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Possible Evidence for Person-to-Person Transmission of Alzheimer's Pathology

2015-09-11
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       Prions are the misshapen proteins that replicate by inducing normal proteins to misfold and aggregate in the brain, leading to rare diseases such as mad cow and kuru. In recent years, scientists have discovered that similar processes of protein misfolding are at work in many neurodegenerative disorders, including Alzheimer’s, Parkinson’s and Lou Gehrig’s disease. Now, a study in Nature reveals the first evidence for human-to-human transmission of the misfolded proteins that underlie the pathology of Alzheimer’s disease.

    Yet, a new study from researchers at the University College London suggests the possibility, that under a particular set of circumstances, amyloid-β (the main peptide that comprises amyloid plaques of AD patients) may potentially be transmissible through certain medical procedures.

 

    “Our findings relate to the specific circumstance of cadaver-derived human growth hormone injections, a treatment that was discontinued many years ago,” explained senior co-author John Collinge, M.D., director of the Medical Research Council Prion Unit at the UCL Institute of Neurology. “ It is possible our findings might be relevant to some other medical or surgical procedures, but evaluating what risk, if any, there might be, requires much further research. Our current data have no bearing on dental surgery and certainly do not argue that dentistry poses a risk of Alzheimer’s disease.”

 

    The findings from this study were published recently in Nature through an article entitled “Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy.”

 

    The UCL researchers conducted autopsy studies that included brain tissue sampling from eight patients ranging in age from 36-51. All eight patients had been diagnosed previously with iatrogenic Creutzfeldt–Jakob disease (CJD), which they acquired after subsequent treatment with prion-contaminated human growth hormone (HGH).

 

    The investigators found that in addition to CJD pathology, six exhibited some degree of amyloid beta pathology—with four of those cases having some degree of cerebral amyloid angiopathy (CAA). Of particular interest to the researchers was that typically such pathology is rare within this age range and none of the patients was found to have mutations associated with early-onset AD.

 

    Additionally, the UCL scientists could find no evidence of tau protein pathology characteristic of AD. The researchers went on to examine a cohort of 116 patients with other prion diseases and found no evidence of amyloid beta pathology in the brains of patients of similar age range or a decade older who did not receive HGH treatment.

 

    “This is potentially very important research from the UCL Institute of Neurology Prion Research Group,” noted Mike Hanna, M.D., director of the UCL Institute of Neurology. “It could inform our understanding of the molecular mechanisms leading to Alzheimer’s disease.”

 

    While the study was small and the results preliminary, the results should at least prompt investigation into whether other known iatrogenic routes of prion transmission, including surgical instrument use and blood transfusion, could also be relevant to the transmission of AD pathology or other neurodegenerative diseases.

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