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Brain PD > Week 1 part 1 > Flashcards

Week 1 part 1 Flashcards

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1
Q

How much is spent on treatment for mental disorder in England in 2011/2012 DH?

A

£12 billion

11% of NHS budget

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2
Q

What is the percentage of burden of disease in UK due to mental disorder WHO?

A

30.3%

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3
Q

Wha is one of the most impactful component of the cost of healthcare?

A

Burden of mental disorders

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4
Q

Where is there a lot of investment in?

A

Cancer

Catch up with the impact of cancer on awareness

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5
Q

Why do we need to address the issue of mental disorders?

A

Alleviate the suffering
Cost of quality of life
Integrate into society and have a meaningful life

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6
Q

What are the challenges in the development of successful therapies in neurology and psychiatry?

A
  1. Understanding disease cause and evolution
  2. Understanding the pathophysiology
  3. Availability of adequate animal models of the disease
  4. Do the drugs teach the target?
  5. Patient response variability
  6. Identification of novel targets
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7
Q

What does the challenges in the development of successful therapy in 2019 span?

A

Neurology and psychiatry

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8
Q

What is treated by a psychiatry?

A

Schizophrenia and Depression

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9
Q

What is treated by a neurologist?

A

Parkinson disease

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10
Q

What is found in neurological disease?

A

Neural inflammation

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11
Q

What is found in psychiatric and many more evolutionary diseases?

A

Demyelination signal

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12
Q

Availability of adequate animal models of the disease?

A

Superimposed ethical issues
Are they good or bad?
Can we use lower species to model human conditions
Is it ethical in terms of harming the animals
How we have control of the animals for medical research
Validity done on each model

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13
Q

How are drugs prescribed?

A

In a very routine manner

Quite stereotype manner

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14
Q

What is schizophrenia?

A

Severe psychiatric disorder characterised by psychotic and cognitive symptoms

Leading cause of global disease burden

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15
Q

What is schizophrenia preceded by?

A

Prodromal phase of attenuated psychotic symptoms and functional impairment

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16
Q

What is increasing evidence of schizophrenia?

A

Involvement of neuroinflammatory processes

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17
Q

History of schizophrenia: where was patients submitted to?

A

Very strange paradigms of treatment

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18
Q

What is schizophrenia a disease of?

A

Changes life significantly by individuals affected by it

It affects personal life

Cost of worldwide and it is not going away

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19
Q

What age group does schizophrenia affect?

A

People in their early 20’s

Age 16-30 (women tend to have a later onset)

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20
Q

What percentage of population is affected by schizophrenia?

A

1%

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21
Q

The percentage of population is similar across what?

A

Different countries
Cultural groups
Sexes

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22
Q

The evolution of schizophrenia is what?

A

Heterogenous

The condition persists throughout a patients lifetime

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23
Q

What is schizophrenia characterised by?

A

Triad of core symptoms:
Positive
Negative
Cognitive

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24
Q

What are the positive symptoms?

A

Hallucination
Delusion
Agitation
Disorganised thinking/speech

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25
Q

What are the negative symptoms?

A 
Introversion 
Apathy
Low self-esteem
Personal neglect 
Total lack of interest in anything
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26
Q

What are the cognitive symptoms?

A

Poor memory
Attention Deficit
Executive dysfunction

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27
Q

What are the structural and functional changes in schizophrenia?

A

Larger ventricles

Smaller mesial temporal lobe structures

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28
Q

What does structural FMRI of schizophrenia patients show?

A

Shrinkage of Brain
Some loss of brain matter
Some loss of white matter

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29
Q

What has been possible to do in the past 15 years?

A

A more dynamic assessment of the progression of structural changes in schizophrenia

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30
Q

What happens as you grow up and your brain matures?

A

Lose some percentage of brain matter in particular as the brain continues to sculpture itself

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31
Q

What does the normal adolescent show in a structural FMRI?

A

Loss of brain matter due to sculpturing of the brain measured by an average annual loss from blue to purple

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32
Q

What does schizophrenic patients such in a structural FMRI?

A

Colours are more vivid and more intense

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33
Q

What can be used for parameters to be measured objectively to get a stimulation response?

A

Event related potential (ERP)

Simple electrical signature when exposed to a sensory stimulus

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34
Q

What does computerised tomography show?

A

Ventricular enlargement

Generalised loss of brain tissue in patients

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35
Q

What does structural MRI show?

A

Additional volume deficit in the prefrontal and temporal lobes
Thalamus is also reduced in volume

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36
Q

What is schizophrenia characterised by?

A

Abnormal PFC interaction with other cortical areas

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37
Q

What is an important concept of schizophrenia?

