Memory Flashcards

1
Q

retrograde amnesia

A

can form new memories but forget old ones (can be temporally graded - only remember childhood for ex.)

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2
Q

anterograde amnesia

A

can’t form new memories but remember old ones

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3
Q

patient HM

A

went through bilateral medial temporal lobectomy to treat epilepsy. anterograde amnesia, but working memory intact.

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4
Q

implicit memory

A

unconscious thought

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5
Q

explicit memory

A

can be actively recalled

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6
Q

memory consolidation

A
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7
Q

subtypes of explicit memory

A

episodic & semantic

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8
Q

Episodic memory

A

personally experienced events

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9
Q

Semantic memory

A

facts and general knowledge

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10
Q

long-term potentiation

A

memory at a cellular level; persistent strengthening of synapses in a neuronal network (the stronger the synapse, better the memory)

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11
Q

patient KC

A
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12
Q

where are implicit memories processed

A

cerebellum and basal ganglia

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13
Q

where are explicit memories processed

A

hippocampus, frontal and temporal lobes

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14
Q

hippocampal indexing theory

A

informations get indexed together in one spot in hippocampus. later only one needs to be triggered to generate recall of others. stronger connections are made.

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15
Q

lesion on hippocampus

A

dysfunction in consolidating new long-term memories

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16
Q

cell changes during LTP

A

large influx of glutamate binds to AMPA receptors, causing depolarization and telling magnesium that blocks NMDA receptors. glutamate then binds do NMDAr. high glutamate in cell causes more AMPAr to come to surface of membrane (positive feedback cycle)

17
Q

functional changes during LTP

A

AMPA receptors recruited to membrane to allow for more signals to occur; lasts for a couple hours.

18
Q

structural changes during LTP

A
19
Q

early onset AD

A

familial or genetic

20
Q

defining characteristics of AD

A

Brain volume decreases
Neurofibrillary tangles
Amyloid plaques

21
Q

Neurofibrillary tangles

A

Hyperphosphorylated tau aggregates and axon disintegrates. Intracellular marker

22
Q

Amyloid plaques

A

beta-amyloid proteins don’t break properly from APP and clump together forming plaques around the neuron. Extracellular marker

23
Q

time course of AD

A

neurodegeneration is happening before symptoms. amyloid plaques starts to form, triggering neurofibrillary tangles at one point; neuronal integrity is decreasing.

24
Q

AD biomarkers

A

through CSF: lower beta-amyloid, higher tau levels