Ever since they have been diagnosed, neurological disorders have been somewhat of a mystery to medical science. Now it may be possible that the underlying cause of those issues, including Parkinson’s disease, Alzheimer’s and schizophrenia, may be traced back to our immune system.
Alzheimer’s is often attributed to a buildup of proteins in the brain that forms plaques and tangles. This is thought to lead to the loss of brain connections.
Scientist Beth Stevens, however, has a theory that the underlying cause of degenerative neurological conditions takes place before the build up of proteins. Along with researchers from MIT and Harvard, she believes that aberrant synaptic elimination is to blame.
Our brain is constantly going through a process in which damaged or weak synapses are being cleared out. This helps to keep everything running smoothly. The cells that are responsible for “pruning” faulty synapse are known as microglia. Until recently, the scientific community has largely overlooked those cells.
Microglia were thought to be nothing more than a neurological janitorial service. When we have damaged brain cells, Microglia eat away at the injured bits while another type of glia, known as astrocytes, create scar tissue. This is a process known as gliosis.
Ben Barres, a Stanford biologist and Steven’s mentor, has been studying microglia for many years. He feels that the discovery is fascinating.
The great mystery was: what is the point of this gliosis? Is it good? Is it bad? Is it driving the disease process, or is it trying to repair the injured brain?
He found that a protein called C1q marks the unused or injured cells for elimination and it is what triggers the pruning process. The brain only needs synapse that are actually in use, so the C1q protein is important for healthy brain development. In healthy neurons that are fully developed, the C1q protein is practically absent.
Both bars and Stevens conducted research on mice bred so that they would develop neurological disorders. They found that the C1q was present in adult cells but it also appeared before any other sign of the disease. It is even found before the cells started dying.
Stephen McCarroll PhD was part of a study that identified a similar protein, C4, has been activated in schizophrenic brains. He says:
I think the implication of that is they could be lifelong diseases.The disease process could be going on for decades and the brain is just compensating, rewiring, making new synapses.
McCarroll, Stevens and a team at the broad Institute of MIT Harvard published a paper in January. It shows that aberrant microglia could contribute to or even cause massive cell loss. In turn, this could lead to cognitive defects, like schizophrenia.
What does this mean for treatment of those who have the disease? Is it possible that neurological conditions such as schizophrenia, Alzheimer’s and Parkinson’s could be halted by targeting the suppression of synapse proteins?
A company called Annexon Biosciences was founded by Barres to develop a drug that could block C1q. Recently, Stevens, Barres and their colleagues published a paper showing that the drug could prevent mice bred to develop Alzheimer’s from showing signs of the disease.
Within the next two years, the company hopes to start human trials. Although they admit they are a ways away from a cure, they feel they definitely have a path forward.
Via: Second Nexus
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