A

Hypofrontality

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38
Q

What is used to see hypofrontality in schizophrenia patients?

A

FMRI

  • interrogate the brain to see how the brain mobilises in its resources to perform a certain task
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39
Q

What is observed for schizophrenic patients when FMRI is used?

A

Much more difficulty in recruiting brain areas which are necessary to perform well at a certain task

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40
Q

What is Hypofrontality?

A

A state of decreased blood flow in the prefrontal cortex of the brain

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41
Q

Hypofrontality - schizophrenic patient - what does it show?

A

There is a performing metabolic deficit

You can’t really recruit blood flow, glucose and metabolites

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42
Q

What is the earliest seed of neurodevelopment?

A

Intellectual activity are extremely limited

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43
Q

What causes schizophrenia?

A

A combination of physical, genetic, psychological and environmental factors can make a person more likely to develop the condition

-stressful or emotional life event might trigger a psychotic episode

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44
Q

What is the abnormalities in schizophrenia which suggest an impaired neurodevelopment

A 
Brain asymmetry 
Corpus callosum dysgenesis 
Abnormal correlation between regional cortical volume measurements 
Absence of gliosis 
Minor physical anomalies 
Early childhood behaviour abnormalities
45
Q

What is gliosis?

A

Nonspecific reactive change of glial cells in response to damage to the CNS

46
Q

What increases the risk of later schizophrenia?

A

Prenatal and birth complications

Unfavourable changes e.g extreme hypoxia of the foetus

47
Q

What does schizophrenia till this day remain?

A

Polymorphic disease

48
Q

What does the node diagram for schizophrenia patient show?

A

Emergence of the condition and you can see any pattern

How variable the disease is

49
Q

What component is found in schizophrenia?

A

Genetic

The more related you are to someone who is schizophrenic, the more of a risk you will have it yourself

50
Q

After the genome project was completed, there was an enrichment in the understanding of what?

A

Genetic components of disease

51
Q

Whole chromosomal complement

A

Gene changes scattered all over

52
Q

Genetics of schizophrenia - examples

A

Try and understand the biological plausibility

What is in the gene that will increase the risk of schizophrenia disorder

53
Q

What doesn’t the genetic component of schizophrenia show?

A

Where the final product is

If the protein is really changed

54
Q

What are examples of genes and function?

A 
PRODH
NRG1
RGS4
EPN4
COMT
55
Q

PRODH

A

Involved in the metabolism of proline (proline oxidase)

Dysfunction in glutamate transmission

56
Q

NRG1

A

Involved in neuronal development and survival

57
Q

RGS4

A

Linked to GTPase activation

Involved in the activity of several receptor families

58
Q

EPN4

A

Epsin 4

Involved in the intracellular trafficking of proteins

59
Q

COMT

A

Involved in the metabolism of dopamine

60
Q

DISC1

A

Gene that confers risks
Discovered in Scottish population
When you manipulate these genes experimentally, you reduce neuronal growth

61
Q

What is the function of DISC1

A

Restricted expression in adult breaks

  • dentate gyrus granule cells
  • olfactory bulb

DISC1 binds to molecules involved in neural development (e.g. NDEL1)

62
Q

What is the In vitro impairment of DISC1?

A

Reduced neurite growth

63
Q

What is the In utero interference with DISC1?

A

Retarded migration and mis-orientation of dendrites of cortical cells

64
Q

What will occur when you have variation of DISC1 and an individual in a cognition test?

A

An engagement of the brain

65
Q

What is observed in the variation of DISC1?

A

Decrease in grey matter in the hippocampus

What you can measure functionally is a decrease in engagement of the hippocampus in an episodic memory task

66
Q

What progressed schizophrenia into a full blown disease ?

A

Genetic predisposition

Environmental risk factor

67
Q

What is one strong association of risk linked to schizophrenia?

A

The use of cannabis during adolescence

68
Q

What happens when you have a certain mutation in the COMT gene?

A

It will take you over the threshold to develop schizophrenia

69
Q

What was the accidental discovery for the treatment of schizophrenia?

A

Looking at antihistamine and sedative compounds

70
Q

What was the greatest accidental discovery in medicine?

A

Chlorpromazine
Has a characteristic of blocking dopamine receptors of D2 types
Essential for antipsychotic activity

71
Q

What do all antipsychotic drugs have?

A

Efficacy

72
Q

What is activity and efficacy correlated with?

A

Plasma concentration of the drug

Ability to block the receptors

73
Q

Where do we have antagonist activity at?

A

5-HT2 receptors

74
Q

Why is clozapine unique?

A

Allows treatment of resistance to schizophrenic patients

75
Q

Why can’t clozapine be used in all patients?

