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Psychology & Neuroscience of Affective Disorders > Introduction to the complex world of mood > Flashcards

Introduction to the complex world of mood Flashcards

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1
Q

What are affective disorders?

A

Neuropsychiatric conditions broadly divided into 2 conditions:
- Depressed mood (MDD, clinical, unipolar, or major depression)

  • Bipolar disorder

= Mood disorders
- conditions characterised by a disturbance in one’s mood

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2
Q

What do the DSM and ICD offer?

A
  1. Common language, standard criteria
    - help mh professionals determine/communicate patient’s diagnosis
  2. Diagnostic criteria for research
  3. Resource for health insurance, pharmaceutical companies, and legal system
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3
Q

What are the comorbidities associated to affective disorders?

A
  • Anxiety disorders
  • Substance use disorders
  • Impulse control disorders
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4
Q

What is the association between mood disorders and dementia?

A

Increased risk of dementia

  • over 60,000 individuals, depression associate with 2-fold increased risk of developing dementia in older age
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5
Q

How does the identification of correlates and causes differ in mood disorders?

A

Correlates are more easily identifiable than causes in mood disorders

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6
Q

What is aetiology of an affective disorder?

A

> Nurture: environment/experience

> Nature: genes

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7
Q

What can improve our understanding of affective disorders?

A

> Engagement and communication with patients and their families

> Evaluation of underlying biological factors

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8
Q

How can you evaluate the underlying biological factors of affective disorders?

A
  1. Examining patients’ blood, saliva, hair, nails, urine, faecal matter
  2. Imaging techniques (patients vs. controls)
  3. Post-mortem sampling
  4. iPS cells
  5. Use of genome association and animal models
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9
Q

What is the benefit of using animal models for understanding mood disorders?

A

> Provide behavioural readouts

> Enhance understanding of biological underpinning through brain-behaviour associations

> Help identify new underlying pathways, drug targets, test protective interventions

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10
Q

What are the four types of environmental manipulations (procedures) we can operate in animal models?

A

> Social isolation

> Unpredictable chronic mild stress

> Social defeat (introduction of agressive animal)

> Physical manipulations

  • restraint stress
  • maternal deprivation
  • sleep deprivation
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11
Q

What are the three types of internal alterations we can operate in animal models?

A

> Permanent

  • olfactory bulbectomy (removal of olfactory bulb)
  • adrenalectomy (removal of adrenal glands)

> Transient

  • manipulation of immune/stress systems
  • disruptions induced by changing dietary composition

> Genetic modifications

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12
Q

Which genetic modifications can be made in animal models?

A

> Transgenic and knock-out animals with genetically altered systems

> Selection of extreme types from an animal population

> Use of inbred strains

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13
Q

What is the purpose of pharmacogenetics?

A

Identify genetic variants that control efficacy and possible adverse reactions to drugs

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14
Q

What is the genetic contribution to unipolar depression (Craddock and Forty, 2006)

A

Between 33-42%

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15
Q

What is the genetic contribution to bipolar disorder (Craddock and Forty, 2006)?

A

Between 80-90%

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16
Q

What did the mega-analysis of genome-wide association studies for major depressive disorders (Ripke et al., 2013) show?

A

> No single nucleotide polymorphisms (SNPs) reaching genome-wide significance

> Lack of result might be due to underlying heterogeneity of MDD cases part of the study

17
Q

What is the limit of most studies that try to identify the genetic contribution to depression?

A
  • Insufficient power

- Need of large sample size and/or decrease in heterogeneity of selected cases

18
Q

Which neuroimaging techniques indirectly measure neuronal activity?

A
  • PET
  • SPECT
  • fMRI
19
Q

Which neuroimaging techniques directly measure electrical activity?

A
  • MEG

- EEG

20
Q

How do PET and SPECT scans indirectly measure neuronal activity?

A

Look at distribution and density of neurotransmitter receptors in certain areas

21
Q

How does grey matter vary in depressive disorders (Redlich et al., 2014)?

A

Individuals with bipolar depression (BD) had decreased grey matter in sagittal and coronal slices of hippocampus and amygdala
vs. those with unipolar depression UD)

22
Q

What is the effect of electroconvulsive therapy (ECT) on the cortical structures of patients with major depression (Joshi et al., 2016)?

