Baylor University Medical Center Proceedings July 2017 - 363

Evidence now predominantly
points to the failure of perivascular lymphatic drainage of Aβ
as a major common factor in
the pathogenesis of both CAA
and AD. Elimination of Aβ is a
multistep pathway involving enzymatic degradation of the parent
protein, absorption of the components into the blood, and drainage
of the components along perivascular lymphatic channels. Each
of these individual elimination
c
d
mechanisms appears to fail as the
aging brain experiences reduction
of enzymatic activity and stiﬀening of cerebral arteries, resulting
in decreased absorption into the
blood and impaired drainage. This
in turn results in accumulation of
Aβ in the brain (3).
While amyloid plaques could
previously be visualized only at
autopsy, a new imaging technique, amyloid PET scan, allows
for the direct visualization of the
Figure 2. Normal Amyvid scan at the level of (a) the Sylvian fissures and (b) the lateral ventricles. Note the greater overall burden and distribution
accumulation of the radiotracer within the white matter (arrows) as opposed to the cortical gray matter (arrowheads), pattern of amyloid plaques via the
resulting in clear gray-white matter distinction. Abnormal Amyvid scan at the level of (c) the Sylvian fissures and (d) the
high-aﬃnity binding of Amyvid
lateral ventricles. Note the increase in radiotracer accumulation throughout the gray matter resulting in diffuse loss of
(Florbetapir F-18) or other similar
gray-white matter distinction (arrows). Amyvid tracer localizes specifically to amyloid plaques. This positive scan indicates
radioisotopes to amyloid plaques
the presence of an extensive plaque burden.
in the brain. A positive amyloid
scan, as seen in our patient, is indicative of moderate to frequent
however, have made neuroimaging, including brain MRI and
amyloid plaques. Of note, there is no similar biomarker for CAA,
PET, a useful adjunct in diﬀerentiating dementia from normal
and based on imaging it is possible that our patient has both dissequelae of aging.
orders. Since a degree of amyloid plaque accumulation can also
MRI, speciﬁcally susceptibility-weighted sequences, aid
be seen in elderly patients without AD, amyloid imaging should
signiﬁcantly in the detection of cerebral amyloid angiopathy
be used as an adjunct to clinical diagnostic evaluation. A nega(CAA), a cerebrovascular disorder characterized by accumulative amyloid scan indicates sparse to no amyloid plaques and is
tion of cerebral beta amyloid protein (Aβ) in the tunica media
inconsistent with a diagnosis of AD (5). A negative amyloid scan
and adventitia of leptomeningeal and cortical vessels. One maniin a patient who has a clinical diagnosis of AD has been shown to
festation of this disorder is the accumulation over time of many
be of great clinical value, as it suggests a misdiagnosis and often
small, often clinically silent microhemorrhages, as was demonresults in changes to subsequent therapeutic planning (6).
strated in our patient. Other presentations include acute lobar
Currently, there is a lack of eﬃcacious drugs targeted for
hemorrhage, small-vessel infarcts, and leukoencephalopathy (2).
removing or reducing production of amyloid. However, several
CAA is a degenerative disease found primarily in the elderly,
new targeted drugs for AD therapy are being researched and,
and while evidence of CAA is found incidentally at autopsy in
should a drug prove eﬀective, it is reasonable that diagnosis of
30% of asymptomatic elderly individuals, it is found at a much
AD at the earliest possible stage would be advantageous in terms
higher rate (90%-96%) in autopsies of patients with AD (3).
of initiating treatment and slowing progression of the disease.
Studies have shown that AD results from abnormal deposition
Amyloid PET imaging, particularly as part of a multimodality
of the same amyloid protein subtype-Aβ-as seen in CAA
neuroimaging approach in combination with MRI, is a valuable
(3). Whereas in CAA the deposition of Aβ is within the vascuadjunct to standard neuropsychological testing in this context.
lature, in AD it is within the brain parenchyma itself (4). This
results in the formation of amyloid plaques in the brain. While
1. World Health Organization and Alzheimer's Disease International.
these plaques can be found normally in the aging brain, they
Dementia: A Public Health Priority. Geneva, Switzerland: WHO, 2012.
are found in far greater number and with a more widespread
2. Chao CP, Kotsenas AL, Broderick DF. Cerebral amyloid angiopathy: CT
distribution in the AD brain.
and MR imaging ﬁndings. Radiographics 2006;26(5):1517-1531.
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Usefulness of PET to detect cerebral amyloid as a means to diagnose neurodegenerative disease

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Table of Contents for the Digital Edition of Baylor University Medical Center Proceedings July 2017