Lecture - Nervous System (Neuroanatomy 5 Liu)

Question 1

Slide 4:

1. What are the two types of long term memory?
2. What is the hippocampus, medial temporal lobe and neocortex involved in in terms of memory?

Answer 1

1. Declarative (explicit) and non-declarative (implicit)
2. They are involved in episodic long-term declarative memory (personal episodes in time and space)
   - the other explicit/declarative is semantic (facts, meaning, knowledge etc - lateral and anterior temporal cortex and prefrontal cortex

Question 2

Slide 5:

1. Where is the hippocampus in relation to the lateral ventricle?

Answer 2

1. This is actually written on slide 6 but the hippocampal formation is on the medial wall of the inferior horn of the lateral ventricle

Question 3

Slide 6:

1. In this image, what is every sticky?

Answer 3

1. Starting from the left: ignore that one, the red arrow is hippocampus, the hole is the inferior horn of the lateral ventricle, and then the temporal lobe and then finally the lateral sulcus

Question 4

Slide 6/7:

1. So you have identified where the hippocampus is, but what is the parahippocampal region?
2. Therefore, what is the parahippocampal gyrus?
3. Imagine in your head the hippocampus - now tell me where the three parts of the parahippocampal region are
4. Now, on slide 7, there is an image of the constituents of everything - just read it and try to remember the starred things (even scientists don’t agree on what the hippocampal formation includes. Just remember the hippocampus and the parahippocampal region/gyrus)

Answer 4

1. The parahippocampal region is the entrorhinal cortex, the perirhinal cortex and the parahippocampal cortex
2. The hippocampus gyrus is the parahippocampal region, I thinkkkkk since “The parahippocampal gyrus (Syn. hippocampal gyrus) is a grey matter cortical region of the brain that surrounds the hippocampus and is part of the limbic system.”
3. Look at the image for the parahippocampal gyrus
4. So now you know where the hippocampus sits (medial part of inferior horn of lateral ventricle), and the region surrounding it is the parahippocampal region/gyrus (entro-, perirhinal and parahippocampal cortex). And all of this is collectively known as the medial temporal lobe memory system (because it is on the medial part of the temporal lobe)

Question 5

Slide 11:

1. What is the anterior part of the hippocampus responsible for?

Answer 5

1. Critically involved in spatial learning and memory

Question 6

Slide 13: AD

1. So we know that it is progressive and degenerative, but what are the three characteristics?
2. This is from another lecture but we know that AD is a dementia - are all dementias progressive?

Answer 6

1. Increasing memory loss, other cognitive decline and changes in behaviour, personality and judgement + activites of daily living
2. Yes and AD is the most common

Question 7

Slide 14:

1. What are time early warning symptoms of AD? Name 3-4

Answer 7

Not being able to drive at night is a big one (from the AD lecture) because driving is complex and during the day, it’s fine bc there are cues to tell us how to drive but at night, there are no cues.

Question 8

Slide 15 and 16:

1. What can a person do/not do in severe AD?
2. What is the prevalance of AD related to?

Answer 8

1. The person can’t communicate verbally, understand words/instructions, recognise self in mirror/pics (face recognition is part of temporal lobe) or recognise fam, and they can’t care for themself. Usually die in 15y
2. Ageing is major risk factor. But after about 95, if still no dementia/AD then likely won’t get it.

Question 9

Slide 17:

1. So clearly there is atrophy (neuronal loss) of the brain in AD, and there are very narrow gyriand wide sulci…but what parts are severely affected?
2. What happens to the ventricles?

Answer 9

2. Large ventricles bc the surrounding sutff is lost

Question 10

Slide 18

1. What are the three things you see in the neuropathology in AD?

Answer 10

2 - Neurofibrillary tangles (Neurons contin microtubules for transmitting nutrients from cell body to the terminal. SO () is microtubule twisted and tangled and eventually loss of function so cell just dies. Intracellular neuronal tangles). This is INTRAneuronal

1. # 1 - Senile plaques in brain - amyloid plaques (bc they contain amyloid protein). These are INTERneuronal

Question 11

Slide 19: So carrying on from the nruopathology….

1. What is APP?
2. What happens in AD vs normal people in the processing?
3. So the protein that forms is t___ and s____

Answer 11

1. APP is the amyloid procursor protein
2. In normal people, form the non-amylogenic processing so don’t get the formation of the amyloid protein. In AD, there is amylogeni processing and you do form the myloid protein
3. Toxic and sticky

Question 12

Slide 20
1. So now that there is amyloid deposites, what is that going to affect?

Answer 12

1. It is going to affect the synapses because there is reduced spine densitiy (spines are the varicotities on the axons that are involved in other synapses) so affect the cell-to-cell communicaiton

Question 13

Slide 21 and 22

1. So we talked about tangles being one of the three neuropathologies in the AD brain - what is the specific protein involved in these tangles?
2. AD amyloid/senile plaques - is there any distinct patttern in terms of the vdevelopment of them?
3. What about tangles?
4. What is one place you don’t find the tangles?

Answer 13

1. Every cell contains tau proteins and these are there to keep the microtubules aligned down the lenght of the neuron so the neurotransitters and nuttirents can get to the terminal. But in AD, the tau protein is hyperphosphorylated or something so this new tau protein will aggregate and make the MT tangled and if no neutransmitter or nutrients to be delivered, cell just dies.
2. Nope
3. Yes - picture
4. Cerebeullum!

Question 14

Slide 25:

1. What does this graph mean?

Answer 14

Sticky =

Small number of tangles in the area of 35 (perirhinal cortex)

So when we are getting older, the tangles are getting more and more

Tangles develop initially in the perirhinal cortex but dont know why

Question 15

Slide 26:

1. Loss and atrophy of _____ __ _____ _____ _____ ______ in elderly people with mild cognitive impairment?

Answer 15

Layer 2 of the entorhinal cortex form this group of dark stained paramidal(?) cells - Lost these cells in AD

Entro cortex provides direct projection to the CA1 gyrus etc - basically major corticoal inputs to the hipppo

Clinically, try to use scan to see the size of the entorhinal cortex ot detect AD but it can only be detected when it is too late….

Question 16

Slide 28 and 32:

1. What is the amyloid cascade hypothesis?
2. Is this cascade the cause of AD?

Answer 16

1. If for whatever reason there is increased production and reduced clearnace of a-beta (the amyloid protein thing), then you get accumulation - key factor leading to AD. They think that tangles are downstream problem of this accumulation.
2. “The amyloid hypothesis, time to move on: Amyloid is the downstream result, NOT CAUSE, of AD.

Question 17

Slide 29
1. It was said that ACh producing cells are also lost, so you have low levels of ACh in the brain. What are the treatments of this?

2. Does it work?

Answer 17

NO CURE!

Question 18

Slide 31:

1. What are some other AD treatments (well, one)

Answer 18

1. Some research says in AD, there is over-excitation of nerve cells and eventually, kils neurons so this () can be used to treat

Question 19

Is the amyloid thing specific to AD?

Answer 19

No, can be found in normal peeps too (slide 34)