By: Alexandria Addesso
Memory loss and absent-mindedness has long been seen as an inevitable flaw that comes with old age. Although there is a slew of medications on the market that are prescribed for those suffering from Alzheimer’s Disease, none seem to change it by too large of a margin. This has led scientists to rethink what in particular is the root cause of Alzheimer’s.
New studies done on laboratory test rodents have found that there is a marked loss of synapses, which are a junction between two nerve cells, consisting of a minute gap across which impulses pass by diffusion of a neurotransmitter. Specifically synapses that are located in brain regions that are highly significant and key to memory.
These junctions between nerve cells are where neurotransmitters are released to spark the brain’s electrical activity. Currently, all pharmaceutical drugs on the market for the treatment of Alzheimer’s, focus on eliminating β amyloid, a protein that forms telltale sticky plaques around neurons in people with the disease. But, more β amyloid does not always mean more severe symptoms such as memory loss or poor attention.
Researchers at the University of Virginia, School of Medicine, in Charlottesville found that a protein called ‘C1q’ sets off a series of chemical reactions that ultimately mark a synapse for destruction. After this occurs immune cells called microglia-glial cells derived from mesoderm that function as macrophages (scavengers) in the central nervous system and form part of the reticuloendothelial system, destroy or “eat” the synapse.
“It is beautiful new work brings into light what’s happening in the early stage of the disease,” said one of the researchers at the University of Virginia School of Medicine neuroscientist Jonathan Kipnis.
These findings could mean that treatment that blocks C1q could be pivotal and highly successful in fighting Alzheimer’s Disease. When researchers gave the laboratory rodent test subjects an antibody to stop the destruction of cells by microglia, synapse loss did not appear. This could also mean a slowing in cognitive decline, but according to Edward Ruthazer, a neuroscientist at the Montreal Neurological Institute and Hospital in Canada, using microglia as such a central role to fight the disease is “still on the controversial side.”
Memory loss and absent-mindedness has long been seen as an inevitable flaw that comes with old age. Although there is a slew of medications on the market that are prescribed for those suffering from Alzheimer’s Disease, none seem to change it by too large of a margin. This has led scientists to rethink what in particular is the root cause of Alzheimer’s.
New studies done on laboratory test rodents have found that there is a marked loss of synapses, which are a junction between two nerve cells, consisting of a minute gap across which impulses pass by diffusion of a neurotransmitter. Specifically synapses that are located in brain regions that are highly significant and key to memory.
These junctions between nerve cells are where neurotransmitters are released to spark the brain’s electrical activity. Currently, all pharmaceutical drugs on the market for the treatment of Alzheimer’s, focus on eliminating β amyloid, a protein that forms telltale sticky plaques around neurons in people with the disease. But, more β amyloid does not always mean more severe symptoms such as memory loss or poor attention.
Researchers at the University of Virginia, School of Medicine, in Charlottesville found that a protein called ‘C1q’ sets off a series of chemical reactions that ultimately mark a synapse for destruction. After this occurs immune cells called microglia-glial cells derived from mesoderm that function as macrophages (scavengers) in the central nervous system and form part of the reticuloendothelial system, destroy or “eat” the synapse.
“It is beautiful new work brings into light what’s happening in the early stage of the disease,” said one of the researchers at the University of Virginia School of Medicine neuroscientist Jonathan Kipnis.
These findings could mean that treatment that blocks C1q could be pivotal and highly successful in fighting Alzheimer’s Disease. When researchers gave the laboratory rodent test subjects an antibody to stop the destruction of cells by microglia, synapse loss did not appear. This could also mean a slowing in cognitive decline, but according to Edward Ruthazer, a neuroscientist at the Montreal Neurological Institute and Hospital in Canada, using microglia as such a central role to fight the disease is “still on the controversial side.”
