Biological Basis of Nervous System Disorders
High-Yield Summary
- Schizophrenia: mostly genetic (10x risk to first-degree relatives), plus birth hypoxemia and adolescent marijuana use as risk factors. Dopamine hypothesis = excess dopamine; neuroleptics (antipsychotics) treat it by blocking dopamine receptors.
- Depression: decreased norepinephrine, serotonin, and dopamine (monoamine theory — actual production reduced, not just reuptake/breakdown); also high amygdala glucose metabolism, hippocampal atrophy, elevated cortisol.
- Bipolar disorder: increased norepinephrine and serotonin (opposite direction from depression); higher risk with a bipolar parent or with multiple sclerosis.
- Alzheimer's genetics: PSEN1 (chr 14)/PSEN2 (chr 1) and APP (chr 21) → early-onset familial cases; APOE (chr 19) modulates late-onset/sporadic risk. Down syndrome → much higher risk.
- Alzheimer's biology: senile plaques = extracellular β-amyloid deposits; neurofibrillary tangles = intracellular hyperphosphorylated tau. Also: ↓acetylcholine, ↓choline acetyltransferase (ChAT), brain atrophy, flattened sulci, enlarged ventricles, ↓parietal/temporal metabolism.
- Parkinson's disease: ↓dopamine production in the substantia nigra → impaired basal ganglia function (movement initiation/termination/smoothing). Symptoms: bradykinesia, resting/pill-rolling tremor, masklike facies, cogwheel rigidity, shuffling gait. L-DOPA (dopamine precursor, crosses blood-brain barrier) is the treatment.
Key Terms
- Dopamine hypothesis
- Schizophrenia is linked to excess dopamine in the brain.
- Monoamine theory of depression
- Decreased norepinephrine, serotonin, and dopamine production underlies depression.
- Senile plaques
- Extracellular deposits of misfolded β-amyloid protein (Alzheimer's).
- Neurofibrillary tangles
- Intracellular aggregates of hyperphosphorylated tau protein (Alzheimer's).
- Substantia nigra
- Brain region that produces dopamine; its degeneration causes Parkinson's disease.
- L-DOPA
- Dopamine precursor that crosses the blood-brain barrier and is converted to dopamine in the brain.
Neurotransmitter Direction by Disorder
| Disorder | Neurotransmitter change |
|---|---|
| Schizophrenia | Excess dopamine |
| Depression | Decreased norepinephrine, serotonin, dopamine |
| Bipolar disorder | Increased norepinephrine, serotonin |
| Parkinson's disease | Decreased dopamine (substantia nigra) |
Alzheimer's: Plaques vs. Tangles
| Feature | Detail |
|---|---|
| Senile plaques | Extracellular; built from β-amyloid |
| Neurofibrillary tangles | Intracellular; built from hyperphosphorylated tau |
Common MCAT Trap
- Direction of neurotransmitter change is the most common trap: schizophrenia = excess dopamine, depression = deficits, bipolar = increases in norepinephrine/serotonin.
- Match the Alzheimer's gene to onset pattern: PSEN1/PSEN2/APP → early-onset familial; APOE → late-onset sporadic risk modulator (not a direct cause).
- Plaques (extracellular, β-amyloid) vs. tangles (intracellular, tau) — different location, different protein.
- L-DOPA is a precursor, not dopamine itself — given because dopamine can't cross the blood-brain barrier but L-DOPA can.
Quick Recall
Why are neuroleptics used to treat schizophrenia?
A CT scan shows extracellular protein deposits in an Alzheimer's patient's brain. Plaque or tangle?
Why is L-DOPA used instead of dopamine to treat Parkinson's disease?
Which Alzheimer's gene is most associated with early-onset familial disease?
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