‘No evidence’ of Alzheimer transmission by neurosurgery

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A study published in the medical journal Nature has provoked media coverage. The study speculated that it might be possible to transmit Alzheimer’s disease during certain surgical procedures. The study looked at the brains of eight people who had died of Creutzfeldt-Jakob disease (CJD) during the 1970s following treatment with brain-derived human growth hormone (HGH). HGH is used to treat short stature and, before the risks of CJD were fully known, was derived from the brain tissue of deceased donors, some of whom had CJD.

The research team found that in four out of the eight brains studied there were also signs associated with Alzheimer’s disease. As these people were outside the age range associated with such signs, the researchers speculate that Alzheimer’s might also have been transmitted by the same route as the CJD. They theorise that it could be possible for Alzheimer’s disease to be transmitted by instruments used in brain surgery that are contaminated with infected brain material.

An UK National Health Service report says this was a small study and this is not evidence that Alzheimer’s disease can be transmitted during neurosurgery or any other form of treatment. There is no suggestion that Alzheimer’s disease is contagious.

UK Chief Medical Officer Professor Dame Sally Davies said: “There is no evidence that Alzheimer’s disease can be transmitted in humans, nor is there any evidence that Alzheimer’s disease can be transmitted through any medical procedure. This was a small study on only eight samples. We monitor research closely and there is a large research programme in place to help us understand and respond to the challenges of Alzheimer’s. I can reassure people that the NHS has extremely stringent procedures in place to minimise infection risk from surgical equipment, and patients are very well protected.”

Dr Doug Brown, director of research at Alzheimer’s Society, said: “There are too many unknowns in this small, observational study of eight brains to draw any conclusions about whether Alzheimer’s disease can be transmitted this way.”

The report says from 1985, the use of brain-derived human growth hormones stopped and a synthetic version was used instead. Modern treatments are regulated, licensed and considered extremely safe. No contagious disease is associated with these modern treatments. As the paper itself says, there is no suggestion that Alzheimer’s disease is contagious.

There has so far been no evidence of Alzheimer’s disease being transmitted through surgery. This study has made a possible link in four cases of specific treatment with growth hormone before 1985, but, the report says, it is important not to jump to conclusions about what this important, but small, research study might mean. There has never been a proven case of transmission by neurosurgery.

The report says this research only relates to treatment by injection with human pituitary-derived growth hormone. Published studies have looked at this question but have found no evidence that blood transfusion is a risk.

Abstract
More than two hundred individuals developed Creutzfeldt–Jakob disease (CJD) worldwide as a result of treatment, typically in childhood, with human cadaveric pituitary-derived growth hormone contaminated with prions1, 2. Although such treatment ceased in 1985, iatrogenic CJD (iCJD) continues to emerge because of the prolonged incubation periods seen in human prion infections. Unexpectedly, in an autopsy study of eight individuals with iCJD, aged 36–51 years, in four we found moderate to severe grey matter and vascular amyloid-β (Aβ) pathology. The Aβ deposition in the grey matter was typical of that seen in Alzheimer’s disease and Aβ in the blood vessel walls was characteristic of cerebral amyloid angiopathy3 and did not co-localize with prion protein deposition. None of these patients had pathogenic mutations, APOE ε4 or other high-risk alleles4 associated with early-onset Alzheimer’s disease. Examination of a series of 116 patients with other prion diseases from a prospective observational cohort study5 showed minimal or no Aβ pathology in cases of similar age range, or a decade older, without APOE ε4 risk alleles. We also analysed pituitary glands from individuals with Aβ pathology and found marked Aβ deposition in multiple cases. Experimental seeding of Aβ pathology has been previously demonstrated in primates and transgenic mice by central nervous system or peripheral inoculation with Alzheimer’s disease brain homogenate6, 7, 8, 9, 10, 11. The marked deposition of parenchymal and vascular Aβ in these relatively young patients with iCJD, in contrast with other prion disease patients and population controls, is consistent with iatrogenic transmission of Aβ pathology in addition to CJD and suggests that healthy exposed individuals may also be at risk of iatrogenic Alzheimer’s disease and cerebral amyloid angiopathy. These findings should also prompt investigation of whether other known iatrogenic routes of prion transmission may also be relevant to Aβ and other proteopathic seeds associated with neurodegenerative and other human diseases.

National Health Service material
Nature abstract


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