Alzheimer’s Disease Mechanism Traced to Genetic Defect That Lowers Levels of a Mitochrondrial Protein

Alzheimer’s Disease Mechanism Traced to Genetic Defect That Lowers Levels of a Mitochrondrial Protein
Researchers at two Norwegian institutions found that deficits in the mitochondrial protein PITRM1 led to an accumulation of amyloid-beta, whose deposits in the brain are known to cause Alzheimer's disease. The findings, drawn from a study of a family with a rare genetic defect, further suggest that mitochondria is a key player in neurodegenerative diseases. The study, Defective PITRM1 mitochondrial peptidase is associated with Ab amyloidotic Neurodegeneration, was published in the journal EMBO Molecular Medicine.
Subscribe or to access all post and page content.