Diseases like Mad Cow, Kuru, and Creutzfeldt-Jakob are caused by misfolded proteins called prions, which propagate by inducing misfolding in normal proteins and cause human to human transmission, when people come in contact with infected brain tissue. Misfolded proteins cause neuronal death due to increased aggregation. Neuronal cell death due to protein aggregation is also responsible for causing diseases like Parkinson's, ALS, and Alzheimer’s disease. However, there have been no reports thus far of human-to-human transmission of factors causing Parkinsons, Alzheimer’s, and ALS.

The scientists used to suspect that there would be a possibility of propagation of misfolded amyloid plaques in Alzheimer’s, similar to that occurring in prion disease. In some studies, when minute amounts of amyloid-beta material were injected into the brains of mice and monkeys, the injected material initiated a chain propagation reaction, leading to the development of full-scale Alzheimer’s disease in the animals.

Now, scientists have discovered possible first evidence for human-to-human transmission of the misfolded proteins of Alzheimer’s disease. Since minute amounts of the brain material may be transferred during neurological/ neurosurgical procedures by re-usage of surgical equipment or hormonal injections derived from brain tissue, the scientists at University College London investigated the presence of amyloid beta proteins in the brains of 8 individuals who died due to Creutzfeldt-Jakob disease. All these eight patients had developed Creutzfeldt-Jakob disease from receiving prion-contaminated growth hormone injections, derived from the pituitary gland extract of Creutzfeldt-Jakob disease individuals. They found that six out of eight individuals also had a widespread presence of amyloid beta proteins. These individuals were in the age group 36 to 51 years, which is too low for the appearance of beta-amyloid proteins in the brain, suggesting that the beta-amyloid material might have been transferred during prion transmission.

The results of the study open up the possibility of human-to-human or animal-to-human transmission of Alzheimer’s disease due to contact with brain tissue, or it may suggest another possibility of prions inducing beta amyloid aggregate formation in infected brains.  This study may have opened a can of worms and suggests a need for further investigation, in order to rule out contagious spread of Alzheimer’s disease, however, remote the possibility.

Written by Dr. Ashish Patil

Primary Reference

Jaunmuktane, Z., Mead, S., Ellis, M., Wadsworth, J., Nicoll, A., Kenny, J.,Brandner, S. (2015). Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy. Nature, 247-250.

DoveMed Resources

Parkinson's Disease (PD). (n.d.). Retrieved September 14, 2015, from http://www.dovemed.com/parkinsons-disease-pd/

Amyotrophic Lateral Sclerosis (ALS). (n.d.). Retrieved September 14, 2015, from http://www.dovemed.com/amyotrophic-lateral-sclerosis-als/

Alzheimer's Disease (AD). (n.d.). Retrieved September 14, 2015, from http://www.dovemed.com/alzheimers-disease-ad/

Additional References

Prusiner, S. (n.d.). Prions are novel infectious pathogens causing scrapie and creutzfeldt-Jakob disease. Bioessays, 281-286