Pathology of Alzheimer's Disease

by Georgina Cornwall, PhD

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    Before we go there, let’s look at these plaques and tangles. First of all, we could have development of plaques. Those plaques happen, the beta amyloid plaques happen between different neurons, so outside of the neuron between neurons and perhaps interrupt signaling. The second component are these neurofibrillary tangles which occur inside the neurons and block the passage of signaling molecules and nutrients to and from the nucleus. Let’s take a closer look at the beta amyloid plaques. We’ll deal with those first to look at where they are derived from. We can see in the first figure here there is what we call amyloid precursor protein. It’s a normal protein in the cell membrane. For some reason, it gets clipped and released. These pieces of beta amyloid are released. The beta amyloid piece of this protein that’s released is particularly sticky. So, it will associate with other pieces that are sticky and cause a beta amyloid plaque, so association of different pieces of the same kind of protein. These occur between neurons, again outside of the cell. They interrupt communication between cells especially at the synapses. When the cells stop communicating with each other, they stop getting signals that’s worth living on. So, the immune response comes in and starts clearing those cells. So, we see degeneration of those neurons. The cells actually undergo apoptosis and are removed which is why we see a decrease in brain size. I’ll show you an image of that shortly. The second component where these neurofibrillary tangles, if you can say that mouthful in front of a camera, good on you, neurofibrillary tangles result from abnormalities in proteins within the cell. First of all, recall that there are microtubules inside of every cell. They’re part of the cytoskeletal network. Microtubules in particular are...

    About the Lecture

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

    Included Quiz Questions

    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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