Alzheimer’s disease is a progressive neurodegenerative disorder that affects memory, cognition and behavior. It is characterized by the accumulation of amyloid beta plaques and neurofibrillary tangles in the brain, which impair the function of neurons and lead to cell death. The exact cause of Alzheimer’s disease is unknown, but genetic, environmental and lifestyle factors are thought to play a role.
However, a new study published in Nature Medicine has found evidence of medically acquired Alzheimer’s disease in living people, raising new questions about the possible transmission of amyloid beta protein through certain medical procedures.
Growth hormone therapy linked to Alzheimer’s
The study, led by John Collinge at University College London Institute of Prion Diseases, involved five adults who had growth hormone deficiency as children and received pituitary growth hormone therapy prepared from cadavers between 1959 and 1985. This treatment was discontinued after cases of Creutzfeldt-Jakob disease (CJD), a rare and fatal prion disease, were found to be associated with the administration of contaminated human growth hormone from cadavers.
The five patients developed early-onset dementia symptoms in their 40s or 50s, such as memory loss, language impairment and personality changes. They also showed signs of cerebral amyloid angiopathy (CAA), a condition that causes bleeding in the brain due to the deposition of amyloid beta protein in blood vessels. CAA is often a precursor to Alzheimer’s disease and can increase the risk of stroke and cognitive decline.
The researchers suggest that the patients’ dementia symptoms and CAA may be the result of the transmission of amyloid beta protein from the contaminated human growth hormone they received decades ago. They performed brain scans and cerebrospinal fluid analysis on the patients and found elevated levels of amyloid beta protein and other biomarkers associated with Alzheimer’s disease. They also analysed archived batches of the cadaver-derived growth hormone and found that they contained amyloid beta protein, which could act as seeds for plaque formation when injected into the brain.
Implications and limitations
The study provides the first reported evidence of Alzheimer’s disease being transmitted through a medical procedure in living people. It supports a controversial hypothesis that amyloid beta protein can be seeded in the brain through material taken from cadavers, such as surgical instruments, blood products or organ transplants.
However, the authors and other experts stress that the study is based on a small number of cases and is related to a medical practice that is no longer used. They emphasize that there is no evidence that Alzheimer’s disease can be spread from person to person through everyday activities or routine care.
The study also has some limitations, such as the lack of autopsy confirmation of Alzheimer’s disease diagnosis in the patients, the possibility of other factors influencing their dementia symptoms, such as genetic mutations or vascular risk factors, and the difficulty of establishing a causal link between amyloid beta transmission and clinical outcomes.
Future directions
The study highlights the need for further research on the potential transmission of amyloid beta protein and other neurodegenerative agents through medical procedures. It also calls for more surveillance and precautionary measures to prevent such transmission and ensure patient safety.
The study also opens new avenues for understanding the pathogenesis and treatment of Alzheimer’s disease and other related disorders. It suggests that amyloid beta protein may have infectious properties similar to prions, which could have implications for developing novel therapies that target its seeding and propagation in the brain.