Memory and Alzheimer's Flashcards

1
Q

What is the definition of learning?

A

Acquisition of new information or knowledge.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the definition of memory?

A

Storage or retention of acquired knowledge.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the definition of engram?

A

Physical representation or location of memory.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the three subclasses of memory?

A

Declarative, emotional and procedural.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What encompasses declarative memory?

A

Daily episodes, words and meanings and history.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What encompasses emotional memory?

A

Preferences aversions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What encompasses procedural memory?

A

Motor skills, associations, priming cues and puzzle solving.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the key brain area involved in procedural memory?

A

Brainstem and spinal motor output.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the key brain area involved in emotional memory?

A

Hypothalamus, autonomic and hormonal output.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the key area involved in declarative memory?

A

The hippocampus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is anterograde amnesia?

A

The loss of ability to create new memories after the event that caused amnesia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Who was Henry Molaison and what happened to him?

A

He suffered from epilepsy and had temporal lobes removed to try and fix his illness. This resulted in him suffering from anterograde amnesia and suffered from retrograde amnesia - (loss of memory before amnesia) for 11 years prior. He could not learn new names or faces from after the surgery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What type of memory loss affected HM?

A

Anterograde amnesia but his working memory and procedural memory were were intact. He could still form long-term procedural memories such as learning new motor skills, even if he couldn’t remember learning them.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the working memory?

A

Short term memory - seconds to minutes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the immediate memory?

A

Fractions of seconds of seconds of memory - immediate memory.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the long term memory?

A

Days-years.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How can a memory be improved?

A

Re-consolidation and reactive the memory.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the classic Pavlovian conditioning?

A

If a bell is shook at the same time a dog is presented with food, if this is repeated the dog will associate the bell with food and will drawl if it hears the bell even if no food is present.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is Hebb’s law?

A

The idea that when two neurones are active (when one repeatedly releases neurotransmitter at the same time as the postsynaptic partner is firing action potentials), then that synapse will become stronger.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is memory dependent on?

A

Populations of interacting neurones.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does rhythmic activity of the short term memory result in?

A

Strengthened synapses - longer term memory.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How is synaptic strengthening studied?

A

Using rat temporal lobes.

23
Q

How are action potentials created?

A

They are glutamate mediated and result in excitatory postsynaptic potentials.

24
Q

What is Long Term Potentiation (LTP)?

A

The increase strength in strength after repeated stimulation of a synapse.

25
Q

What does it mean that long term potentiations have a voltage threshold?

A

That if only low frequency stimulation of a synapse occurs, it will not reach the threshold and there will not be an increase in the strength of the signal.

26
Q

What happens if there is a pharmacological block of NMDAr?

A

There is a prevention of a long term potentiation.

27
Q

What does tetanus do?

A

It induces LTP at the glutamate synapse.

28
Q

What is the effect of reducing extracellular calcium from 2 to 0.2mM?

A

LTPs are prevented.

29
Q

What is th effect of calcium+ through NMDAr?

A

LTPs are induced.

30
Q

What does it mean that the NMDA receptor is dual gated?

A

They are activated by both glutamate and are blocked by Mg2+ - Mg2+ needs to be removed in order for calcium and sodium to flow through the channel.

31
Q

What is Mg-dependent gating important in?

A

Synaptic plasticity, learning and memory.

32
Q

What is the ways in which LTPs can be manifested in postsynaptic neurones?

A

More AMPArs, more sensitive AMPArs, more synapses.

33
Q

What are the ways in which LTPs can be manifested in presynaptic neurones?

A

Increased release, more release sites and more vesicles.

34
Q

What is the induction mechanism of LTP?

A

AMPAr is phosphorylated by PKC and new receptors are inserted by CaMKII. There is synthesis of new receptors. There are retrograde messengers such as nitric oxide that cause presynaptic changes.

35
Q

How is NMDAr involved in memory formation?

A

After learning, the synaptic pathway is short and a memory is created. If the NMDA receptor is inhibited, there is failure to learn/store memory.

36
Q

What is an antagonist of NMDAr?

A

2-AP5.

37
Q

How are NMDAr and AMPA involved in memory?

A

Memory is induced by NMDAr and expressed by AMPA receptors.

38
Q

How are LTPs maintained?

A

Presynaptic alternations of glutamate release and changes in the number and selectivity of posynaptic AMPAr and structural changes.

39
Q

How can your memory be enhanced?

A

Note-taking, understanding, food, sleep, avoiding distraction, revision and cognitive enhancers.

40
Q

What are AMPAkines?

A

Small benzamide compounds that produce positive modulation of AMPA receptors and improve performance on a variety of behavioural tasks.

41
Q

What are some common cognition enhancers?

A

Cholinergic modulators, stimulants, dopaminergics, 5HT drugs, GABAr blockers and mGluR drugs and modafinil.

42
Q

How do cholinergic modulators work?

A

Choline is a precursor molecule for acetylcholine which is involved in memory.

43
Q

What is a common drug that increases choline?

A

Coluracetam.

44
Q

What are some anticholinesterases?

A

Donepezil and galantamine.

45
Q

What are some agonists of acetylcholine receptors?

A

Nicotine and arecoline

46
Q

What are some stimulants that productivity enhancers?

A

Amphetamine, methylphenidate, caffeine.

47
Q

What are the different types of amnesia?

A

Drug induced (alcohol), head trauma and retrograde or anterograde.

48
Q

What is the difference between retrograde and anterograde amnesia?

A

Retrograde amnesia is the loss of memory of events that occurred before the onset of the disease, and anterograde amnesia is the loss of ability to create new memories after the onset of the disease.

49
Q

What is dementia?

A

A syndrome characterized by a decline in cognitive functions sufficient to cause impairment in social and occupational performance.

50
Q

What are the features/symptoms of dementia?

A

Loss of multiple memory categories, inability to form new memories, associated with general cognitive decline, memory impairment first presenting syndrome.

51
Q

What are the types of dementia?

A

Alzheimer’s, vascular dementia, mixed dementia, dementia with Lewy’s body, frontotemporal dementia.

52
Q

What is paraphasia?

A

When the individual employs wrong words or uses words in wrong and senseless combinations.

53
Q

What are the physical changes in the brain of an individual suffering from Alzheimer’s?

A

There is shrinkage of the temporal poles and frontal cortex, along with damange in the entorhinal cortex. The damage is progressive to the whole cortex and subcortical structures.