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New Biological Models of OCD: Implications of Subtypes

Published online by Cambridge University Press:  07 November 2014

Donatella Marazziti
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Extract

Neurobiological studies continue to generate new clues to the pathophysiology of obsessive-compulsive disorder (OCD). Currently, the weight of evidence implicates serotonin (5-hydroxytryptamine, 5-HT) receptor dysfunctions, but there is also evidence for abnormalities in other neurotransmitters, such as dopamine and noradrenaline, in neuropeptides, and for infective and immunological mechanisms. Such findings foster further questions, in particular the identification of the 5-HT receptor subtype involved, the meaning of the serotonergic abnormalities described thus far, and their relationships with the evidence of dysfunctions of other systems.

Certainly, new horizons can now be prospected for biological research in OCD with the ultimate goal of identifying the substrates of the clinical heterogeneity and of offering patients more targeted treatments.

Type
Supplement Monograph
Information
CNS Spectrums , Volume 3 , Issue S1: New Developments in Obsessive-Compulsive and Spectrum Disorders , May 1998 , pp. 24 - 25
Copyright
Copyright © Cambridge University Press 1998

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References

REFERENCES

1.Marazziti, D, Hollander, E, Lensi, P, Ravagli, S, Cassano, GB. Peripheral markers of serotonin and dopamine function in obsessive-compulsive disorder. Psychiatry Res. 1992;42:41–51.Google Scholar
2.Marazziti, D, Rossi, A, Gemignani, A, et al.Decreased H-paroxetine binding in obsessive-compulsive patients. Neuropsychobiology. 1996;34:184–187.Google Scholar
3.Lesch, KP, Hoh, A, Disselkamp-Tietze, J, et al.5-HydroxytryptaminelA receptor activity in obsessivecompulsive disorder: comparison of patients and controls. Arch Gen Psychiatry. 1991;48:540–547.Google Scholar
4.Sasson, Y, Zohar, J. New developments in obsessivecompulsive disorder research: implications for clinical management. Int Clin Psychopharmacol. 1996;11(Suppl 5):3–12.Google Scholar
5.Zohar, J. Is 5-HT1D receptor involved in obsessive-compulsive disorder? Eur Neuropsychopharmacol. 1996;6:54–55.Google Scholar
6.Marazziti, D, Rossi, A, Masala, I, et al.Regulation of the platelet serotonin transporter by protein kinase C in the young and elderly. Biol Psychiatry. In press.Google Scholar
7.McDougle, J, Goodman, WK, Price, LH, et al.Neuroleptic addition in fluvoxamine-refractory obsessive-compulsive disorder. Am J Psychiatry. 1990;147:652–654.Google Scholar
8.Leckman, JF, Goodman, WK, Anderson, GH, et al.Cerebrospinal fluid biogenic amines in obsessive-compulsive disorder, Tourette's syndrome and healthy controls. Neuropsychopharmacology. 1995;12:73–86.Google Scholar
9.Altemus, M, Swedo, SE, Leonard, B, et al.Changes in cerebrospinal fluid neurochemistry during treatment of obsessive-compulsive disorder with clomipramine. Arch Gen Psychiatry. 1994;51:794–803.CrossRefGoogle ScholarPubMed
10. Leckman JF, Goodman WK, North WG, et al.Elevated cerebrospinal fluid levels of oxytocin in obsessivecompulsive disorder. Arch Gen Psychiatry. 1994;51:782–792.Google Scholar
11.Swedo, SE, Leonard, H, Shapiro, MB, et al.Sydenham's chorea: physical and psychological symptoms of St. Vitus dance. Pediatrics. 1993;91:706–713.Google Scholar