A UCLA imaging study has showed that age-related breakdown of myelin, the fatty insulation coating the brain's internal wiring, correlates strongly with the presence of a key genetic risk factor for Alzheimer disease.
The findings are detailed in the January edition of the journal Archives of General Psychiatry and add to a growing body of evidence that myelin breakdown is a key contributor to the onset of Alzheimer disease later in life.
In addition, the study demonstrates how genetic testing coupled with non-invasive evaluation of myelin breakdown through magnetic resonance imaging may prove useful in assessing treatments for preventing the disease.
"Myelination, a process uniquely built up in humans, arguably is the most important and most vulnerable process of brain development as we mature and age," said Dr. George Bartzokis, professor of neurology at UCLA's David Geffen School of Medicine.
"These new findings offer, for the first time, compelling genetic evidence that myelin breakdown underlies both the advanced age and the principal genetic risks for Alzheimer disease."
The Apolipoprotein E (ApoE) genotype is the second most influential Alzheimer risk factor, after only advanced age.
The study used MRI to assess myelin breakdown in 104 healthy individuals between ages 55 and 75 and determine whether the shift in the age at onset of Alzheimer disease caused by the ApoE genotype is associated with age-related myelin breakdown.
The results show that in later-myelinating regions of the brain, the severity and rate of myelin breakdown in healthy older individuals is associated with ApoE status.
Thus both age, the most important risk factor for Alzheimer disease, and ApoE status, the second-most important risk factor, seem to act through the process of myelin breakdown.