Numerous trials have been run hoping to develop and validate drugs which would either slow, stop, or reverse the development of Alzheimer’s in humans. Yet over several decades none have succeeded. Almost all of these attempts have been based on the “amyloid hypothesis”, and consequently, some researchers have started looking in new directions.

One exciting such new direction involves mitochondrial DNA, which we inherit from our mothers, but not our fathers. This difference might account for the fact that people whose family history showed Alzheimer’s on their mother’s side were more likely to get Alzheimer’s than people whose family history only showed Alzheimer’s on the father’s side. So various mitochondrial diseases and failures could be genetically responsible for the development of Alzheimer’s in the brain.

It is widely regarded that most non-human primates do not exhibit Alzheimer’s, although they exhibit related symptoms and brain changes. The new study focused on the idea that thus, Alzheimer’s ought to have come about in human beings due to some evolutionarily recent change in our brains setting us apart from existing primate species. The study focused on one such change, the development of “retrotransposons”, or so-called “jumping genes”.

An excellent extended exposition of this work is available at

When copy-paste attacks: A possible answer to the mystery of Alzheimer’s disease

Another article about the work is

‘Jumping genes’ may set the stage for brain cell death in Alzheimer’s, other diseases

The research publication itself is at

The Alu neurodegeneration hypothesis: A primate-specific mechanism for neuronal transcription noise, mitochondrial dysfunction, and manifestation of neurodegenerative disease

Links to the articles and the research publication have been posted in Alzheimers > Risk Factors > Genetics.