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0:00
Hello, my name is Mar
Hernandez Guillamon,
and I'm a senior researcher at the
Vall d'Hebron Research Institute
in Barcelona, Spain.
This talk aims to provide an
overview of the animal models used
for the study of cerebral amyloid
angiopathy at the pre-clinical level
and to highlight the limitations
and benefits of using CAA models.
0:24
CAA is included in
the group of diseases
caused by the
deposition of amyloid,
most commonly beta-amyloid
in the brain.
The A-beta peptide is a product of
the amyloid precursor protein, APP,
processing by beta
and gamma-secretases,
giving rise to peptides
of different lengths,
including A-beta
40 and A-beta 42.
This amyloid is highly fibrillogenic
and accumulates in the brain,
principally as an
insoluble aggregate,
forming the core of the neuritic
plaques in Alzheimer's disease,
where A-beta 42 is the
predominant A-beta species.
Or on blood vessels,
where A-beta 40 is the
predominant A-beta species,
in using cerebral amyloid
angiopathy, or CAA.
1:12
In fact, CAA is a cerebral
small-vessel disease,
and the principal clinical
manifestations include
lobar intracerebral hemorrhage,
transient focal
neurological episodes,
and cognitive impairment,
independently for
other dementia types.
From a neuroimaging standpoint,
CAA is characteristically
associated with
MRI markers of small
vessel injury,
including hemorrhagic markers as
strictly lobar cerebral microbleeds
and cortical
superficial siderosis.
But also non-hemorrhagic features
as enlarged perivascular spaces
in the semiovale and white
matter hyperintensities.
Despite the prognosis of
CAA-related lobar ICH,
no effective treatments
are available,
and a definitive diagnosis requires
histopathological demonstration.
Although, in clinical practice,
the diagnosis of
possible or probable CAA
can be established following
neuroimaging criteria.
We can see here the different
severity grades of CAA
established by the Vonsattel
diagnostic criteria from brain tissue.
And it can be appreciated
in more severe stages.
Beta-amyloid replaces the smooth
muscle layer of the vessel,
and it has been described
that pathological features
like fibrinoid necrosis found in the later
stage is significantly associated with
intracerebral
hemorrhage occurrence.
