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• Anatomic abnormalities

- Larger ventricles
- Decreased brain volume in medial temporal
areas
- Changes in hipocampus
• Kelainan neurotransmitter
- Dopaminergic system
• Inflammation and immune function
• Genetic
- Kembar monozigot
Kromosom 1q 5q 6p 6q 8p 10p 13q 15q 22q
Mutasi di a-7 nicotinic receptor, DISC 1, GRM 3,
COM NRG 1, RGS 4, and G 72.
• Biochemical
Dopamine Hypothesis
• >> dopaminergic activity
>> release of dopamine
>> dopamine receptors
hypersensi tivity ofthe dopamine receptors to
dopamine
or a combination of these mechanisms.
• Serotonin
• GABA
Loss of GABAergic neuron in the hippocampus
hyperactivity of dopamiergc neurons
• Neuropeptides
Alteration in neuropeptide mechanisms could facilitate,
inhibit, or otherwise alter the pattern of firing these
neuronal systems.
• Glutamate
Neurotoxicity
• Ach and Nicotine
decreased muscarinic and nicotinic receptors in e
caudate-putamen, hippocampus, and selected regions of
the pre frontal cortex.
• Cerebral Ventricles
lateral and third ventricular enlargement and some reduction
in cortical volume.
• Reduced Symmetry
This reduced symmetry is believed by some investigators to
originate during fetal life and to be indicative of a disruption in
brain lateralization during neurodevelopment.
• Lymbic system
- decrease in the size ofthe region, including the amygdala,
the hippocampus, and the parahippocampal gyrus.
- disturbances in glutamate transmission
- Prefrontal cortex
• Thalamus
volume shrinkage or neuronal loss, in particular
subnuclei.
• Basal ganglia and cerebellum
Cell loss, reduction volume of the globu pallidus
and substantitia nigra.
Increase in the number of D2 receptor in
caudate, putamen.

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