Is Alzheimer's Disease Transmissible?

Key points
- In rare circumstances, Alzheimer's disease might be transmissible, a study suggested.
- "In addition to sporadic Alzheimer's disease and inherited or familial Alzheimer's disease, there could also be acquired forms of Alzheimer's disease," according to John Collinge, MD, of University College London, and colleagues.
- But Collinge and outside experts cautioned that the research - based on an observational study of just eight people - is very preliminary and doesn't yet prove that the disease, or even some of its underlying pathology, can be transmitted.
- 10 issue of Nature, Collinge and colleagues reported that autopsies of eight people who died of iatrogenic Creutzfeldt-Jakob disease (CJD) showed four had unexpectedly severe plaques of amyloid-β (Aβ), a protein associated with Alzheimer's.
In rare circumstances, Alzheimer's disease might be transmissible, a study suggested.
"In addition to sporadic Alzheimer's disease and inherited or familial Alzheimer's disease, there could also be acquired forms of Alzheimer's disease," according to John Collinge, MD, of University College London, and colleagues.
But Collinge and outside experts cautioned that the research - based on an observational study of just eight people - is very preliminary and doesn't yet prove that the disease, or even some of its underlying pathology, can be transmitted.
In the Sept. 10 issue of Nature, Collinge and colleagues reported that autopsies of eight people who died of iatrogenic Creutzfeldt-Jakob disease (CJD) showed four had unexpectedly severe plaques of amyloid-β (Aβ), a protein associated with Alzheimer's. Another three patients had lower levels of the protein.
"The Aβ deposition in the gray matter was typical of that seen in Alzheimer's disease and Aβ in the blood vessel walls was characteristic of cerebral amyloid angiopathy," they reported. Moreover, the deposits were not located in the same places where the Creutzfeldt-Jakob prions were deposited.
The eight patients had been treated in childhood with human growth hormone derived from pituitary glands taken from cadavers, a practice that was stopped in 1985 when it was shown that some recipients were developing CJD.
"Very much to our surprise," Collinge told reporters in a telephone briefing, four showed excess amyloid-β, although they were relatively young - ages 36 to 51 - and had none of the genetics associated with early-onset Alzheimer's.
The findings suggested that there might be "proteopathic seeds" of Alzheimer's that can be transmitted in the same way as the prions associated with CJD and other prion diseases.
On the other hand, Collinge said, there was no evidence of the neurofibrillary tangles of tau protein, the other characteristic aspect of Alzheimer's pathology. In addition, none of the patients had developed Alzheimer's before they died of CJD, he stated.
The notion that some neurological diseases might be transmitted in the form of proteopathic seeds has been gaining traction. Indeed, amyloid-β "seeds" can lead to the accumulation of the protein in the brains of experimental mice, noted Mathias Jucker, PhD, of the University of Tübingen in Germany and Lary Walker, PhD, of Emory University in Atlanta.
In an accompanying article in Nature, they argued that the findings by Collinge and colleagues are "fresh support for this seeding concept in a clinically relevant setting."
On the other hand, the finding is likely to "result in a lot of misleading headlines," commented David Allsop, PhD, of the University of Lancaster in England.
Written and revised by
Gerald Hurowitz, M.D.
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