‘Transmissible’ Alzheimer’s theory gains traction

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‘Transmissible’ Alzheimer’s theory gains traction

Dec 26, 2018


Neuroscientists have garnered more evidence for the hypothesis regarding sticky proteins, which is a symbol of neurodegenerative diseases. This can be transferred between people under particular conditions and also cause new damage in a brain of recipient. Their research does not hint that disorders such as Alzheimer’s disease are contagious, however it raises eyebrows that medical and surgical procedures pose a risk of transmitting such proteins between humans. The researchers revealed regarding wide deposits of a protein called amyloid-beta during post-mortem studies of the brains of four people in the United Kingdom. It is treated for short stature during childhood with growth-hormone preparations derived from the pituitary glands of donors after death. The recipients had died in middle-age of a rare but deadly neurodegenerative condition called Creutzfeldt-Jakob disease (CJD), caused by the presence in some of the growth-hormone preparations of an infectious, and misfolded protein or prion, which causes CJD.

Seeds of trouble

Amyloid plaques in blood vessels in the brain are a hallmark of a disease called cerebral amyloid angiopathy (CAA) and cause local bleeding. In Alzheimer’s disease, amyloid plaques are typically accompanied by another protein called tau and lead the researchers concern regarding transmission. The team has squarely tested the hypothesis that these proteins could be transmitted between humans through contaminated biological preparations. When the researchers analysed the samples, their suspicions were confirmed: they found that some of the batches contained substantial levels of amyloid-beta and tau proteins.

Mouse tests

To test whether the amyloid-beta in the batches could cause the amyloid pathology, they injected samples directly into the brains of young mice, which are genetically engineered, to be susceptible to amyloid pathology. The mice had developed extensive amyloid plaques and CAA by mid-life. Control mice that received either no treatment or treatment with synthetic growth hormone didn’t have amyloid build up.

Surgical implications

The transmissibility of the amyloid-beta could be preserved after so many decades underlines that is the need for caution. The sticky amyloid clings tightly to materials used in surgical instruments, resisting standard decontamination methods. But as degenerative diseases take a long time to develop, the danger of any transfer may be in the case of childhood surgery where instruments have also been used on old people.

The epidemiologists have not been able to assess whether a history of surgery increases the risk of developing a neurodegenerative disease in later life. Major population cohort studies, such as the US Framingham Heart Study, are open to collect information about participants’ past surgical procedures, along with other medical data.

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