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Pharmacology CAM202 & 304 > -Dementia > Flashcards

-Dementia Flashcards

1
Q

Which brain regions are active in memory?

A

Hippocampus
Striatum
Neocortex

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2
Q

What is the hippocampus for?

A

The hippocampus is specialized for creating a spatial map of the environment.
Hippocampal lesions can cause a DEFICIT IN WORKING MEMORY
The hippocampus and the temporal lobe are required for relational memory- highly processed sensory information coming into the hippocampus and nearby cortex. Links things happening at the same time.

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3
Q

What is the striatum for?

A

Striatum (caudate nucleus + putamen) is important for procedural memory (habit learning)

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4
Q

What is the neocortex for?

A

storage of temporary information- example repeating a phone number so that you don’t forget

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5
Q

DEscribe Hebbian Learning

A

Cells that fire together WIRE together- EXPERIENCE DEPENDENT PLASTICITY

eg. if cell a fires an action potential that causes neurotransmitter release and an EPSP is evoked in cell B in a coordinated manner, than that syapse will be strengthened.

At the same time, if cell C fires an actionpotential that causes a neurotransmitter release and an ESPSP is NOT evoked in cell B, or occurs in cell B before neurotransmitter release, ie in an uncoordinated manner, that synapse will be weakened.

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6
Q

Explain some of the changes that occur at the cellular level in relation to synaptic plasticity

A

Synaptic plasiticity: changes in spine size, shape, and number (ie. dendritic morphology). Required to regulate connective opportunities for example: alters synaptic strength, synapses can be potentiated or depressed. They can be measured and manipulated experimentally: long term potentiation (LTP); Long term depression (LTD); Changes in protein composition at the post synaptic density.

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7
Q

explain the neuronal relay path between the hippocampus and cortex

A

The hippocampus is the dentate gyrus and Ammon’s horn. (cornu ammonis = CA). 1. Axons in the perforant path relay information from the entorhinal cortex to the dentate gyrus. 2. The dentate gyrus granule cells emit axons called mossy fibers, which synapse on pyramidal neurons in CA3. 3. CA3 axons are the schaffer collaterals which synapse on pyramidal neurons in CA1.

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8
Q

Explain the hippocampus’ role in associative learning

A

Thought to be key to the formation of declarative memories. Eg. See a rose, smell it and see it- you pair the smell and the sight of the rose and hence strengthen the synaptic response; inputs may undergo LTP, thus forming an association between two stimuli

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9
Q

Explain Long term potentiation

A

LTP is triggered by either high frequency stimulation or synchronous activation of synapses, such that postsynaptic CA1 neuron is strongly depolarized. Temporal and spatial EPSP summation- many excitatory synapses are active at the same time. LTP potentiates the post synaptic responses to the presynaptic glutamate signal. Three glutamate receptors are at a synapse: AMPA, NMDA, mGluR. What differentiates synapse from being strengthened or weakened -?-> strength of calcium signal.
Calcium signaling is necessary for both LTP and LTD: Change in calcium conc within postsynaptic density activates CAMKII (get a phosphorylation of lots of things within postsynaptic terminal)

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10
Q

What does LTP potentiate?

A

LTP portentiates the POSTSYNAPTIC RESPONSE TO THE PRESYNAPTIC GLUTAMATE SIGNAL-> through producing a strong strong Ca++ signal, which will cause more AMPA receptors to be inserted into the membrane. This makes it more likely that a presynaptic signal will depolarize the post synaptic membrane: synaptic signaling is potentiated.

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11
Q

What is needed for LTP and LTD?

