Introduction to Affective Disorder

Question 1

What are the two main categories of Affective disorder?

Answer 1

Depressed mood and Bi-polar disorder

Question 2

What are the manuals used to classify disorders and why?

Answer 2

DSM (USA) and ICD (Europe)

To communicate to patients

To communicate to other clinicians

To Communicate to health insurance

Question 3

What Comorbidities do you see with affective disorders?

Answer 3

Anxiety, substance abuse and impulse control disorders

Question 4

What impact do mood disorders have on teenagers, dementia and society?

Answer 4

Early onset, hard to diagnose due to teenage behaviour and drug use

Significant effect on individual and family-increases risk of dementia by 2X (60000n meta-analysis)

Burden to individual and society

Question 5

What is the difference between Causes and Correlates?

Answer 5

Causes: Something that produces an effect

Correlate: Phenomeon that accompanies another Phenomeon, usually in a parallel or related way

Question 6

What are the approaches we can use to research mood disorders?

Answer 6

Engagement and communications-patients and families

Evaluation of underlying biological approaches:

Patients Blood, Saliva, etc,
iPS Cells
Post Mortem Material
Imagining Techniques
Animal Studies

Question 7

How do animal models aid in our understanding of Affective disorders?

Answer 7

Provide a series of behaviours

Enhance understanding of Biological underpinning as brain and behaviour relationship is elucidated

Identify new pathways for drugs and interventions

Question 8

What Animal behavioural/environmental models used? And what Internal alterations are used?

Answer 8

Environmental:
Restraint test

Unpredictable stress

Social defeat

Isolation

Maternal or sleep deprivation

Internal:
Permanent: Adrenal or olfactory removal)

Transient: (Manipulation of)
Immune or stress system
Dietary

Genetic:
Transgenic and KO
Extreme types of pop
Use of inbred Line

Question 9

How do Genes inform research in affective disorders?

Answer 9

Improve prognosis and Diagnosis-predict disease and identify risk groups

Pharmacognetics-Drug efficacy and adverse reactions

Research: Novel targets

Question 10

What is the heritability of unipolar and bi-polar depression?

Answer 10

Unipolar 30-40%

Bi-polar 80-90%

Question 11

What did the GWAS of MDD by Ripke reveal?

Answer 11

That there was no single nucleotide polymorphism responsible for depression.

Heterogeneity and sample size remains an issue.

Question 12

How did the Converge Study deal with the issues of sample size and Heterogeneity?

Answer 12

They streamlined there sample and controls:

Females
Recurrent Depression
over 5000 cases and controls
Only Chinese
interviews fro detailed info on environment

Question 13

What did the Converge study find?

Answer 13

Two loci on chromosome 10 were significant.

Question 14

How can we use imagining approaches to study affective disorders?

Answer 14

Structurally: MRI, CT/CAT, DTI

Functionally: PET and SPECT: distribution of Neurotransmitters

fMRI: Changes in blood flow due to use

The above functional options are indirect examples

Direct functional examples are:

MEG and EEG

Question 15

What did the Redilch et al study show us regarding Brain morphology in unipolar and Bi polar disorders?

Answer 15

Bi-polar patients showed reduced Hippocampus and amygdala.

Question 16

What did Joshi et al find regarding structural plasticity and ECG in MDD?

Answer 16

Patients with MDD all showed lower hippocampal and amygdala volume to start, but increased volume over the course of treatment .

Question 17

What is NICE?

Answer 17

National Institute for Clinical Excellence

Part of the DEPt of Health

Helps to decide best route for treatment in efficacy and economics.

Question 18

What 3 facts do the WHO tell us regarding Depression

Answer 18

It’s the leading cause of disability worldwide,
despite the high number of treatments:
High relapse
Low recovery rate

Question 19

What is the monoamine hypothesis and how did it come about?

Answer 19

It is the theory that depression is caused by the lack of monoamine neurotransmitter levels.

1950’s treatment of TB used the drug iproniazid. This increased mood and was seen to inhibit breakdown of monoamines.

Theory was then that the availability of monoamines was the cause.

Question 20

What was the previous belief regarding neurons?

Answer 20

That the number of neurons were fixed at birth.
Neuroplasticity was due to synaptic strength not neuronal growth.
Research focused on:
NT release and receptors
Number of synapses

Question 21

What was the neurogenesis theory?

Answer 21

That the ability to increase neurons in adults can improve depressive symptoms.

Question 22

Why did the monoamine theory come under fire and what theories have come to rise?

Answer 22

Due to the delayed response of SSRI’s.

HPA dysfunction
Macrophage Theory
Oxidative Stress

Question 23

How did Jacobs et al show the neurogenesis effect on depression?

Answer 23

By using an animal model they showed:

Stress and raised gluccocorticoids decreased neurons and increased depression

Exercise and Antidepressants:

Depression decreased and neurons increased

Question 24

What did Boldrini ert al show regarding Antidepressants and neurons?

Answer 24

MDD have low numbers of neurons.

Those on triciylics increased neurons.

Question 25

Where does the neurogenises tend to take place with antidepressants?

Answer 25

IN the hippocampus, SGZ of Dentate gyrus and SVZ of lateral ventricles.

Question 26

How does the theory of oxidative stress account for depression?

Answer 26

The imbalance of oxidants to anti-oxidants results in decreased neurogenesis or intercellular communication.

Question 27

What does the meta-analysis of oxidative stress by Palta tell us?

Answer 27

That most studies show a significant correlation between oxidative stress and depression.

Question 28

What is the correct way to approach to deal with mood disorders?

Answer 28

In a Holistic way.