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estrogen administration has been found to increase tryptophan hydroxylase

5-HT2A mRNA levels in brain areas relevant for the control of mood, mental state and cognition (Sumner and Fink, 1998) and 5-HTT mRNA when administered for a longer period

n the other hand, estrogen treatment has also been observed to decrease mRNA related to serotonergic neurotransmission

it is established that androgen modulates various neurotransmitters in the CNS. Testosterone decreases γ-aminobutyric acid concentration in the hypothalamus, which is blocked by flutamide, a testosterone receptor blocker (14, 15). Testosterone, probably by its conversion to estradiol, increases serotonin transporter mRNA expression in dorsal raphe nucleus (16), and it also increases the density of 5-hydroxytryptamine receptors and serotonin transporter sites in the forebrain (3, 16) of castrated male rats.

Insulin's effects on cognition may reflect normal regulation of glucose metabolism, long-term potentiation, and neurotransmitter levels

future therapeutic trials should consider the moderating effects of APOE genotype.

Similar patterns of neural activation are implicated in addictive-like eating behavior and substance dependence: elevated activation in reward circuitry in response to food cues and reduced activation of inhibitory regions in response to food intake.

The typical onset of TS occurs at 6–7 years of age and is characterized by the appearance of simple, recurrent motor tics, followed by the manifestation of phonic tics after several months [12]. In most children, TS symptoms undergo a progressive exacerbation, which reaches its zenith at the beginning of puberty (11–12 years of age), and is then followed by a gradual remission in the majority of patients

30–40% of TS-affected children retain their symptoms in adulthood

Multiple neurotransmitters have been implicated in TS, including dopamine (DA), serotonin, norepinephrine, acetylcholine, glutamate and γ-amino-butyric acid (GABA)