A
  1. Calcium Signalling
  2. Different AMPA receptor quantaties
  3. Inhibit receptors
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12
Q

LTP & Depression pathways; calcium signalling

A

(1) Calcium Signalling is necessary

The rate and timing of stimuli will determine whether a synapse is potentiated or depressed.
LTP = high frequency and/or synchronized stimuli : more AMPA receptors
LTD = low frequency and or asynchronous stimuli: less AMPA receptors

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13
Q

LTP & Depression pathways; different AMPA receptor quantaties

A

in LTD, with weak NMDA receptor activation and weak Ca++ signals, AMPA receptors are internalized.
In LTP with strong NMDA receptor activation and strong CA++ signals, more AMPA receptors are recruited to the membrane.

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14
Q

Learning and Memory are therefore potentiation of a synapse

What happens in LTP to receptors?

A

LTP and CAMKII activation- polymerisation of acint (required for spine maturation), activation of local mRNA translation.
More NMDARs, AMPARs, scaffold proteins inserted into the synapse = stronger post synapstic density and synapse

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15
Q

Learning and Memory are therefore potentiation of a synapse

What happens in LTD to receptors?

A

LTD and Calcineurin activation - causing depolymerisation of actin, dephosphorylation of proteins such as AMPARs, causing endocytosis of receptors = WEAKER synapses.

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16
Q

Synapses are remodelled in response to learning-

A

Changing in spine morphology can change synaptic connections: learning a new motor task associated with:

  • formation of new spines
  • stabilisation of dendritic filopodium
  • direct emergence of a new spine that extends towards a nearby axon
  • Elimination of unused spikes
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17
Q

LTP and LTD overview

A

Learning and memory can result from modifications of synaptic transmission.
Synaptic modifications can be triggered by the conversion of neural activity into intracellular second messengers
memories can result from alterations in existing synaptic protesin

18
Q

Multiple receptor types are part of learning and memory formation:

A

acetylcholine receptors,
glutamergic receptors- NMDA, AMPA, mGLUR
Inhibitory receptors: GABA, glycine

19
Q

The diagnosis of dementia needs to be confirmed in at least two of:

A

The diagnosis needs to be confirmed in at least two of:
impaired new learning,
short term memory,
apraxia (inhability to perform learned, purposeful movements),
agnosia (loss of ability to recognize things- people, places objects),
language disturbance,
loss of executive functions.
Attention and concentration are usually unimpaired in mild dementia.

20
Q

Cognitive impairment can be caused by things other than dementia including:

A

Delirium
Depression
Drug effects

21
Q

Important features of:

Alzheimers disease

A

Clinical diagnosis requires memory impairement and impairment of language, executive function, motor function (dyspraxia) or agnosia

22
Q

Important features of:

vascular dementia

A

STEPWISE

Progressive, associated with physical signs of stroke or history of transient ischaemic attack.

23
Q

Important features of:

Lewy Body Dementia

A

Progressive dementia with at least two of the three features of fluctuating cognition visual hallucinations and parkinsonism
Falls are common
Severely intolerant of the adverse effects of antipsychotic drugs
Some evidence for benefit from cholinesterase inhibitors

24
Q

Important features of: Parkinsons disease with dementia

A

ability to function can also be related to adequacy of dopa replacement and is often worse in ‘off’ periods
May be part of a spectrum of disease with dementia with lewy bodies

25
Q

Important features of:

Frontotemporal Dementia

A

Younger patients (less than 645 yo)
Family history of frontotemporal dementia is often found,
‘dysexecutive syndrome’ with change in behavior and personality common
Delusions are common
Also includes progressive fluent and nonfluent aphasia (inability to understand or produce speech) types
Memory is relatively spared
Mini mental state examination is unreliable
Deteriorates with the use of antipsychotics

26
Q

Important features of:

Post Traumatic Dementia

A

History of injury with consistent imagine
Not progressive
Appears to increase the risk of later developing Alzheimers type dementia

27
Q

Important Features of

Toxic Encephalopathy

A

history of toxin exposure

28
Q

What are some non pharmacological treatments of dementia?

