Last year we reported that the protein, alpha-synuclein, behaves in an infectious way in two neurodegenerative diseases: multiple system atrophy and progressive supranuclear palsy (read the article here). Prion diseases are a group of neurodegenerative diseases that are caused by the build up of an abnormal folded version of a naturally-occurring cellular protein. The misfolded prion proteins will induce misfolding of normal prion proteins leading to a kind of chain reaction. The typical feature of prions is that they behave in an infectious manner. For example, variant Creutzfeldt–Jakob disease (vCJD) can be transmitted through eating meat from sick animals.
What is Alzheimer’s?
Alzheimer’s disease is a progressive neurodegenerative disease. Three characteristic changes have been described in the brains of Alzheimer’s disease patients:
(1) senile plaques, (2) neurofibrillary tangles, and (3) brain atrophy.
Senile plaques are extracellular deposits of amyloid-beta, an abnormal protein believed to be toxic to neurons. In addition many Alzheimer’s disease patients also have deposits of amyloid-beta in the blood vessels of the brain, a condition known as cerebral amyloid angiopathy.
Could Alzheimer’s be transmissible?
Amyloid-beta pathology can be induced in mice and monkeys by injecting amyloid-beta extracted from Alzheimer’s diseased brains into the brain of these animals. Last year researchers published a paper in Nature showing that 4 out of 8 people who had developed Creutzfeldt–Jakob disease (CJD) after receiving growth hormone injections derived from people suffering from CJD also had amyloid-beta pathology in their brains. Given the young age of these CJD victims it seems unlikely that the amyloid pathology was spontaneous and more likely that it had been transferred together with the CJD prions in the growth hormone injections. However, none of these patients had the characteristic neurofibrillary tangles in their brain, although it remains possible that they died from the CJD before this hallmark of Alzheimer could develop. It is also noteworthy that a previous study in JAMA Neurology (70: 462) did not find evidence of a higher incidence of Alzheimer’s disease in people who received cadaveric growth hormone injections but this research was based on the death certificates without autopsy data.
Now, a new paper appeared in the Swiss Medical Weekly that shows similar findings in patients who developed CJD after receiving surgical grafts of dura mater (the membrane that covers the brain and spinal cord). These patients underwent brain surgery that required a dura mater graft 11 to 25 years before the death. Five of the seven studied patients (aged between 28 and 63 years) had amyloid-beta deposits in the blood vessels and in the brain matter. The youngest patient was 6 at the time of surgery and needed a dura mater graft after an injury. Twenty-two years later the patient died from CJD and when his brain was investigated it contained amyloid-beta plaques. Amyloid-beta plaques are highly unusual that this young age. However, it should be pointed out that this study cannot eliminate the possibility that the trauma or underlying disease leading to the need for a dura mater graft or the neurosurgery contributed to the amyloid-beta pathology.
The combined evidence from these two studies together with the animal research suggests that amyloid-beta may be transferred from one person to another through contaminated biological materials. Furthermore, prion diseases are also known to be transmissible through surgical instruments and previous research has found that amyloid-beta remains infectious in mice after a two year long storage in formalin (Acta Neuropathol 128: 477). However, more evidence is needed before we can unequivocally establish that amyloid-beta is transmissible.
Read more in Nature
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