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Principles of Neuroscience > L27 - 29 - NS Disorders > Flashcards

L27 - 29 - NS Disorders Flashcards

1
Q

Four Categories of NS Disorders

A

1) Mental diseases - if you can’t see anything wrong, attributed to mental state, functional (the subject of psychiatry without an organic cause) (software issue)
2) Neurological disorders - pathological condition in tissue, organic disorder (the subject of neurology) (hardware issue)
3) Learning and developmental disabilities
4) Substance abuse disorders

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2
Q

Learning and developmental disabilities

A

Includes functional limitations that manifest in infancy or childhood as a result of disorders of or injuries to the developing NS

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3
Q

Males or females have higher rates of ADHD, autism and substance use disorders?

A

Males

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4
Q

Males or females have higher rates of major depressive disorder, most anxiety disorders and eating disorders?

A

Females

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5
Q

Prior to any schizophrenic psychotic episodes people with it may exhibit prodromal (period between appearance of symptoms and full development) signs such as? Why are they known as negative symptoms?

A
  • Social withdrawal
  • Neglect of personal hygiene
  • Odd ideas and behaviours
  • Flattened affect and paucity of speech
  • Negative symptoms - theses signs are an absence of normal actions
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6
Q

Schizophrenic non-psychotic signs may include

A
  • Tendencies to become overloaded with info
  • Difficulty in crowed rooms or when lots of people are talking
  • Easily distracted
  • Periods of great mental activity, creativity and excitement
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7
Q

Acute psychotic episodes are charactered by? Commonly auditory or visual?

A

Delusions of paranoia, grandiosity (extremely narcissistic - believing you are really important), spiritual or supernatural experiences. Auditory hallucinations are more common.
*Patients also experience the feeling that they are being controlled by external forces and loss of insight

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8
Q

Does schizophrenia have a genetic component to it?

A

Yes - If you are identical twins, and one has it, the other has a 48% chance of having it too.
*The more related you are to someone that has it, the more likely you will have it

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9
Q

Schizophrenia - what is a sign in the brain structures that indicate the presence of it?

A

Enlarged ventricles and loss of excitatory synapses, not enough loss of inhibitory synapses
*There is also enlarged ventricles in huntingtons

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10
Q

What antagonists can be used in treatment of schizophrenia?

A

Dopamine D2 receptors antagonists

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11
Q

Schizophrenia - What are the problems with the dopamine hypothesis?

A

1) Long duration before relief of symptoms
Dopamine antagonists can be shown to bind to receptors a short time after administration, but relieve of symptoms takes several weeks (as with antidepressants).

2) PCP (angel dust) acts on glutamate receptors instead
Paranoid delusions and hallucinations that control the person) but it acts on a subclass of glutamate receptors not dopamine receptors.

3) Some people don’t respond to D2 blockers, but to drugs that show broad monoamine antagonism.

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12
Q

NEUROLOGICAL DISEASE: ALZHEIMER’S DISEASE – what is it? What is it characterized by?

A

Form of dementia (deterioration of intellectual function and other cognitive skills). Characterized by deposition of amyloid protein (leading to aggregation of tau protein, a microtubule stabilizer, hence cell doesn’t function well because of the neurofibularly tangles formed-> leads to cell death) and the disruption of the neuronal cytoskeleton
*Amyloid plaque and neurofibularly tangles prevalent in parietal, occipital and medial temporal region

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13
Q

NEUROLOGICAL DISEASE: Epilepsy – what is it? What is it characterised by?

A

Common brain disorder characterized by two or more unprovoked seizures (affects 1% of population). It is more a symptom of a disease than a disease itself. Seizures are discrete events caused by transient, hyper-synchronous, abnormal neuronal activity.

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14
Q

Grand Mal Seizure

A

A generalized tonic-clonic seizure — features a loss of consciousness and violent muscle contractions. It’s the type of seizure most people picture when they think about seizures in general.

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15
Q

Seizures may occur in close temporal association with _, _ or _.

A

Acute stroke, sepsis or alcohol withdrawal

*Most cases have no immediate identifiable cause

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16
Q

Epilepsy - The recording of the small _____ ____ in the brain is generated by _____ oriented ______ neurons.

A

Electrical fields, orthogonally, cortical

17
Q

Epilepsy – 3 categories

A

1) Idiopathic epilepsy (e.g. childhood-onset absence epilepsy) which is thought to have a genetic basis (10%)
2) Secondary or symptomatic epilepsy, which is caused by a known CNS injury or disorder (e.g. infection, stroke or traumatic injury) (20%)
3) Cryptogenic epilepsy, for which there is no clear evidence of an etiological (origin) `factor (60%)

18
Q

What genetic mutations are affected in inherited/familial epilepsies?

A

Genes encoding proteins directly associated with neuronal excitability e.g. ion channels, NT receptors

19
Q

Multiple Sclerosis - what is it characterized by? What does it affect?

A

A chronic, autoimmune disease characterized by destruction of myelin in the CNS. Symptoms include changes in sensation, visual problems, muscle weakness, depression, coordination and speech difficulty, severe fatigue, cognitive impairment, balance problems, overheating and pain.

20
Q

ASD – what is it? Characterized by?

A
  • Heterogeneous neurodevelopment disorder.

- Characterized by impaired social interaction, communication deficits, stereotyped repetitive behaviour.

21
Q

ASD – affects F or M more?

A

Males, 4:1 *affects 1 in 68 children

22
Q

Is Asperger’s syndrome part of ASD?

A

Yes

23
Q

ASD – How long does it last? Treatment?