A

MONITOR GENERAL HEALTH other chronic conditions: cardiovascular risk factors, optimize health and independence.
PSYCHOSOCIAL INTERVENTION for carers: teaching specific problem solving skills: more effective if the patient is also involved. STRUCTURED INDIVIDUAL COUNSELING; involvement of the extended family and consistent professional long term support. Can helpt o reduce psychological buden and reduce the need for institutional care of the patient.
COMMUNITY BASED OCCUPATIONAL THERAPY: aims to improve the patients daily function.

29
Q

Maintaining Cognitive, physical and social activity

A

Helps to improve quality of life for the patient. Reduces the burden of care. Also improved by education about symptom progression, burden management and enabling appropriate access to services including respite care. Local patient support organisations can be useful resources for this. It is also important that carers maintain a relationship with their own general practitioner so that their own needs are addressed. No supportive evidence for aromatherapy, music therapy, transcutaneous electrical nerve stimulation (TENS), bright light therapy.

30
Q

Name some of the drug classes used in treating dementia:

A

Cholinesterase inhibitors

NMDAR antagonist

31
Q

What is the function of Cholinesterase inhibitors

Name some of teh drugs

A

Prevent breakdown of ACh at the synapse
Donepezil
Galantamine
Rivastigmine

32
Q

Who benefits from the use of Cholinesterase inhibitors

A

.Alzheimer’s disease: early research indicated that cholinergic neurons were vulnerable to degeneration. There is a statistical benefit of cholinesterase inhibitors in mild to moderate AD, conflicting data as to whether taking a cholinesterase inhibitor improves cognition and function at one year and delay in nursing home placement
Vascular dementia and dementia with Lewy bodies: same evidence for efficacy in these conditions although not yet approved for these indications.

33
Q

What are adverse effects of Cholinesterase inhibitors

& CONTRAINDICATIONS

A

Common: nausea, vomiting, diarrhoea (can be reduced with dose titration).

Not as common- bronchoconstriction (asthma patients), bradycardia, cramps and vivid dreams

Galantamine is contraindicated in severe renal failure

34
Q

What is the function of NMDAR antagonists

Name some of teh drugs

A

MENTAMINE - moderate to severe AD, vascular D

N-methyl D-aspartate receptor antagonists : Thought to protect neurons from overstimulation and excitatory damage which is associated with glutamate transmission and calcium overload. Calcium dysregulation hypothesis of Alzheimers disease. Also thought to be useful in dementia with a strong vascular component.
It is available on the PBS as a potential alternative for those who can’t tolerate cholinesterase inhibitors.

It requires dose titration over a month to minimize adverse effects

35
Q

What are adverse effects of NMDAR antagonists

& CONTRAINDICATIONS

A

Adverse: agitation, hallucination and headache. May also increase the risk of seizure activity.

Metabolism: Excreted in the urine and is no suitable for use in those with renal impairment. But can be used in combination with cholinesterase inhibitors ?

36
Q

Some therapies target PPAR mediated transcription, why?

A

Through FIBRATES

ApoE normally facilitates the clearance of Abeta from the brain.
ApoE transcription is under the control of PPARgamma in cooperation with the liver X receptors in and retinoid X receptors.
Recent animal studies have demonstrated that bexarotene, an agonist of the LXR and the RXR can enhance Abeta clearance and cognitive performance in mice…

37
Q

Drugs for delerium

A

Delirium (clouding of conscious state, disorientation, impaired attention and memory): a course of THIAMINE (vitamin B1) can be trialled.
Thiamine deficiency can lead to Wernicke’s encephalopathy and Korsakoff’s psychosis, especially in people who abuse alcohol

38
Q

Drugs for delerium

A

THIAMINE OR BENZO’s

Benzodiazapines can be used to treat delirium to control associated anxiety, agitation, aggression, hallucinations, an dellusions.

39
Q

Drugs for Depression

A

SSRIs

40
Q

Behavioural Distrurbance

A

antipsychotics help reduce hallucination and delusion

Pharmacology CAM202 & 304 (5 decks)

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