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3D mini-brains against multiple sclerosis

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3D mini-brains against multiple sclerosis

The technologies available today allow us to access new and detailed knowledge, never before possessed. An immense amount of data. The challenge is to be able to interpret them correctly to understand the complex processes underlying the disease. But to win the battle it is necessary to be united and share knowledge with experts on other neurodegenerative diseases. To be able to develop new human models with the ultimate goal of identifying innovative treatments to protect the nervous system.

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The data collected on biological and genetic research

Covid, vaccines, war are changing our life, history, geography and our imagination. Science also faces an epochal challenge, which can change the history of many diseases and the lives of many people. Industry and large private and public lenders are investing huge capital to build what are called Human Atlases of biological, genetic data and knowledge and so on. These atlases represent a kind of very high resolution 2.0 reference map for organs and tissues, including the brain.

Linking multiple sclerosis with other neurodegenerative diseases

Regarding multiple sclerosis (Sm), these very high resolution studies can allow us to identify mechanisms of response and progression to damage, common to several brain diseases. Therefore, the challenge of connecting multiple sclerosis with other neurodegenerative diseases – a topic chosen by the FISM (Italian Multiple Sclerosis Foundation) in its recent congress with the aim of finding with the scientific community new ways to stop progression and neurodegeneration and restore brain function of people with multiple sclerosis – strongly depends on the ability of us scientists to look in detail, go beyond the old dogmas, interpret these new data provided by human atlases, generate and verify mechanism hypotheses that are shared.

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The brain aging process

Sharing, of knowledge as well as of intentions, is in fact the starting point of a new scientific era that aims to understand in order to slow down the progressive loss of resilience to the disease; to check to identify how “confusing” the brain aging process is; and finally to generate alliances without borders of disease to try to identify the most suitable treatments to protect the nervous system from neurodegeneration mechanisms and try to save the neurological reserve we are endowed with from birth.

To help us better interpret these big human data in the field of multiple sclerosis, it will be crucial to develop new human models – whether they are alternative or complementary to the animal ones – that allow us to observe what can happen when the disease develops.

Minibrain studied in the laboratory

In my Regenerative Neuroimmunology laboratory in Cambridge, for this purpose, we have developed several human models, some more mature and others yet to be optimized. In particular, we have generated a new version of human brain organoids (called minibrains) – classically used to study the development of the human brain in three dimensions starting from pluripotent stem cells – in which we have seeded what we believe to be one of the germs that contribute to reduce the resilience of the brain during progressive multiple sclerosis and accelerate the aging process.

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The use of a human model in three dimensions, such as the one we are still developing, is one of the new ways in which to study and try to correct the progressive loss of resilience to the disease that characterizes progressive multiple sclerosis.

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Study of cellular metabolism and mitochondria

Another innovative point of research on progressive multiple sclerosis concerns the study of cellular metabolism and mitochondria, which are the seat of respiration reactions and the cell’s central energy production. Research in recent years has shown that cells of the innate immune system, particularly microglia and macrophages, are the ones most involved in secondary multiple sclerosis. Within the central nervous system, in fact, their persistent activation is highlighted which determines neuro-degeneration.

Our challenge is to understand why all this happens and if, by depriving microglia and macrophages of the fuel necessary for this chronic inflammation process to self-maintain exclusively in the brain, we are able to preserve what is globally called the neurological reserve.

Treatments that help the brain increase its resilience

To change the history of the disease and the lives of people with progressive multiple sclerosis we must therefore, first of all, find those treatments that help the brain increase its resilience, its resistance to the disease and thus slow down its premature aging.

For this reason, the time has come to change the design of clinical research for the progressive forms of multiple sclerosis, exploring the impact that a treatment can have on the patient’s neurological reserve, not exclusively or mainly on the ambulatory capacity, but also on the cognitive activity, memory or residual motor functions of the upper limbs.

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* Stefano Pluchino, Professor of Regenerative Neuroimmunology at the Department of Neurological Sciences of the University of Cambridge in Great Britain. He coordinates an international research group on the role of metabolism and mitochondria in chronic brain inflammation processes (with Luca Peruzzotti-Jametti), and the role of cellular senescence in the mechanisms of brain resilience to progressive SM (with Alexandra Nicaise)

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