00:01 In this lecture, weāll take a look into Parkinsonās and Huntingtonās disease and discuss all of the things that you need to know about both of those. Beginning with Parkinsonās disease, it is a little bit different than Alzheimerās because this is a disease that affects movement first rather than memory. 00:24 So, it is a progressive neurodegenerative disorder. It involves damage to dopaminergic neurons in the basal ganglia. Weāll take a look more closely at that shortly. Youāre probably familiar with this fairly standard presentation of Parkinsonās. We see the tremors with a little bit of shakiness and stiffness, slowed movements that appear to be sort of difficult to start. Balance issues also arise. 00:56 Now, the basal ganglia, to give us some orientation are a number of nuclei in the subcortical area of the brain. The ones that weāre particularly interested in are the substantia nigra and the striatum. 01:14 It turns out that thereās communication between these two regions of the brain that gets broken down in Parkinsonism. So, letās take a little bit closer look at the two pathways involved in controlling movements. First of all, we have a direct pathway in which the substantia nigra has dopaminergic neurons that signal the striatum. Dopamine is deposited in the striatum. 01:40 Then that message is then passed on through the thalamus into the cortical regions of the brain that are appropriate for the desired movements. Now, this is an excitatory pathway where weāre acting to increase the level of movement. So, I like to use the thalamus as an example of an analogy here, a puppy or a little dog that lives in the thalamus. Heās very excited and stimulated through this substantia nigra striatum pathway with dopamine. So dopamine makes the dog pretty happy. 02:16 He could run all over the cortex but thatās not going to go so well. So, we have also an indirect pathway that works through a number of other neurons, nuclei in the basal ganglia. That acts more like a leash holding the dog in the realm that it should be. So, we have a direct pathway that acts to increase movements and an indirect pathway that acts to decrease or fine tune the movements. 02:51 That is the leash. When we consider Parkinsonās, weāre looking at this direct pathway and having a problem with increasing the movements. So thatās where we see the symptoms of Parkinsonās, it being difficult to initiate movement because this nigrostriatal pathway is shut down. 03:17 It is shut down due to an accumulation of Lewy bodies. Where have you heard me mention Lewy bodies before or maybe you havenāt. But if you have, it was in another lecture where we were considering Alzheimerās and different sorts of dementia, not only Alzheimerās but there was a Lewy body dementia. Now, Iām going to speak a little bit more about these Lewy bodies because thereās something that you need to understand. First of all, understand that we donāt really know quite how they function but Iāll let you know what we do know. 03:57 First of all, we do know that these Lewy bodies involve a protein called Ī±-synuclein and accumulation of it, so again, clamping of a protein that interferes in signaling. 04:11 Thus, a neuron thatās no longer sending signals tends to degenerate and eventually will result in neuronal death. We can see these clusters of proteins interfering with mechanisms of the cell. 04:25 When 80% of the neurons at the nigrostriatal pathway have degenerated, signals have become low enough or slow enough that we start seeing this bradykinesia. Bradykinesia is that slowed, hard initiation of movement patterns. It tends to look fairly rigid so movements are no longer smooth and coordinated. Theyāre a little bit jerky. Thatās where we may see the tremors. 05:03 The sad thing is with Parkinsonās, we also see spreading to other regions of the brain where we start seeing progression into dementia later on in the disease. So Lewy bodies, we know some about. The question is though, are they a cause of or a result of Parkinsonās disease? It turns out that we are not really too certain about that. The cause of Parkinsonās is still fairly much of a mystery. Most cases seem to be idiopathic which really means we donāt know. 05:49 They appear to arise spontaneously. Fifteen percent or so of cases do have a genetic link. 05:57 We know that there are some serious environmental factors that are associated with Parkinsonās disease. The first and I think the most controllable that we have are these pesticide exposures or other chemical exposures. Thereās a high correlation between people that are working in farm and the farming industry where pesticides are applied heavily to crops having a very high incidence of Parkinsonās disease. Also individuals that experience a lot of cleaning chemicals and have inhalation of heavy metals, so all these chemicals affecting the neurons and generation of these Lewy bodies. Also, youāve probably heard quite a bit about having history of concussions leading to some dementias as well as Parkinsonās disease. 06:55 So, those are certainly risk factors also. With Parkinsonās, it seems to show up more frequently in males than it does females. So, we have increased gender risk in the case of Parkinsonās disease.
The lecture Anomalies of the Aging Brain: Parkinson's Disease by Georgina Cornwall, PhD is from the course Aging.
Which of the following statements regarding the onset of Parkinson's disease is true?
Which of the following is true regarding the pathophysiology of Parkinson's disease?
Which of the following symptoms is typically not seen until the end-stage of Parkinson's disease progression?
Which of the following has NOT been linked to the development of Parkinson's disease?
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Very clear and thorough, liked it a lot thank you Dr Cornwall!
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