Great presentation here
Professor Michal Schwartz, recorded on 16 August 2010. She is from the Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
She talks about using immune cells to repair injured CNS/brain. By using BLOOD macrophages (as opposed to microglia/macrophages already present in the CNS) and T lympocytes – CD4 positive T cells, they managed to reverse spinal cord injury, PTSD and MD, and stress induced anxiety in mice.
She talks about those 'imported' M2-type activated macrophages (from blood) being protective and healing, maintaining brain plasticity etc.
T-cells that recognise brain antigen (mentioned myelin specifically) are protective
Part of what those good T cells are doing is recruitment of BLOOD monocytes to sites of injury
In injured brain: resident macroglia do the first response job (get activated/inflamed) and by staying activated they recruit blood monocytes to come help. Those newcomer monocytes will then calm down activated resident microglia and terminate their response (this doesn't happen in autism but just goes on ...ME?), and this process is dependent on IL-10 ! (if no IL-10 this will not happen)
Failed NSAID trials - why anitinflammatory drugs fail in neurodegenerative disease/alzheimers with local inflammation (as opposed to systemic, such as MS): Her proposal: because mononcytes are also need in Alzheimers, and by lowering microglia inflammation (which are activated in order to summon monocytes) we are blocking recruitment of those blood monocytes!! [is this why minocyline accelerated ALS progression instead of stopping it??]
Their theory: chronic neuroinflammatory disease risk factor is present before visible onset. Onset happens when the equilibrium is lost, when the immune system stops responding to need. See slide at 38 minutes for possible reasons why (peripheral loss of immunity etc)
They observed lack of brain plasticity and neurogenesis in immune-deficient animals. They had poor memory, high neurotoxicity etc. In aged animals those that have more memory loss are those whose immune system ages fast, with higher levels of surpressive regulatory T-cells! By reducing levels of those Reg T cells they were able to boost brain activity and memory in aged mice.
HOW TO boost blood monocytes? ... By boosting levels of regulatory T-cells, which are needed for their recruitment. By boosting peripheral immunity … Mentions stem cell treatment and bone marrow transplant
She talks about their findings in schizophrenia
Summary slide at 1:02 min
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Professor Michal Schwartz, recorded on 16 August 2010. She is from the Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
She talks about using immune cells to repair injured CNS/brain. By using BLOOD macrophages (as opposed to microglia/macrophages already present in the CNS) and T lympocytes – CD4 positive T cells, they managed to reverse spinal cord injury, PTSD and MD, and stress induced anxiety in mice.
She talks about those 'imported' M2-type activated macrophages (from blood) being protective and healing, maintaining brain plasticity etc.
T-cells that recognise brain antigen (mentioned myelin specifically) are protective
Part of what those good T cells are doing is recruitment of BLOOD monocytes to sites of injury
In injured brain: resident macroglia do the first response job (get activated/inflamed) and by staying activated they recruit blood monocytes to come help. Those newcomer monocytes will then calm down activated resident microglia and terminate their response (this doesn't happen in autism but just goes on ...ME?), and this process is dependent on IL-10 ! (if no IL-10 this will not happen)
Failed NSAID trials - why anitinflammatory drugs fail in neurodegenerative disease/alzheimers with local inflammation (as opposed to systemic, such as MS): Her proposal: because mononcytes are also need in Alzheimers, and by lowering microglia inflammation (which are activated in order to summon monocytes) we are blocking recruitment of those blood monocytes!! [is this why minocyline accelerated ALS progression instead of stopping it??]
Their theory: chronic neuroinflammatory disease risk factor is present before visible onset. Onset happens when the equilibrium is lost, when the immune system stops responding to need. See slide at 38 minutes for possible reasons why (peripheral loss of immunity etc)
They observed lack of brain plasticity and neurogenesis in immune-deficient animals. They had poor memory, high neurotoxicity etc. In aged animals those that have more memory loss are those whose immune system ages fast, with higher levels of surpressive regulatory T-cells! By reducing levels of those Reg T cells they were able to boost brain activity and memory in aged mice.
HOW TO boost blood monocytes? ... By boosting levels of regulatory T-cells, which are needed for their recruitment. By boosting peripheral immunity … Mentions stem cell treatment and bone marrow transplant
She talks about their findings in schizophrenia
Summary slide at 1:02 min
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