A
  • Patients with refractory depression showed smaller hippocampal volumes at baseline compared to controls
  • Increase in hippocampal and amygdala volumes after ECT treatment in relation to improvement in symptoms
23
Q

What is the National Institute for Health and Care Excellence (NICE)?

A

Public organisation which is part of Department of Health in UK

  • helps clinicians to choose the best therapies for their clients based on research, therapeutic outcomes, and health economics
24
Q

What is the leading cause of disability worldwide according to the World Health Organization (WHO, 2018)?

A

Depression

- high rate of relapse despite wide range of psychological/pharmacological treatments available

25
Q

What is the monoamine hypothesis of depression?

A

Depression is due to deficiency of neurotransmitter levels or signalling in the brain

26
Q

How did the monoamine hypothesis of depression emerge?

A
  • First antidepressants (isoniazid, iproniazid) first used as medication for tuberculosis in 1950s
  • Doctors noticed patients using this medication showed improvement in mood
  • it inhibited monoamine oxidase (break down enzyme of monoamine NTs)

-> it was concluded that depression likely caused by lack of neurotransmitters

27
Q

What are the three major monoamine neurotransmitters?

A
  • Serotonin (5HT)
  • Dopamine (DA)
  • Norepinephrine (NE)
28
Q

What makes serotonin, dopamine and norepinephrine monoamines?

A

They all have an amino group.

29
Q

What were the common misconceptions on neurons?

A

> Number of neurons in adult brain fixed in early life, with majority formed during pre-natal and perinatal stages

> Neuroplasticity in nervous sustem achieved by ‘strengthening’ without any addition of new neurons

30
Q

Which theories emerged from the discovery of adult neurogenesis ?

A

> Neurogenesis hypothesis/alterations

> Hypothalamic-pituitary-adrenal axis dysfunction

> Inflammatory alterations - Macrophage Theory of Depression

> Oxidative stress system alterations

31
Q

What does the neurogenesis hypothesis (alterations) of depression propose?

A

Changes in neurotransmission occur shortly after intake of antidepressants
BUT effects take 2 to 6 weeks

-> depression cannot be solely due to a lack of neurotransmitters

32
Q

Which findings support the adult neurogenesis explanation of depression?

A

> Altered rates of neurogenesis in adult hippocampus might underlie either development of major depression or recovery from it

  • stress / raised glucocorticoids decrease neurogenesis and increase depression levels
  • antidepressants and exercise increase neurogenesis and decrease depression levels

> Antidepressants increase neural progenitor cells in human hippocampus

  • low numbers of new neurons in individuals with depression
  • increased number of new neurons in individuals taking tricyclic antidepressants
33
Q

What is the association between adult neurogenesis and mood (Borsini et al., 2015)?

A

Process of neurons growing and forming new connections

  • takes several weeks
  • AND is associated with improvement in mood
34
Q

What did animal studies show on the effects of antidepressants and depression treatment (e.g. ECT)?

A

Antidepressants and treatment for depression (e.g. ECT) induce growth and enhanced branching of neurons in hippocampus
(cf. increased size of hippocampus)

35
Q

What is oxidative stress?

A

Consequence of biological imbalance between oxidants (Reactive Oxygen Species, ROS) and antioxidants

36
Q

What are the effects of oxidative stress?

A

> Decreases neurogenesis

> Can lead to loss of control in intracellular signalling pathways

37
Q

What do intracellular signalling pathways refer to?

A

Extracellular stimuli can induce chain of reactions which transmits signals from cell surface (through ligand binding, G-protein receptors) to intracellular target enzymes (including transcription factors)

= intracellular signal transduction

-> alters the regulation of gene expression

38
Q

What is the evidence on the association of depression and oxidative stress?

A

Meta-analysis of observational studies (Palta et al., 2014):

- correlation between depression and different levels of oxidative stress in individuals

39
Q

Which approach is most beneficial to individuals suffering of affective (mood) disorders?

A

A holistic approach

  • psycho-social factors, culture
  • nutrition
  • genetics
  • inflammation
  • early trauma
  • endocrine and immune system
  • oxidative stress

Psychology & Neuroscience of Affective Disorders (16 decks)

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