Learning, Memory and Alzheimer's Flashcards

1
Q

Where are memories stored?

A

Diffusely across the brain

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2
Q

Who is HM, what happened to him and what did this teach us?

A

HM most famous px in neuroscience, has bicycle accident causing LOC and epileptic seizures, neurosurgeon determined seizures were happening in temporal lobes so both were removed = cured epilepsy but caused anterograde amnesia and partial retrograde amnesia = temporal lobes critical for forming long term memories

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3
Q

differentiate between the 2 types of long-term memory

A

declarative: can explain to others, can be episodic: breakfast this morning or semantic: PM name
procedural: things you know that you can show by doing them, can be skill learning: skiing, bike riding, priming: using recently learnt word or conditioning: salivating when seeing steak

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4
Q

where are new episodic memories formed?

A

medial temporal lobes

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5
Q

what parts of brain control motor skill and memory?

A

motor cortex and basal ganglia

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6
Q

describe the pathway to storing long-term memories

A

sensory info -> short term memory -> rehearsal -> consolidation -> long-term memory

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7
Q

describe donal hebb’s theory involving cell A and cell B

A

when an axon of cell A excited cell B repeatedly, growth process/metabolic change occurs in one or both cells so A’s efficiency as one of the cells firing B is increased

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8
Q

What effect does increased glu/synaptic activity have in hippocampal synapses and NMDA-Rs?

A

increased synaptic activity forces magnesium block out, allowing entry of Ca2+ causing greater depolarisation, activating CAMKII which increases AMPA sensitivity to Glu -> LTP

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9
Q

differentiate normal transmission at hippocampal synapse (low synaptic activity) to transmission after conditioning train

A

normal transmission: only AMPA receptors are activated -> brief depolarisation -> excitation
after conditioning train: AMPA, NMDA-R and metabotropic receptors activated -> increased calcium and activation PKC and NOS -> sustained depolarisation -> excitation -> long term changes eg learning

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10
Q

What special protein kinase does calcium activate and what effect does this have on AMPA receptors?

A

calcium activates CAMKII which makes AMPA receptors more responsive by increasing amount of them at synapse

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11
Q

What effect does CREB have on long term potentiation?

A

CREB is activated in LTP and activates gene expression -> more ion channel receptors and new synapses which reinforce synaptic connections between two repeatedly communicating neurons

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12
Q

list the different types of dementia

A

alzheimer’s, vascular, frontotemporal, lewy body

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13
Q

describe the impact dementia has on aus population

A

2ND leading COD

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14
Q

Describe Alzheimer’s

A

memory deteriorating quicker than normal ageing population, progressive, anterograde and retrograde amnesia, impaired short term and implicit memory for verbal and perceptual material, leads to death of neurons in lower brain regions, changes in brain can be happening for 10 years > before symptoms show

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15
Q

where are signs of alzheimer’s first noticed in brain?

A

entorhinal cortex then hippocampus

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16
Q

What is the prognosis of Alzheimer’s?

A

8-12years

17
Q

What can be seen in brain of Alzheimer’s patients?

A

amyloid plaques between cells and neurofibrillary tangles within individual neurons

18
Q

Describe how amyloid plaques are made and build up

A

Amyloid precursor protein is broken down by series of secretases, normally cut twice at specific spots and two insoluble pieces travel away, if cut at wrong spot, amyloid is sticky and will stick to other sticky amyloids around

19
Q

describe function of microtubules in cells

A

act like railroad tracks that transport supplies to and from nucleus of neuron

20
Q

describe function of tau proteins in cells

A

act like railroad ties that stabalise microtubule structure

21
Q

what happens to tau proteins and microtubules in AD and what effect does this have

A

tau proteins become tangles, destabalising microtubules in neuron causing loss of axonal transport = cell death

22
Q

what neurons are affected in AD

A

neurons using Ach

23
Q

Describe mechanism of drugs for AD with NMDA glu receptors as the target and the effects of high and low concentrations

A

block NMDA receptor ion channel, high concentrations can inhibit learning and memory, low concentrations promote synaptic plasticity and preserve excitotoxic destruction due to death of neurons