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— BUSM researchers develop blood test to detect membranous nephropathy — Research conducted by a pair of physicians at Boston University School of Medicine (BUSM) and Boston Medical Centre (BMC) has led to the development of a test that can help diagnose…
— New hip implants no better than traditional implants — New hip implants appear to have no advantage over traditional implants, suggests a review of the evidence published on bmj.com today…
— Action needed to improve men's health in Europe — Policies aimed specifically at men are urgently needed to improve the health of Europe's men, say experts on bmj.com today…
— Probiotics reduce infections for patients in intensive care — Traumatic brain injury is associated with a profound suppression of the patient's ability to fight infection. At the same time the patient also often suffers hyper-inflammation, due…
— High blood sugar levels in older women linked to colorectal cancer — Elevated blood sugar levels are associated with an increased risk of colorectal cancer, according to a study led by researchers at Albert Einstein College of Medicine of Yeshiva University.…
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The protein APC slows Lou Gehrig's disease in mice
Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, is a neurodegenerative disease that causes progressive weakness, disability, and death. Treatments are largely palliative. Using mice carrying the mutated form of the human SOD1 gene that causes inherited forms of ALS, however, Berislav Zlokovic and colleagues, at the University of Rochester Medical Centre, Rochester, have now found that administration of the protein APC slows disease progression and extends survival. The authors therefore suggest that strategies designed to activate APC might be of benefit to patients with inherited, and possibly sporadic, ALS. However, in an accompanying commentary, Charles Esmon and Jonathan Glass warn that such an approach would not be without risks.
In the study, administration of both APC, whose main function is to prevent blood clotting, and APC analogues with a reduced ability to prevent blood clotting slowed disease progression in the mutant SOD1 - expressing mice and extended their survival, even when the compounds were administered after disease onset. Further analysis indicated that these compounds were able to access the brain and that once there, they worked by decreasing expression of the mutant SOD1 in several cell types in the brain, including the nerve cells destroyed in individuals with ALS. This study therefore indicates that APC can have a neuroprotective effect in mouse models of inherited ALS.
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