More than a million people in France have Alzheimer's disease. This pathology results from the slow and propagative degeneration of the brain's neurons, which occurs in association with two cerebral lesions characteristic of the disease: β-amyloidosis, i.e. the accumulation of microscopic clumps of proteinaceous matter (called amyloid plaques), and tauopathy, i.e. the accumulation of abnormal tau proteins (called neurofibrillary tangles). Alzheimer's disease is associated with the aging of the brain and, in some cases, genetic factors. But can it be transmitted via contamination from one person to another?
In humans, epidemiological data already suggest that β-amyloidosis can be transmitted in exceptional circumstances, such as the injection of brain-derived growth hormones or neurosurgery procedures involving brain tissue grafting. To date, tauopathy transmission has not been clearly established, and importantly, the literature has not reported any neurodegenerative processes resulting from the transmission of these lesions.
However, researchers from MIRCen's neurodegenerative diseases laboratory recently showed that the injection of extracts from the brains of human patients with Alzheimer's disease into the brains of gray mouse lemurs (a non-human primate), caused, in these latter, memory disorders and neurodegenerative disease characterized by neuronal loss, impaired neuronal activity, and brain atrophy. Furthermore, they also observed the transmission of the two characteristic lesions, β-amyloidosis and tauopathy.
Their work is the first illustration of the induction of clinical signs associated with neurodegenerative disease via the injection of human Alzheimer's disease brain extracts. It is also the first demonstration of tauopathy induction by contamination from a primate brain (humans being primates) to another.
The team's study in no way implies that Alzheimer's disease is contagious in normal conditions. It does however underline the need for specific precautions in certain neurosurgical procedures where brain-to-brain contamination is a possibility. Such precautions are already taken for prion diseases, which may also be transmitted by brain-to-brain contamination. Particularly, the results reported by the MIRCen team will lead to the exploration of novel mechanisms in Alzheimer's disease and thus a better understanding of the causes of neuronal loss.
Also, the study's results may be interpreted in the setting of the "prion hypothesis" of Alzheimer's disease. In prion diseases, pathogenic prion proteins transmit their misfolded form to healthy prions, thus propagating the pathology. The transmission of Alzheimer-characteristic lesions observed in the MIRCen study suggests that β-amyloid and tau proteins may indeed behave like pathogenic prions. That observation argues in favor of the currently-controversial prion hypothesis in Alzheimer's disease as well as in other neurodegenerative pathologies, such as Parkinson's or Huntington's diseases.