The paper
B. Eftekharzadeh et al., “Tau protein disrupts nucleocytoplasmic transport in Alzheimer’s disease,” Neuron, 99:925–40.e7, 2018.
Dotted along the edges of neuronal cells’ nuclei are protein complexes that act like border agents, carefully monitoring the RNAs and proteins that move into and out of the command center of the cell. Disruptions at the border—such as an improper flux of certain proteins—can cause problems for the cell and may underlie Alzheimer’s disease (AD) and other neurological conditions.
Researchers have previously linked defects in the gatekeeping protein structures—called nuclear pore complexes—with aging, amyotrophic lateral sclerosis, and other neurological diseases. But a new study “demonstrates that nuclear pore impairment seen in AD is likely a primary target of the disease, rather than a nonspecific defect,” Hong Joo Kim, a cell and molecular biologist at St. Jude Children’s Research Hospital who was not involved in the work, tells The Scientist.
Past studies have ...
