A molecular model for bipolar affective disorder

Herbert M. Lachman, D. F. Papolos

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

The biological basis of bipolar disorder is not known. Models for the illness have been proposed that were based on the neurobiological effects of pharmacological agents that affect mood. Although of great interest, these models have not adequately explained the striking clinical pattern of illness in which patients may experience either unipolar episodes or bipolar cycles of mania and depression. We now present a new model suggesting that the unique clinical heterogeneity found in patients with bipolar disorder could be explained by a defect in a 'downstream' portion of a signal transduction pathway that can regulate two or more neurotransmitter systems that have opposite effects on neuronal activity. This model may target specific candidate genes for involvement in bipolar disorder.

Original languageEnglish (US)
Pages (from-to)255-264
Number of pages10
JournalMedical Hypotheses
Volume45
Issue number3
DOIs
StatePublished - 1995

Fingerprint

Molecular Models
Mood Disorders
Bipolar Disorder
Neurotransmitter Agents
Signal Transduction
Pharmacology
Depression
Genes

ASJC Scopus subject areas

  • Medicine(all)
  • Developmental Biology
  • Drug Discovery

Cite this

A molecular model for bipolar affective disorder. / Lachman, Herbert M.; Papolos, D. F.

In: Medical Hypotheses, Vol. 45, No. 3, 1995, p. 255-264.

Research output: Contribution to journalArticle

Lachman, Herbert M. ; Papolos, D. F. / A molecular model for bipolar affective disorder. In: Medical Hypotheses. 1995 ; Vol. 45, No. 3. pp. 255-264.
@article{d02eba3dd11847d8a9274a76d46b73bd,
title = "A molecular model for bipolar affective disorder",
abstract = "The biological basis of bipolar disorder is not known. Models for the illness have been proposed that were based on the neurobiological effects of pharmacological agents that affect mood. Although of great interest, these models have not adequately explained the striking clinical pattern of illness in which patients may experience either unipolar episodes or bipolar cycles of mania and depression. We now present a new model suggesting that the unique clinical heterogeneity found in patients with bipolar disorder could be explained by a defect in a 'downstream' portion of a signal transduction pathway that can regulate two or more neurotransmitter systems that have opposite effects on neuronal activity. This model may target specific candidate genes for involvement in bipolar disorder.",
author = "Lachman, {Herbert M.} and Papolos, {D. F.}",
year = "1995",
doi = "10.1016/0306-9877(95)90114-0",
language = "English (US)",
volume = "45",
pages = "255--264",
journal = "Medical Hypotheses",
issn = "0306-9877",
publisher = "Churchill Livingstone",
number = "3",

}

TY - JOUR

T1 - A molecular model for bipolar affective disorder

AU - Lachman, Herbert M.

AU - Papolos, D. F.

PY - 1995

Y1 - 1995

N2 - The biological basis of bipolar disorder is not known. Models for the illness have been proposed that were based on the neurobiological effects of pharmacological agents that affect mood. Although of great interest, these models have not adequately explained the striking clinical pattern of illness in which patients may experience either unipolar episodes or bipolar cycles of mania and depression. We now present a new model suggesting that the unique clinical heterogeneity found in patients with bipolar disorder could be explained by a defect in a 'downstream' portion of a signal transduction pathway that can regulate two or more neurotransmitter systems that have opposite effects on neuronal activity. This model may target specific candidate genes for involvement in bipolar disorder.

AB - The biological basis of bipolar disorder is not known. Models for the illness have been proposed that were based on the neurobiological effects of pharmacological agents that affect mood. Although of great interest, these models have not adequately explained the striking clinical pattern of illness in which patients may experience either unipolar episodes or bipolar cycles of mania and depression. We now present a new model suggesting that the unique clinical heterogeneity found in patients with bipolar disorder could be explained by a defect in a 'downstream' portion of a signal transduction pathway that can regulate two or more neurotransmitter systems that have opposite effects on neuronal activity. This model may target specific candidate genes for involvement in bipolar disorder.

UR - http://www.scopus.com/inward/record.url?scp=0028810958&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028810958&partnerID=8YFLogxK

U2 - 10.1016/0306-9877(95)90114-0

DO - 10.1016/0306-9877(95)90114-0

M3 - Article

C2 - 8569548

AN - SCOPUS:0028810958

VL - 45

SP - 255

EP - 264

JO - Medical Hypotheses

JF - Medical Hypotheses

SN - 0306-9877

IS - 3

ER -