You Can’t Catch Alzheimer’s Disease, Can You?

You Can’t Catch Alzheimer’s Disease, Can You?

By Guest Blogger,
Tyler Kokjohn, PhD.

Transmissible ADAlzheimer’s disease (AD) does not spread from person to person like a cold virus, but some recent findings suggest the unsettling possibility it might be transmitted through medical procedures (1).

Deadly diseases have been transmitted through medical procedures such as blood transfusions, organ transplants and surgery.  In fact, this new concern about AD was sparked by the grim legacy of a past medical practice in which hormone preparations obtained from human cadavers were injected into children who were not growing normally.  What the physicians did not know at the time was that pathologic prions, abnormally shaped proteins producing the rapidly lethal neurodegenerative illness known as Creutzfeldt-Jakob disease (CJD), contaminated some of these hormone preparations.  Over two hundred cases of fatal CJD appeared ultimately in patients who had received cadaveric growth hormone supplements (2).

An unforeseeable sequence of events is thought to have led to the cadaveric growth hormone therapy tragedy.  CJD is a rare disease most often appearing in persons over age 60 (3).  Although clinically obvious CJD is rare, protein mis-folding occurs spontaneously during normal aging and many outwardly healthy persons die with some pathologic prions in their brains.  Perhaps these individuals would have succumbed to CJD if they had lived a little longer.  Hormone therapy necessitated pooling pituitary tissue from large numbers of deceased donors some of whom probably harbored toxic CJD prions without exhibiting any signs or symptoms of disease.  Unfortunately, over 200 hormone recipients received enough pathologic prions during their treatments to develop CJD in short order.

Examination of brain tissue samples from a small group of the growth hormone recipients who died of CJD revealed half of them had amyloid deposits reminiscent of those found in AD patients.  However, these patients were much younger than the typical AD patient and finding such amyloid deposits in them was unexpected.  After ruling out the possibility the results could be explained by genetic mutations linked producing early onset AD, the investigators recognized there was an alarming possibility some CJD prion-contaminated growth hormone injections also transmitted this key pathologic change linked to AD dementia as well.

Another medical procedure, transplantation of cadaveric dura mater, the tough outer covering of the brain, has also been recognized to have transmitted CJD.  A second study of several deceased CJD patients who had received transplants of cadaveric dura mater (the tough outer covering of the brain) revealed the presence of AD amyloid pathology in some of them.  The observations may be explained in several ways, but the results are consistent with the idea that that dura mater transplants also promoted amyloid pathology development.

These new observations have potentially staggering implications.  Scientists do not know how prions produce the massive neurodegeneration characteristic of CJD, but they have convincing evidence the process begins when a normal protein changes its shape.  These abnormal prions seed and spread this neurotoxic change throughout the brain by initiating a relentless chain reaction which forces their remaining normal relatives to adopt the pathologic shape.  The toxic seeds may appear spontaneously, but CJD has been confirmed to have been transferred through several types of medical interventions including contaminated growth hormone injections, surgical procedures and transplants.  Pathological changes associated with several neurodegenerative disorders may spread through the brain using similar prion-like mechanisms (4), prompting concern that medical procedures could also spread AD and other conditions as well.  Discovering some recipients of cadaveric growth hormones and dura mater grafts who died of CJD (5) also had amyloid deposits suggests these treatments introduced the seeds necessary to initiate both CJD and AD-like pathologic changes.

CJD is a rare disease and to see an explosion of cases due to hormone replacement therapy and transplants was shocking.  Cadaveric pituitary hormone replacement therapy was eliminated over 30 years ago when brain extracts were supplanted by synthetic preparations and dura mater grafts are no longer performed.  While the epidemic of induced CJD seems to have subsided, the question now is whether another problem has been exposed.  AD is a far more common affliction than CJD, suggesting that hormone replacement injections and transplants were much more likely to have introduced amyloid seeds than CJD prions.  The true proportion of persons injected with cadaveric hormones or receiving dura mater transplants who consequently developed amyloid deposits in their brains is unknown.  This group is still comparatively young and only a small number of them have come to autopsy and been studied to date.  Conceivably a high proportion of them are incubating prions today and could go on to ultimately develop dementia or suffer the toxic effects of amyloid deposits.

Unfortunately, because AD is widespread, if the ideas as to how this pathology extends itself are correct the number of persons being seeded with toxic amyloid through medical procedures might be enormous.  Pathologic prions are notoriously difficult to inactivate (6) and with neurosurgery where there is a high risk they might be present, stringent methods are employed to prevent their spread.  Because pathologic prions are so tough to eliminate there is a possibility that medical protocols performed with less stringent precautions such as general surgery conducted at other body sites, transplants and blood transfusions have all been inadvertently spreading the seeds of toxic amyloid.  It is important to note that what has been seen in the deceased pituitary hormone and dura mater graft recipients is not precisely AD, but an apparent transmission of amyloid pathology similar to that typical of demented patients.  In addition, to date only brain-associated materials have been identified as a possible source of putatively neurotoxic amyloid seeds.  However, even if ‘only’ an amyloid pathology was seeded and spread within these patients, such deposits are potentially toxic and therefore cause for great concern.

AD is not contagious, but is it transmissible by medical procedures?  At this point we still have only a vague understanding of the natural history of prion diseases.  Newly arising information suggests a pathological change linked to AD, amyloid deposits, could be seeded or accelerated by some invasive medical interventions, but the frequency of such events and the degree of threat posed by them is uncertain.  Work is in progress to confirm these observations and establish their potential implications for human health

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(1)   A. Abbott.  2016. The red-hot debate about transmissible Alzheimer’s.  Nature 16 March 2016. http://www.nature.com/news/the-red-hot-debate-about-transmissible-alzheimer-s-1.19554

(2)   B. S. Appleby et al.  2013.  Iatrogenic Creutzfeldt-Jakob disease from commercial cadaveric human growth hormone.  Emerging Infectious Disease. 19(4): 682–684. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3647424/)

(3)   Creutzfeldt-Jakob Disease Fact Sheet.  http://www.ninds.nih.gov/disorders/cjd/detail_cjd.htm

(4)   G. Miller. 2009.  Could they all be prion diseases? Science 326:1337-1339.  http://science.sciencemag.org/content/326/5958/1337.full

(5)   A. Abbott.  2016.  More evidence emerges for ‘transmissible Alzheimer’s’ theory.  Nature 26 January 2016. http://www.nature.com/news/more-evidence-emerges-for-transmissible-alzheimer-s-theory-1.19229

(6)   D. Dormont.  2002.  Prion diseases: Pathogenesis and public health concerns. FEBS Letters 529:17-21.  http://onlinelibrary.wiley.com/doi/10.1016/S0014-5793(02)032684/abstract;jsessionid=A70616D5CBA695BB66402DBAB86FBBEC.f04t02

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