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Pathology of Alzheimer's Disease

by Georgina Cornwall, PhD
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    The lecture Pathology of Alzheimer's Disease by Georgina Cornwall, PhD is from the course Aging.


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    1. Beta-amyloid plaques build up in the synaptic region between neurons and block inter-neruonal signalling.
    2. Beta-amyloid plaques build up inside neurons and block passage of neurotransmitters from the nucleus to the synapse.
    3. Tao protein tangles build up in the synaptic region between neurons and block inter-neuronal signalling.
    4. Beta-amyloid plaques interrupt the integrity of microtubules in a neuron.
    5. Tao protein plaques attach to neurotransmitters and block synaptic communication between neurons.
    1. They are an accumulation of parts of clipped cell membrane proteins that build up between neurons, blocking communication at the synapse.
    2. They are mutated proteins inside a neuron.
    3. They clog up normal transport via microtubules in a neuron.
    4. They are due to an immune response that destroys cells.
    5. They are direct antagonists to receptors on neurotransmitters and block their effect at the synapse.
    1. Most of the time, Alzheimer's disease is first manifested as negative effects on one's speech and communication.
    2. The accumulation of neurofibrilary tangles inside neurons block the passage of neurotransmittors from the nucleus to the synaptic region of a neuron.
    3. The accumulation of beta-amyloid plaques between neurons interrupts neurotransmitter signals at the synapse.
    4. The body's immune response initiates apoptosis of neurons that are unable to communicate causing brain atrophy.
    5. Alzheimer's is a neurodegenerative disorder.
    1. Learning disability and memory loss
    2. Loss of capacity for complex thinking and future planning
    3. Loss of sense and awareness of surrounding environment
    4. Affected speech and communication
    5. Change in personality and emotional behavior
    1. It increases the amount of time acetylcholine remains at the synapse, increasing it's potential for neuronal communication.
    2. It decreases the amount of time acetylcholine remains at the synapse, increasing it's potential for neuronal communication.
    3. It acts as an antagonist against glutamate receptors in the synapse.
    4. It acts to dissolve amyloid plaques in the synapse.
    5. It acts to stabilize microtubules for improved transport of neurotransmitters.

    Author of lecture Pathology of Alzheimer's Disease

     Georgina Cornwall, PhD

    Georgina Cornwall, PhD


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