Study links fatty myelin breakdown to Alzheimer’s
WASHINGTON (Reuters) – The breakdown of myelin, a sheet of
fat that insulates nerves and helps speed messages through the
brain, appears to be a key contributor to the onset of
Alzheimer’s disease, a study published on Monday said.
Researchers at UCLA, who reported their findings in the
journal Archives of General Psychiatry, used magnetic resonance
imaging to assess the breakdown of myelin in 104 healthy adults
between the ages of 55 and 75.
They found the severity and rate of myelin breakdown was
correlated with the type of APOE, or apolipoprotein-E, gene a
person had. Previous research has shown APOE status to be the
second biggest risk factor for the disease after aging, with a
version called APOE-4 putting persons at highest risk.
The study found the breakdown of myelin, a natural part of
the aging process, proceeded most rapidly for those with
APOE-4, less so for those with APOE-3 and most slowly for those
with APOE-2. APOE-2 is thought to offer some protection from
Alzheimer’s, while APOE-3 is seen as neutral.
“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,” said Dr. George Bartzokis, professor of neurology at
UCLA’s David Geffen School of Medicine.
Myelin has a very high cholesterol content. As it builds
up, cholesterol levels in the brain increase and eventually
promote the production of a toxin that attacks the myelin.
Bartzokis said in an interview the study opened up a
potential avenue to preventive care since it showed you could
track one of the underlying factors for the progressive brain
disorder, which afflicts an estimated 4.5 million Americans.
Combining genetic testing with an MRI evaluation of myelin
breakdown could help assess potential preventive treatments, he
Alzheimer’s disease, the most common form of dementia, is
an irreversible disorder that results in memory loss and a
decline in cognitive abilities.