It's not contagious
LifeSciencesToday based on Penn Medicine: Penn Study Confirms No Transmission of Alzheimer's Proteins Between HumansIntercellular transmission is a common pathway for the spread and progression of Alzheimer's disease, Parkinson's disease and other neurodegenerative diseases.
Apparently, being transmitted from cell to cell, improperly folded toxic proteins damage more and more new areas of the patient's brain, depriving the affected neurons of the ability to perform their functions. However, there is no reason to fear that abnormal proteins characteristic of these diseases can be transmitted from person to person.
Pathological deposits of proteins (shown by arrows) associated with Alzheimer's disease and Parkinson's disease in human pituitary gland samples. (A – beta-amyloid, the main component of beta-amyloid plaques in Alzheimer's disease, B – tau protein, the main component of neurofibrillary tangles in Alzheimer's disease, C – alpha-synuclein, the main component of Levi's bodies in Parkinson's disease).
(Photo: University of Pennsylvania School of Medicine)
An ever-increasing amount of data indicates that pathological proteins associated with the onset and progression of neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, frontotemporal lobar degeneration, amyotrophic lateral sclerosis, are able to spread from cell to cell in the brain of patients suffering from these diseases and thereby "spread" the disease between interconnected areas.
However, in a study conducted by scientists at the Perelman School of Medicine at the University of Pennsylvania, no evidence was found that these abnormal proteins are "contagious" and can be transmitted from person to person or from animals to humans.
"After a thorough analysis of the existing database with information about a group of well–studied patients, we came to the conclusion that there is no evidence that Alzheimer's disease or Parkinson's disease can be transmitted from person to person," comments the results of the study, its head John Trojanowski, MD, PhD, professor of pathology and Laboratory Medicine, co-director of the Center for the Study of Neurodegenerative Diseases (Center for Neurodegenerative Disease Research, CNDR) of the University of Pennsylvania. "We can now redouble our efforts to find treatments using immunotherapy or other approaches to stop the intercellular spread of these toxic proteins."
In order to test whether pathological proteins can be transmitted from person to person, the researchers analyzed data related to a group of patients who received human growth hormone (hGH) from cadaveric pituitary glands (c-hGH) under the national program for the treatment of growth retardation (treatment was carried out before the appearance of a synthetic analogue of this hormone). In the United States, almost 7,700 patients received c-hGH injections between 1963 and 1985.
In the mid-1980s, more than 200 patients worldwide who received c-hGH accidentally contaminated with prion proteins from donor pituitary tissue developed an acquired form of Kreutzfeldt-Jakob disease, a rare, invariably fatal degenerative brain disease caused by pathological prion proteins, which are also the cause of mad cow disease. Since then, scientists have been tracking the appearance of new cases of Kreutzfeldt-Jakob disease in patients of this group and currently have detailed medical histories of a large number of patients aged 30 and older (this method of treatment was banned after the establishment in 1985 of a link between c-hGH and Kreutzfeldt-Jakob disease).
In this study, the researchers looked for signs of an increased risk of developing Alzheimer's disease, Parkinson's disease, frontotemporal lobar degeneration and amyotrophic lateral sclerosis in this group and found that none of the c-hGH recipients developed Alzheimer's disease, Parkinson's disease, or frontotemporal lobar degeneration. Three cases of amyotrophic lateral sclerosis have been identified, but given that no traces of ALS-related proteins (TDP-43, FUS and Ubiquilin) have been found in the pituitary gland of these patients, scientists cannot yet explain the significance of these data. At the same time, pathological proteins of Alzheimer's disease (tau and beta-amyloid) and Parkinson's disease (alpha-synuclein) were present in the brains of these patients. This means that c-hGH recipients were most likely exposed to the proteins of these neurodegenerative diseases, but this did not lead to human-to-human transmission of the disease.
"This group is an invaluable resource, and it is imperative to continue monitoring it, especially since we are increasingly understanding how pathology progresses in neurodegenerative diseases," said David Irwin, MD, a researcher at CNDR and the Department of Neurology at the Perelman School of Medicine, lead author of an article about the study published on–online in the journal JAMA Neurology.
The work was attended by specialists from the Centers for Disease Control and Prevention of the United States (U.S. Centers for Disease Control and Prevention) and the U.S. Department of Health and Human Services (U.S. Department of Health and Human Services).
Article by David J. Irwin et al. Evaluation of Potential Infectivity of Alzheimer and Parkinson Disease Proteins in Recipients of Cadaver-Derived Human Growth Hormone Alzheimer and Parkinson Potential Infectivity published in JAMA Neurology
Portal "Eternal youth" http://vechnayamolodost.ru08.02.2013