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28, 2020 /--- In a recent study published in the journal Science Advance, researchers at the La Jolla Institute for Immunology (LJI) reported that the nervous system may contribute to the death of pancreatic Beta cells.
their new findings in mouse models suggest that blocking nerve signals in the pancreas can prevent patients from developing type 1 diabetes.
, senior author of the study, said: "This process may be halted by the influence of neurons.
" (Photo: www.pixabay.com) von Herrath Labs has long struggled to find the cause of type 1 diabetes.
the disease has environmental and genetic risk factors, the onset of type 1 diabetes appears to be random.
for more than a year, researchers have been looking for causes of beta cell death.
theory is that these cell deaths stem from differences in blood supply around them, or are damaged by immune attacks triggered by viral infections.
to test this theory, the researchers used a mouse model that could artificially induce beta cell death.
they "weaken nerves" through surgery or the use of neurotoxins or pharmacological methods, blocking the sensory nerve signals of most pancreas.
, the researchers used imaging devices to track the pattern of beta cell death in mice.
team found that blocking nerve signals protected mice from beta cell death compared to mice that were not treated and those who were given only beta blockers.
"We found significant differences in these neuroresistants in affecting the onset of diabetes.
" is much more than explaining cell death in type 1 diabetes.
it is well known that several autoimmune diseases have similar events of cell death.
such as vitiligo and arthritis.
Von Herrath believes that breakthroughs in neuroimmune science may have broad implications for explaining why the body reverses its own organs in many autoimmune diseases.
the future, the authors hope to study the cellular mechanisms between the nervous system and the onset of type 1 diabetes.
, Aug. 28, 2020 /--- In a recent study published in the journal Science Advance, researchers at the La Jolla Institute for Immunology (LJI) reported that the nervous system may contribute to the death of pancreatic Beta cells.
their new findings in mouse models suggest that blocking nerve signals in the pancreas can prevent patients from developing type 1 diabetes.
, senior author of the study, said: "This process may be halted by the influence of neurons.
" von Herrath laboratory has long struggled to find the cause of type 1 diabetes.
the disease has environmental and genetic risk factors, the onset of type 1 diabetes appears to be random.
for more than a year, researchers have been looking for causes of beta cell death.
theory is that these cell deaths stem from differences in blood supply around them, or are damaged by immune attacks triggered by viral infections.
to test this theory, the researchers used a mouse model that could artificially induce beta cell death.
they "weaken nerves" through surgery or the use of neurotoxins or pharmacological methods, blocking the sensory nerve signals of most pancreas.
, the researchers used imaging devices to track the pattern of beta cell death in mice.
team found that blocking nerve signals protected mice from beta cell death compared to mice that were not treated and those who were given only beta blockers.
"We found significant differences in these neuroresistants in affecting the onset of diabetes.
" is much more than explaining cell death in type 1 diabetes.
it is well known that several autoimmune diseases have similar events of cell death.
such as vitiligo and arthritis.
Von Herrath believes that breakthroughs in neuroimmune science may have broad implications for explaining why the body reverses its own organs in many autoimmune diseases.
the future, the authors hope to study the cellular mechanisms between the nervous system and the onset of type 1 diabetes.
(bioon.com) Source: Blocking nerve signals to the pancreas halts type 1 diabetes onset in mice Original source: "Processing with pancreaticsing signaling halts the onset of diabetes in mice" Science Advances (2020). advances.sciencemag.org/lookup . . . 1126 / sciadv.abb2878.