PSYB64H3 Lecture Notes - Lecture 11: Chronic Traumatic Encephalopathy, Amyloid Precursor Protein, Traumatic Brain Injury

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25 Jul 2016
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Week 11 Chapter 15: Neurocognitive Disorders
Neuropsychology: field within clinical psychology that seeks to understand and treat patients
with cognitive impairments
Neuropsychologists: licensed doctoral level clinical psychologist who undergoes additional
training in the neurosciences
Neurocognitive Disorders
Disorder characterized by a decline in function in cognition (attention, executive
function, learning and memory, perception and movement, or social cognition) following
a known challenge to the nervous system
Despite the protection from the skull bones, cerebrospinal fluid, and blood-brain barrier
provide to the brain, damage can still occur due to interruptions in the brain’s blood
supply and from blows to the head
Alzheimer’s Disease
An age-related neurocognitive disorder resulting in gradual loss of cognitive function
Associated with aging that results in dementia
Dementia: loss of normal cognitive and emotional function
Probable Alzheimer’s disease is diagnosed on the basis of genetic testing or family
history, clear evidence of learning and memory impairments, and a steady gradual loss of
cognitive function without plateaus
In a small percentage of patients, disease can be inherited as dominant trait due to
mutations in one of three genes
oGenes for amyloid precursor protein (APP) on chromosome 21
oPresenilin 1 (PSEN1) on chromosome 14, or
oPresenilin 2 (PSEN2) on chromosome 1
For majority of patients, the e4 variant of the gene APOE that is located on chromosome
19 is the most reliable genetic risk factor for this disease
oIndividuals with one e4 allele have three times the risk for developing this disease
Behaviourally, Alzheimer’s disease usually beings with mild memory loss but as it
progresses, problem solving, language, and social behaviour deteriorate
This disease is also associated with atrophy of the cerebral cortex and contains a
characteristic pattern of neural degeneration
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oEmergence of neurofibrillary tangles that is a trademark feature
Results when tau (protein that normally holds structural microtubules in
place) breaks off and the microtubules are unable to hold their structure
any longer and so fall apart and breakdown, leading to the neuron to fold
in on itself and collapse
oBeta amyloids are misfolded proteins that form fibrous clumps and contribute to
the detachment of tau and subsequent cell structure
oIn addition, beta amyloid proteins collect in plaques (abnormal patches) on axons
of affected neurons and within blood vessels that serve the brain
Vascular Disease (Stroke)
Occurs when the brain’s blood supply is interrupted by either hemorrhage (bleeding) or
the blockage of a blood vessel (ischemia)
Risk factors for stroke include age, hypertension (high blood pressure), smoking,
diabetes, high cholesterol levels, obesity, use of alcohol, cocaine, amphetamines, heroin,
and other drugs
Risk is also increased when arteries are narrowed gradually by a condition such as
arteriosclerosis (hardening of the arteries)
Excess glutamate release produces neural damage due to excitotoxicity
Cell death following strokes is largely caused by excess glutamate activity triggered by
disruptions in the delivery of oxygen
oExcess glutamate entering a neuron causes abnormal level of calcium activity in
the cell that then stimulates four “executioner” enzymes that damage the cell’s
energy stores, membranes, cytostructure, and DNA
Neural cell death occurs immediately after a stroke, but prompt medical attention can
save the neurons and glia in the penumbra (the area immediately surrounding an infarct)
Treatments approved for ischemic stroke involve the use of drugs that reduce blood
clotting
Cerebral hemorrhage (bleeding in the brain)
Generally results from hypertension or structural defects in the arteries serving the brain
Some hemorrhages occur due to the rupture of aneurysms (balloon-like bulges in the
walls of arteries)
Others can result from diseases such as leukemia or exposure to toxic chemicals
Can also be hereditary
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Are frequently fatal due to the brain damage they produce interfering with the blood
supply to neurons and by flooding areas of the brain with salty blood that then dehydrates
and kills nearby neurons
Ischemia (low oxygen levels) that results from blockages of blood vessels
80% of all strokes
Results in death of neural tissue, producing an infarct (area of dead tissue)
oInfarcts cause changes in consciousness, sensation, or the ability to move,
depending on their size and location
oTransient ischemic attacks (TIAs): produce brief episodes, typically 24 hours or
less, of stoke symptoms
oAre strong predictors of subsequent stroke
Material that causes the blockage of a blood vessel can be labelled as either a thrombosis
or an embolism
oThrombosis: blockage that doesn’t move from its point of origin in the blood
vessel
oEmbolism: a blockage that originated elsewhere and travelled to its current
location
Cells in the middle layers of the cortex and cells in the hippocampus appear to be the
most vulnerable to ischemic attacks
Autopsy results of patients that died following ischemia showed that only certain cells
appeared to be damaged
oIf cell death occurred only because of a lack of oxygen, the damage should have
been more widespread  meaning that other processes must be involved in brain
damage following ischemia
Traumatic Brain Injury (TBI)
Result of physical damage to the brain (traffic accidents, gunshot wounds, falls, etc)
Types of TBI
oOpen head injuries (penetration of the skull)
Closed head injuries (concussions)  blow to the head without penetration of the brain or
from a blow to another part of the body that results in force transmitted to the brain
Range from mild (no or very brief period of unconsciousness) to severe
(coma)
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