiple Sclerosis

Importance of the Atg7 gene for the recovery from inflammation in the central nervous system

Multiple sclerosis (MS) is an inflammatory disease of the central nervous system (CNS) which in the majority of cases comes in bouts causing severe neurological symptoms, such as loss of sensation and trembling, difficulties walking and maintaining balance, memory failure and visual impairment. Subsequently there is usually a certain amount of recovery the gradual loss of function over time however is inevitable. Currently used treatments can reduce the frequency and damaging effects of the disease bouts. For the progressive worsening phase, which usually occurs when the patient has had the disease for 10 to 20 years, there is only one approved drug and more research about the mechanisms behind this disease phase is needed.

From the left: André Ortlieb Guerreiro-Cacais, Maja Jagodic, Rasmus Berglund and Tomas Olsson. Photo: Ulf Sirborn

Maja Jagodic, Associate Professor of experimental medicine and Group Leader at CMM, has led a study investigating the molecular processes occurring in progression of MS, using an MS-like disease in mice as a model. The results were recently published in Science Immunology in a paper with the title “Microglial autophagy-associated phagocytosis is essential for recovery from neuroinflammation”.

MS progression has previously been linked to the activation of a CNS-specific immune cell type called microglia. In MS myelin sheaths surrounding nerve threads (axons) become destroyed. Microglia play an important role in the phagocytic clearance of tissue debris and maintenance of brain homeostasis, a capacity which is impaired in some neuroinflammatory conditions such as MS.

Rasmus Berglund, PhD student in Tomas Olsson’s Group is the first author of this paper, in which the role of the Atg7 gene in autophagy processes in relation to neuroinflammatory disease is investigated. Rasmus and his colleagues from CMM, other colleagues from Karolinska Institutet as well as Amsterdam UMC and Queen Mary University of London, show that the Atg7 gene is important for the regulation of autophagy in the context of neuroinflammation.

They found that Atg7 is critical for a specific form of autophagy that was thus impaired in mice lacking Atg7 in the microglia. This caused an accumulation of phagocytosed myelin and lack of recovery from MS-like disease in these mice. The results shed new light on the microglia function in MS, and especially during disease progression.

Another significant insight from the study is that microglia from aged mice resemble the cells from young mice that lacked Atg7 since both displayed deficiencies in the autophagy process, which had a negative effect on the course of the disease. It is an important finding because age is a risk factor for the progressive phase of MS.

Interestingly, by inducing autophagy using he plant and fungi-derived sugar Trehalose, Rasmus and his colleagues could reverse the age-related progression of the MS-like disease in mice. “By enhancing this process we hope one day to be able to treat and prevent age-related aspects of neuroinflammatory conditions,” says Rasmus Berglund in the Karolinska Institutet press release about the study.

 

Link to the publication here.

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