Scientists have long known that amyloid β (Aβ) deposits in
the brain are a hallmark of Alzheimer disease and that this neurotoxic protein
is somehow connected with damage to mitochondria that triggers the generation
of free radicals and death of neurons. Now, an international team of researchers
has identified a direct link between these two elements, providing a potential
new target for treating the brain-ravaging disorder (Science. 2004;304:228-452).
Researchers from Columbia University in New York City, and colleagues
at other institutions in the United States, China, and Scotland, discovered
that Aβ enters the mitochondria of brain cells and interacts there with
an enzyme called Aβ-binding alcohol dehydrogenase (ABAD) to form a complex.
Aβ-ABAD complex was present in the brain of patients who died of Alzheimer
disease and in mice that are genetically engineered to produce a precursor
for Aβ, but little was found in brain tissue from nondemented age-matched
patients or from control mice.
Stephenson J. New Alzheimer Disease Target Identified. JAMA. 2004;291(17):2063. doi:10.1001/jama.291.17.2063