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Treatment of dementia and Alzheimer’s disease | Mental health | NCLEX-RN | Khan Academy

Treatment of dementia and Alzheimer’s disease | Mental health | NCLEX-RN | Khan Academy

– [Voiceover] Scientists and
physicians continue to learn more and more about Alzheimer’s
disease and dementia in general, but unfortunately,
they still haven’t found a cure. With that said, though,
there are medications that can help lesson the
symptoms of dementia, like memory loss and confusion. Currently, all the medications approved by the Food and Drug
Administration or the FDA are aimed at either one
of two neurotransmitters: acetylcholine or glutamate. The first class of drugs are
cholinesterase inhibitors. Acetylcholine is a really
important neurotransmitter in our brain and nervous system. Even though it has important
functions in other parts of our body, in our brain, it
helps our neurons communicate. And it’s this communication of our neurons that allows our brain
to think and do things like sustain attention,
sense things, learn and remember things. Okay, so, say we have
these two neurons here that are trying to communicate, one transmitting neuron
and one receiving neuron. The transmitting neuron releases the neurotransmitter
acetylcholine, which then binds to an acetylcholine receptor
on the receiving neuron. And this is how these two
neurons communicate, right? To sort of regulate this
process, though, you have this enzyme that constantly
breaks down the acetylcholine that’s being released and
this sort of makes sure that too much doesn’t build up. And this guy is called
acetylcholinesterase, and it breaks acetylcholine
down into acetic acid and choline. Think of acetylcholinesterase like Pac-Man and all of these acetylcholines
as the little dots that he eats. He’s constantly going
around eating the dots, but some of them may get by to communicate between the neurons. So, it’s like this balance,
right, of some of the dots being eaten and some communicating. Acetylcholinesterase is
a type of cholinesterase. So, if we throw a cholinesterase
inhibitor into the mix, like the ghost in Pac-Man,
then we inhibit or stop our Pac-Man from doing his
job of eating the dots, right? Which means more of these dots build up, and we tilt the balance
in favor of the dots or acetylcholine. Now, patients with
Alzheimer’s disease, though, already have decreased levels
of dots in the first place. So, with Pac-Man there,
they have even less. But if we inhibit Pac-Man,
then we have less dots being eaten, right? And so, we end up with
more active acetylcholine. And by doing this, by stopping
the enzyme that breaks down acetylcholine, we can
help neurons communicate in people with Alzheimer’s disease. And this medication can
help delay worsening of dementia symptoms for
about six to 12 months on average, for about half of
the patients that take them. And although they’re usually
pretty well tolerated, some side effects can
include nausea, vomiting, and loss of appetite. All right, so that’s the
first type of medication for Alzheimer’s disease. The second type targets the
neurotransmitter glutamate, and is called memantine. Just like acetylcholinesterase inhibitors, memantine is prescribed to
help patients with symptoms related to memory, attention, reasoning, and language skills. Instead of acetylcholine,
though, now we focus on this neurotransmitter called glutamate. Glutamate, when at normal
levels, actually helps our learning and memory, and is considered an excitatory neurotransmitter. When glutamate levels
get too high, though, it’s actually toxic to the cell. And we use the word called excitotoxicity, where the cell gets actually
too stimulated and may die as a result. Having too much glutamate
is thought to be one possible way that people
with Alzheimer’s disease lose nerve cells and
therefore have problems with learning and remembering new things. So, again, we’ve got our
two neurons transmitting and receiving, right? And we have this receptor
on the receiving neuron called the NMDA receptor,
which is also like this channel or gateway that lets in
ions to the receiving cell. Now, this gateway lets them
in when glutamate binds to it. So, if there’s too much
glutamate and this gateway is always open, then the
receiving neuron can suffer from excitotoxicity,
because it’s like always being stimulated. Now, memantine blocks this
receptor for glutamate, so it keeps this channel closed more. And when it’s closed more,
we bring down the stimulation to normal levels and
avoid killing the cell by overstimulating it. Think of glutamate like
this key that opens the door to this party down here,
letting all the ions in. If too many get in, though,
the party gets too big and too crowded and out of control. If we put a different lock on the door, memantine, then the key won’t open it, and the party stays at reasonable levels. Now, memantine is used most
often to treat moderate to severe Alzheimer’s disease,
and will often be taken alongside cholinesterase inhibitors. Some side effects can
be things like headache, confusion, and dizziness. So, switching gears a little
bit, other forms of treatment often target behavioral
symptoms, like agitation, irritability, aggression, and anxiety. Usually, it’s preferred
to focus on treatments that don’t use medications
for these, though, like behavioral modification, since a lot of medications
intended to treat behavioral symptoms can
actually increase confusion and can even be associated
with increased mortality.

