Mitochondria are the powerhouses of the cell, generating the energy needed to function and survive. In Alzheimer's disease, abnormal levels of beta-amyloid damage brain mitochondria, leading to neuronal dysfunction. A team led by investigators at Columbia University, New York City, found that beta-amyloid interacts with mitochondria by binding to a mitochondrial enzyme called ABAD (beta-amyloid-binding alcohol dehydrogenase) (Yao et al., 2011). Treating Alzheimer's model mice with a peptide that blocks beta-amyloid binding to ABAD improved mitochondrial function and also alleviated the mice's memory deficits. This study strongly implicates mitochondrial beta-amyloid as a critical player in the development of Alzheimer's disease.
Synapses depend on nearby mitochondria to generate the energy needed for proper functioning. A study led by Harvard University, Cambridge, MA, researchers showed that abnormal forms of tau disrupt this process (Kopeikina et al., 2011). In mice expressing a mutant form of human tau, neurons lacked the mitochondria needed for proper functioning; similar abnormalities were seen at autopsy in people diagnosed with Alzheimer's. The researchers also found that tau does not have to form thread-like fibrils to disrupt mitochondria from delivering energy to synapses. Rather, reduced levels of normal tau in mouse models are enough to disrupt the process.