A

Lasts lifelong, no treatment

*Even the cause of movement disorders/repetitive behaviour in ASD is unknown

24
Q

T/F: ASD people can be hyper agile

A

T

25
Q

ASD - Co-morbidties

A
  • GI symptoms
  • Sensory defects
  • Motor disorders
  • Anxiety
  • Sleep disorders
  • Seizure
  • Aggression
26
Q

Motor disorders in ASD

A

• All ASD patients have repetitive behaviours
- These can include hand flapping, echolalia, spinning, pacing..
• 60-80% of ASD patients have hypotonia (low muscle tone), gait problems, toe walking, and apraxia
• Both gross and fine motor impairments are common
• Gait, handwriting, maintaining constant grip force

27
Q

Brain regions involved in movement disorders

A
  • Regions involved in motor activity include the cerebellum and basal ganglia:
  • Dorsal striatum (caudate nucleus and putamen)
  • Ventral striatum (nucleus accumbens and olfactory tubercle)
  • Globus pallidus, ventral pallidum, substantia nigra, subthalamic nucleus
  • These regions are involved in Tourette syndrome, OCD and Parkinson’s disease.
28
Q

If you are an identical twin with a sibling with ASD, you are _ to _% likely to have ASD too. For non-identical twins this is up to _%

A

60-90, 20

*More than 100 genes associated with ASD

29
Q

Many mutations that cause autism alter _____

A

Synapses - e.g. Neuroligins, neurexins and Shank

30
Q

Autistic mice: model validity - what are the 3 validities?

A
  1. Construct validity: similar etiology to patients e.g. gene mutation
  2. Face validity: similar traits to patients “endophenotypes”
  3. Predictive validity: response to clinically effective treatments
31
Q

Mouse models of autism
• > 30 mouse models of autism – Includes transgenic, phenotype-first (using whatever mouse in the lab that has the phenotype first) and environmental models
• Show at least one endophenotype similar to core traits in patients (i.e. social, communication and repetitive behaviours such as excess grooming)
• Many show altered synaptic function
• Many show increased motor learning– Could this indicate repetitive behaviour?

A

Mouse models of autism
• > 30 mouse models of autism – Includes transgenic, phenotype-first (using whatever mouse in the lab that has the phenotype first) and environmental models
• Show at least one endophenotype similar to core traits in patients (i.e. social, communication and repetitive behaviours such as excess grooming)
• Many show altered synaptic function
• Many show increased motor learning– Could this indicate repetitive behaviour?

32
Q

Neuroligin-3 (NL3) are extremely rare

  • NL3 (R451C - Arginine at position 451 changed into cysteine) was found in two brothers with ASD
  • NL3 deletion was identified in 2 families
A

Neuroligin-3 (NL3) are extremely rare

  • NL3 (R451C - Arginine at position 451 changed into cysteine) was found in two brothers with ASD
  • NL3 deletion was identified in 2 families
33
Q

What does mutating NL3 do in mice? (In regards to Social, Communication and Repetition)

A
  • Social: increased aggression (reversed by risperidone)
  • Communication: reduced vocalizations in early development (postnatal day 8)
  • Repetitive: both NL3-R451C and NL3-KO mice show improved motor learning (Rothwell et al., Cell, 2014)
34
Q

NL3 mutant mice have improved motor learning
The rotarod test is a simple assay (increase the speed and time how long for the mouse to fall off)
-NL3 knockout mice are better at this test

A

NL3 mutant mice have improved motor learning
The rotarod test is a simple assay (increase the speed and time how long for the mouse to fall off)
-NL3 knockout mice are better at this test

35
Q

What are the 3 experiments we would do to test brain area that causes mice to be better at rotarod?

A
  1. Transgenic mice (mice bred with genes deleted or mutated) – e.g. NL3 KO
    - NL3 KO mice stay on rotarod longer
  2. Conditional mutants (genes deleted or mutated in specific brain regions – or at a specific stage in development)
    When NL3 is deleted from some neurons in the striatum (includes dorsal striatum and nucleus accumbens), motor learning is increased
    - This experiment deleted NL3 in neurons in the dorsal striatum and the nucleus accumbens (so we need to have viral constructs to figure out specifically which of the two structures it affects)
    - The D1-cre promoter deleted NL3 only in neurons expressing the D1 receptor only in neurons expressing the D1 receptor (D1-medium spiny neurons)
  3. Viral constructs (inject virus so that the gene mutation is expressed in a small area of the brain)
    - Inject a viral construct targeting all neurons
    - Only green fluorescent neurons at the injection site have NL3 deleted
36
Q

What brain area is involved in motor learning in NL3 KO mice?

A

The nucleus accumbens

37
Q

Experimental strategies to understand other autism endophenotypes
Compare mice using a simple assay
- In this case, the rotarod test (increase the speed and time how long for the mouse to fall off)
- Other tests for different endophenotypes e.g. video of grooming, aggression test etc

Generate mice with different patterns of gene expression and compare using the assay

  • Transgenic, conditional mutants, viral injection
  • But note that these experiments are very expensive and time consuming
A

Experimental strategies to understand other autism endophenotypes
Compare mice using a simple assay
- In this case, the rotarod test (increase the speed and time how long for the mouse to fall off)
- Other tests for different endophenotypes e.g. video of grooming, aggression test etc

Generate mice with different patterns of gene expression and compare using the assay

  • Transgenic, conditional mutants, viral injection
  • But note that these experiments are very expensive and time consuming
38
Q

T/F: ASD is homogeneous

A

FALSE - Autism (ASD) is heterogeneous

Principles of Neuroscience (25 decks)

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