A

Decreases in white blood cells count

76
Q

Aripiprazole

A

Complex pharmacodynamics

Partial agonist

77
Q

What does every country have in treating schizophrenia?

A

It’s own guidelines

Put forward by organisation NICE

78
Q

What are examples of typical antipsychotics

A 
Chlorpromazine 
Thioridazine
Fluphenazine 
Haloperidol
Flupenthixol
79
Q

What are examples of atypical antipsychotics ?

A 
Risperidone 
Olanzapine
Clozapine 
Queriapine
Paliperidone
Aripiprazole
80
Q

What does clozapine block?

A

D4 receptors with high affinity

81
Q

What can atypical antipsychotics improve?

A

Cognition in some patients

82
Q

What is the issue of schizophrenia?

A

Due to hyperdopaminergic state subcortically (ventral stratium)
But there is hypodopaminergic state in the prefrontal region

83
Q

What are other neurotransmitter abnormalities in schizophrenic patients?

A

Alteration in glutamatergic and GABAergic transmission

84
Q

Cytoarchitectural defects in schizophrenia?

A 
Abnormalities in the cortical layers:
Decreased layer thickness 
Decreased size of pyramidal cells 
Decreases in GABAergic interneurons 
Decreased complexity of dendritic arbors
85
Q

Prefrontal pyramidal neurons in schizophrenia

A

Fewer spines on dendrites

86
Q

What is small changes of schizophrenia?

A

Reduced interneuron activity

Excessive excitatory pruning

87
Q

What is criteria for validity of animal models?

A

Face validity - “looks like the disease”
Construct validity - “has a sound casual rationale”
Predictive validity - “drugs work in it”

88
Q

What is the overview of models of schizophrenia?

A
  1. Early lesion models
  2. Stress models
  3. Prenatal viral infections or evoked immune response
  4. Perinatal treatment with phencyclidine
  5. Disruption of Neurogenesis
89
Q

Disruption of neurogenesis

A

Methylazoxymenthanol exposure (man model)

90
Q

What is man model based on?

A

Disruption of neurodevelopment with a toxin

91
Q

Method of man model

A

Inject at day 17 in rat dams and this can be also be done in nice
They then give birth
Look at brain characteristics
They have a smaller brain size

92
Q

Non-exposed rats and schizophrenic patients have anatomical abnormalities which are similar

A

Increased ventricular size

Decreased size of key brain regions cortical network

93
Q

Behavioural changes: amphetamine

A

Inject amphetamine in animals and get them to present with a high sensitivity

94
Q

What is amphetamine?

A

Psycholytic compound

95
Q

Schizophrenia patients

A

Hyper-sensitive to amphetamine

96
Q

MAM-animals give amphetamine

A

Much more active

They will mimic hyper-sensitivity to amphetamine

97
Q

What is disrupted in schizophrenic patients?

A

Social behaviours
Impaired interaction
Mimicked in rodents

98
Q

What can cognition modelling in rodents be supported by?

A

Morris water maze
Put rodent in a little bath of Luke-warm water
Ask them to remember the location of the platform
See how fast they learn
Simple way to test their learning and memory
Twist in the maze - show flexibility cognitive

99
Q

Morris water maze - reference memory

A

No difference between normal and MAM-exposed animals
Cognition function of schizophrenic patients are perfectly normal
Their flexibility is problematic

100
Q

Morris water maze - reversal memory

A

Adolescence rats have a problem for reverse memory

Much difficult task as learn platform changes

Animal with MAM-exposure are much more confused by it

101
Q

What is the difficulty in having cognitive ability and making decisions reminiscent of?

A

Difficulties experienced by patients in the Wisconsin Card Test

102
Q

Schizophrenic patients

A

Diminished abilities to change rules
Cannot focus
No cognitive abilities
Cannot make decisions faster

103
Q

In schizophrenia what is affected?

A

Interneurons

104
Q

What is “PV-expressing neurons?”

A

In the prefrontal cortex
Protein that is enriched in interneurons
Detected in the PFC and hippocampus

105
Q

What are parvalbumin neuron involved in?

A

Gamma alteration in the brain

Electrical manifestation of cognitive processing

106
Q

What is schizophrenia associated with?

A

Demyelination

107
Q

Overview of the MAM model of schizophrenia

A

The model is based on the neurodevelopmental theory of schizophrenia

The model reproduced regional abnormalities in corticolimbic circuits

Fundamental abnormalities such as decreased density of synaptic spines

Animals also display a behaviour which reproduces the positive, negative and cognitive spectrum of symptoms

108
Q

Why may patient not respond well to existing drug?

A

Variation in metabolism of drug e.g. cytochrome P450

Brain PD (15 decks)

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