A lot of good notes in the exam review lecture: NPB173-L17
For each:
Root Cause
- How deep do we understand level?
- Genetic? Environment?
- Neurological? Psychiatric?
Symptoms - Clusters? Triads?
- etc?
Treatments - How do they work?
- Future ideas?
Before Saying its understood…
Dive into the bigger idea for each disease.
What idea is it exposing?
- Epigentics?
- Dynamic systems?
- Activation networks?
How do those interface with content? Large impacts?
And theeenn..
Top it off by answering learning objectives
Fragile X
Autism
ADHD
Anxiety
Depression
Schizophrenia
Cause
Super high heritability, neurodevelopmental in nature. Starts in late adolescence / early adulthood
Symptoms
Postive:
Hallucinations, dellusions, disorganized thoughts
Neg
REduced speech (alogia), lack of emotional and facial expression (affective flattening), diminished ability to begin and sustain activities (avolition), decreased ability to find pleasure in everyday (anhedonia), social withdrawal
Cognitive
Memory, Attention, Planning, Decisionmaking
Treatment
Typical antipsychotic. These inhibit the inhibitory D2 receptors (afffects to the striatum).
- Reduce the positive symptoms, but no improvement to negative / cognitive decifics
- Many side effects: dy mouth,weight gain, movement disorders referred to as extrapyramidal symptoms (EPS)
- EPS involves disregulation of movement control circuits, involving basal ganglia through inhibition of D2 receptors
Atypical Psychotic: Doesn’t just inhibit D2 receptors, but 5-HT2A (serotonin) receptors too
- EPS involves disregulation of movement control circuits, involving basal ganglia through inhibition of D2 receptors
- one of 5-HT2A receptors effects if inhibition of dopamine neurons. If inhibited, leads to release of more dopamine neurons
- So, preventing D2 receptros at the same time potentially allowing more dopamine neurons to fire
- Potential to be just as effective as typical antipsychotics, but less side effects
Time scale is days to weeks