University of Minnesota Medical School researchers have identified one of the earliest neurologic fingerprints associated with neurodegenerative diseases such as Alzheimer's— an abnormal buildup of a protein in the brain called "tau."
According to neuroscientists Karen Ashe, Ph.D., from the University of Minnesota and the Minneapolis VA Health Care System, and Dezhi Liao, Ph.D., from the University of Minnesota, a buildup of tau can disrupt the brain's communication abilities even before noticeable symptoms occur.
The research, published in the December 22 issue of the journal Neuron may help guide development of therapeutic strategies that precede irreversible degeneration in some parts of the brain. Such degeneration is a defining feature of neurodegenerative disorders called “tauopathies,” which include Alzheimer's disease and other dementias.
Normally, tau proteins act as stabilizers in the body's cells – most notably within the central nervous system. When defective, prior research has shown that abnormal tau levels can form brain-damaging deposits, and that too much of the protein can contribute to Alzheimer's disease and other dementias.
“Research has shown that in neurodegenerative disorders such as Alzheimer's, that more tau is present in the cell body, and that an accumulation of tau proteins can induce neurodegeneration,” said Ashe, the study's lead author. “But no prior study has addressed how tau diminishes brain function. Our study was designed to show how tau can impact the decline of brain functioning so that therapies can be designed to combat the trend.”
Ashe and Liao found that early accumulation of tau in the portion of the brain responsible for conducting electrochemical stimulation – structures known as dendritic spines– are directly correlated to neurodegenerative disorders. To prove the correlation, the researchers expressed fluoresced tau proteins into neurons and directly monitored the communication along dendritic spines. These structures are sites where there lies a link between two neurons.
“The abnormal accumulation of tau proteins in dendritic spines, which are the fundamental computation units in the brain just like the 1 and 0 in computers, causes early memory deficits by directly disrupting neuronal communication,” said Liao. “These findings capture what is likely the earliest synaptic dysfunction that precedes synapse loss in neurodegenerative disorders.” “Understanding the key interactions that occur prior to neuronal loss will become increasingly important as preventative strategies shift the timing of interventions to pre-degenerative phases of disease,” added Ashe.
Adapted from the University of Minnesota