Interleukin-1beta - Helpful In Alzheimer's Disease
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Individuals with Alzheimer's disease (AD) suffer from the formation of amyloid plaques, made up of the peptide amyloid beta (Abeta), in brain tissue. The role, if any, of inflammation in AD remains somewhat of a mystery. Although the levels of some proinflammatory proteins are elevated in AD brain tissue, whether these proteins have negative or positive effects is still unclear. In the Journal of Clinical Investigation, M. Kerry O'Banion and colleagues from University of Rochester Medical Center examined a mouse model of AD and found that overexpression of the proinflammatory molecule interleukin-1beta (IL-1beta) in the hippocampus resulted not in the expected worsening of Abeta deposition common to AD, but instead in the lessening of plaque formation in brain tissue.
In an accompanying commentary, Cynthia A. Lemere from Harvard Medical School comments that "the IL-1beta results reported here provide much food for thought and will undoubtedly encourage much-needed future investigation into a positive role for inflammation in neurodegenerative diseases, including AD. Manipulation of the immune system may be a potential therapeutic approach to protect against AD, although further studies are needed to understand all of the downstream effects of this manipulation."
Alzheimer's Donation
Donate Online Now
.
Individuals with Alzheimer's disease (AD) suffer from the formation of amyloid plaques, made up of the peptide amyloid beta (Abeta), in brain tissue. The role, if any, of inflammation in AD remains somewhat of a mystery. Although the levels of some proinflammatory proteins are elevated in AD brain tissue, whether these proteins have negative or positive effects is still unclear. In the Journal of Clinical Investigation, M. Kerry O'Banion and colleagues from University of Rochester Medical Center examined a mouse model of AD and found that overexpression of the proinflammatory molecule interleukin-1beta (IL-1beta) in the hippocampus resulted not in the expected worsening of Abeta deposition common to AD, but instead in the lessening of plaque formation in brain tissue.
In an accompanying commentary, Cynthia A. Lemere from Harvard Medical School comments that "the IL-1beta results reported here provide much food for thought and will undoubtedly encourage much-needed future investigation into a positive role for inflammation in neurodegenerative diseases, including AD. Manipulation of the immune system may be a potential therapeutic approach to protect against AD, although further studies are needed to understand all of the downstream effects of this manipulation."
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