Could Alzheimer’s be infectious?
Comments (0) A recent paper in the journal Science provides some evidence that Aβ can, like the prion protein, initiate the nucleation-polymerization in cells into which it is introduced.
Meyer-Luehmann, et al used two strains of transgenic mice in their experiments. Mice of one strain (APP23) over-produce the 40-amino-acid Aβ peptide, while mice of the other strain (APPPS1) over-produce the 42-amino acid peptide. In both strains, Aβ plaques are deposited in the brain as the animals age, but the strains differ in the distribution and appearance of the plaques.
The experiments involved taking brain extracts from deceased Alzheimer’s patients or from aged mice of both strains, and injected them into the brains of young mice of both strains, before they had developed the symptoms of the disease. It was observed that all extracts had a seeding activity in both strains of mice – they induced the deposition of the Aβ peptide, which aggregated to form plaques in the brains of the mice into which they had been injected. The seeding activity was both time- and concentration-dependent (i.e. seeding increased with time, and with greater concentrations of Aβ in the extracts), but differed depending on the strain of mouse the extract was taken from, and the strain it was injected into.
However, if the extracts were treated with anti-Aβ antibodies, or heated so that the structure of the Aβ molecules was destroyed, the seeding activity was abolished. Similarly, if the host mice were immunized against Aβ before they were injected with the extracts, seeding did not occur. Finally, no seeding activity was observed when any brain extract was injected into the brain of normal mice, suggesting that, if Alzheimer’s was indeed found to be infectious, an infected individual would have to be genetically predisposed to the condition in order for it to develop.
One could predict that the accumulation of abnormal proteins in other neurodegenerative diseases – e.g. alpha-synuclein in Parkinson’s Disease and huntingtin in Huntington’s Disease, may also occur as a result of a prion-like seeding process. But for me, the most puzzling question of all is this: how would an Alzheimer’s infection be transmitted?
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