23 thoughts on “Treatment of dementia and Alzheimer’s disease | Mental health | NCLEX-RN | Khan Academy

  1. It is an appalling news to my family after my granddad was diagnosed with dementia. It is even more miserable to know drugs can't help recover his cognitive functions.

  2. How Does Our Brain Work and How Can We Treat Alzheimer's Disease?
    Our brain merely moves our consciousness back and forth thru time and televises the image of the past event that is occurring this very moment…Since the past, present, and future are all occurring simultaneously. So the brain is not storing information, but rather producing an image occurring in some element of time (past, present, or even future i.e. Psychics; Deja Vu),much like televisions of old, received transmitted signals from television stations. Hence, our brains are chronovisors… An artificial chronovisor is known to be located in the Vatican capable of televising the crucifixion of Jesus Christ in real time. Furthermore, the Chronovisor is stated to be capable of producing images in the future.
    So, Alzheimer's Disease occurs when the brain loses its capacity to shift consciousness back and forth thru time and subsequently remains locked in the present. But to fully understand Alzheimer's disease, let's use another analogy. Imagine a radio that has excellent reception, particularly when its antenna is fully extended. Now again, imagine dipping this same radio antenna in plaster. Once the plaster hardens on the radio antenna, the radio reception, subsequently, becomes very poor. Memories are Not With in…. They are With out. Alzheimer's disease diagnostically has neurofibrallary tangles and amyloid plaques on the brain's cerebral cortex. Hence, Alzheimer's disease is equivalent to dipping the antenna, ie brain, in plaster and thus destroying the brain's reception capacity. Occasionally, a frequency may get pass the amyloid plaques and neurofibrallary tangles, particularly if enough energy or stimulation is applied.
    Hence, the treatment for Alzheimer's disease that will invariably develop, will be a prosthetic device or electrode head cap that will allow a bypass of the diseased cerebral cortex which contain neurofibrallary tangles and amyloid plaques. Furthermore, this head cap will also have electrodes leading to the interior of the brain. Upon electrical stimulation, memory will be substantially improved. Despite the ultimate cure for Alzheimer's disease being the resolution and removal of neurofibrallary tangles and amyloid plaques, the proposed electrical cerebral prosthetic device will potentially slow the Alzheimer's disease process and substantially improve patient memory leading to a significant improvement of quality of life.
    Dr. Robert E. Rainer, MD

  3. Bloody love this video! I rely on visual aids and this vid has explained things PERFECTLY! THANK YOU!!! I am subscribing!!!

  4. Behavioral modification sounds great. But tell that to my mother in law who is now suffering from major anxiety and depression herself due to her husbands dementia. The only solution was medication sadly because there was no way in hell we could have resolved anything at this stage in life with his aggresion.He was always a difficult man and we've never really told him he has alzheimers/dementia. He just thinks his memory is failing. On the upside, in addition to donepezil, quetiapine has kept him at home and more tollerable but this disease steals lives. My mother in law is now on anti-anxiety and depression meds and as their primary caretaker, my life has been turned upside down.

    Thank you so much for the explanation of how the meds work. Now I can use the pac-man example when explaining donepezil to family and friends. Great video!

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