Since the 1960s and 1970s, especially after the discovery of the very rare Creutzfeldt-Jakob degenerative brain disease (CJD), some researchers have hypothesized about the transmission of neurodegenerative diseases between humans. Among them Alzheimer’s himself. In this regard, a scientific article has been published in Nature that, according to Dr. Sagrario Manzano Palomo. Neurologist and coordinator of the Behavior and Dementia Study Group of the Spanish Neurology Society, she has not been correctly interpreted by the media.
From the Spanish Society of Neurology they have launched an informative press release on the scientific publication and the conclusions reached by said study in which they wanted to point out several controversial points:
• These headlines have been generated secondary to a scientific article published in a medical journal where the theoretical possibility of transmission of a type of dementia is discussed. Transmission and contagion are totally different words in the field of medicine . Contagion is when there is the possibility of the spread of a disease from one individual to another and in no case has it been discussed in said study. Also, Alzheimer’s and dementia are not synonymous.
• This study has analyzed the brains of some patients who as children were treated with human growth hormone obtained from the cadaver . A practice that was carried out long before it could be obtained artificially, as it is done today.
• According to the study, a small group of these children obtained this hormone from corpses that had a prion disease, Creutzfeldt-Jakob disease (CJD). Creutzfeldt-Jakob disease is a tremendously rare disease and very different from Alzheimer’s disease . For this disease, which conditions rapidly progressive dementia, there are both genetic and sporadic cases that are contracted iatrogens (by transmission). The cases analyzed in the article (only 8 patients) developed the disease decades later, with all the peculiar brain changes that prion disease entails.
• In the study led by researchers John Collinge and Sebastian Brandner, the word Alzheimer’s is never mentioned . He mentions a protein called “abnormally folded beta-amyloid.” Having this altered protein is not synonymous with having Alzheimer’s disease, as there are other diseases in which it is also altered (such as Creutzfeldt-Jakob disease) and they are not Alzheimer’s disease. Furthermore, the existence of another alteration in the brains of these patients, very characteristic of Alzheimer’s disease, which is neurofibrillary tangles, is not mentioned, therefore it cannot be extrapolated that these subjects have Alzheimer’s.
• Furthermore, clinically, these 8 patients developed dementia associated with their prion disease, not Alzheimer’s disease. Therefore, this is a misguided interpretation that must be clarified for the good of all.
• There have therefore been several misinterpretations of the work carried out by researchers John Collinge and Sebastian Brandner, making amyloid plaques equivalent to Alzheimer’s disease and also between transmission and contagiousness.
• Furthermore, although the published article is very interesting because it talks about the (theoretical) possibility that the introduction of beta-amyloid protein in a healthy brain could generate amyloidosis , it is not definitive either. You have to analyze the data with caution, like everything in medicine, and see if they are reproducible.
• The Study Group on Behavior and Dementias of the Spanish Neurology Society asks, in view of this type of information, caution when trying to simplify scientific terms and more so when it comes to medicine. Headlines such as those that have been generated as a result of the misinterpretation of this study, can generate a lot of fear and uncertainty among patients and their families.
