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0:00
My name is
Tammaryn Lashley.
I'm a research fellow at
Queen Square Brain Bank
at the institute of
neurology at ULC.
I'll be giving an overview
of the neuropathology
found in neurodegenerative diseases.
0:12
The nuerodegenerative diseases
that I will be discussing
are Alzheimer's disease,
dementia with Lewy bodies,
frontal temporal dementias,
and the familial British
and Danish dementias.
0:24
For each of these
neurodegenerative diseases,
I will discuss the
macroscopic features
that are characteristic
to the diseases,
the major pathological proteins
that are involved in those diseases,
the microscopic pathological
lesions present,
and how we diagnose
the different diseases
from the pathological features,
and also discuss the importance
of the clinical pathological
studies that will help in earlier
and correct diagnosis
of future cases.
0:50
Alzheimer's disease is the
most common form of dementia,
with dementia being defined
as a clinical decline
in daily functioning due
to cognitive impairment.
The prevalence of AD
increases with age.
And from epidemiological
studies in 65 to 69-year-olds,
the prevalence of dementia is
approximately one in a hundred,
and for every subsequent five
years, the prevalence doubles.
There are several risk factors
associated with dementia.
By far, the most
important risk factor
is age, followed by family
history of dementia,
hypertension, and diabetes.
Nueropathologically, brains
reveal a global brain atrophy,
abundant amounts of amyloid
plaques composed of Aβ
and neurofibrillary
tangles composed of tau.
Inherited forms of AD
account for less than 5%
of the total number of
cases, and early onset AD
is caused by mutations in the
amyloid precursor protein.
Over 30 different
pathological mutations
have been identified, and mutations
in the Presenilin-1 and -2
proteins.
The majority of mutations are found
in PS-1, while only 14 mutations
have been found in the PS-2 gene.
The genetics of late onset AD
are considerably more challenging
than early onset AD, and variations
in the apolipoprotein E and TREM2
gene have been shown
to increase the risk
of developing late onset
Alzheimer's disease.
