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It is hypothesized that retrotransposons have played a fundamental role in primate evolution and that enhanced neurologic retrotransposon activity in humans may underlie the origin of higher cognitive function. As a potential consequence of this enhanced activity, it is likely that neurons are susceptible to deleterious retrotransposon pathways that can disrupt mitochondrial function. An example is observed in the  TOMM40  gene, encoding a β‐barrel protein critical for mitochondrial preprotein transport. Primate‐specific  Alu  retrotransposons have repeatedly inserted into  TOMM40  introns, and at least one variant associated with late‐onset Alzheimer's disease originated from an  Alu  insertion event. We provide evidence of enriched  Alu  content in mitochondrial genes and postulate that  Alus  can disrupt mitochondrial populations in neurons, thereby setting the stage for progressive neurologic dysfunction. This  Alu  neurodegeneration hypothesis is compatible with decades of research and offers a plausible mechanism for the disruption of neuronal mitochondrial homeostasis, ultimately cascading into neurodegenerative disease.

alzheimer's and dementia

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