The blood–brain barrier in psychosis

Thomas A Pollak; Svetlana Drndarski; James M Stone; Anthony S David; Philip McGuire; N Joan Abbott

doi:10.1016/S2215-0366(17)30293-6

The blood–brain barrier in psychosis

Thomas A Pollak, Svetlana Drndarski, James M Stone, Anthony S David, Philip McGuire, N Joan Abbott

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215 Citations (Scopus)

Abstract

Blood–brain barrier pathology is recognised as a central factor in the development of many neurological disorders, but much less is known about the role of the blood–brain barrier in psychiatric disorders. We review post-mortem, serum-biomarker, CSF-biomarker, and neuroimaging studies that have examined blood–brain barrier structure and function in schizophrenia and related psychoses. We consider how blood–brain barrier dysfunction could relate to glutamatergic and inflammatory abnormalities, which are increasingly understood to play a part in the pathogenesis of psychosis. Mechanisms by which the blood–brain barrier and its associated solute transporters moderate CNS availability of antipsychotic drugs are summarised. We conclude that the complex nature of blood–brain barrier dysfunction in psychosis might be relevant to many aspects of disrupted neuronal and synaptic function, increased permeability to inflammatory molecules, disrupted glutamate homoeostasis, impaired action of antipsychotics, and development of antipsychotic resistance. Future research should address the longitudinal course of blood–brain barrier alterations in psychosis, to determine whether blood–brain barrier dysfunction is a cause or consequence of the pathology associated with the disorder.

Original language	English
Journal	The Lancet Psychiatry
DOIs	https://doi.org/10.1016/S2215-0366(17)30293-6
Publication status	E-pub ahead of print - 3 Aug 2017

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title = "The blood–brain barrier in psychosis",

abstract = "Blood–brain barrier pathology is recognised as a central factor in the development of many neurological disorders, but much less is known about the role of the blood–brain barrier in psychiatric disorders. We review post-mortem, serum-biomarker, CSF-biomarker, and neuroimaging studies that have examined blood–brain barrier structure and function in schizophrenia and related psychoses. We consider how blood–brain barrier dysfunction could relate to glutamatergic and inflammatory abnormalities, which are increasingly understood to play a part in the pathogenesis of psychosis. Mechanisms by which the blood–brain barrier and its associated solute transporters moderate CNS availability of antipsychotic drugs are summarised. We conclude that the complex nature of blood–brain barrier dysfunction in psychosis might be relevant to many aspects of disrupted neuronal and synaptic function, increased permeability to inflammatory molecules, disrupted glutamate homoeostasis, impaired action of antipsychotics, and development of antipsychotic resistance. Future research should address the longitudinal course of blood–brain barrier alterations in psychosis, to determine whether blood–brain barrier dysfunction is a cause or consequence of the pathology associated with the disorder.",

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T1 - The blood–brain barrier in psychosis

AU - Pollak, Thomas A

AU - Drndarski, Svetlana

AU - Stone, James M

AU - David, Anthony S

AU - McGuire, Philip

AU - Abbott, N Joan

PY - 2017/8/3

Y1 - 2017/8/3

N2 - Blood–brain barrier pathology is recognised as a central factor in the development of many neurological disorders, but much less is known about the role of the blood–brain barrier in psychiatric disorders. We review post-mortem, serum-biomarker, CSF-biomarker, and neuroimaging studies that have examined blood–brain barrier structure and function in schizophrenia and related psychoses. We consider how blood–brain barrier dysfunction could relate to glutamatergic and inflammatory abnormalities, which are increasingly understood to play a part in the pathogenesis of psychosis. Mechanisms by which the blood–brain barrier and its associated solute transporters moderate CNS availability of antipsychotic drugs are summarised. We conclude that the complex nature of blood–brain barrier dysfunction in psychosis might be relevant to many aspects of disrupted neuronal and synaptic function, increased permeability to inflammatory molecules, disrupted glutamate homoeostasis, impaired action of antipsychotics, and development of antipsychotic resistance. Future research should address the longitudinal course of blood–brain barrier alterations in psychosis, to determine whether blood–brain barrier dysfunction is a cause or consequence of the pathology associated with the disorder.

AB - Blood–brain barrier pathology is recognised as a central factor in the development of many neurological disorders, but much less is known about the role of the blood–brain barrier in psychiatric disorders. We review post-mortem, serum-biomarker, CSF-biomarker, and neuroimaging studies that have examined blood–brain barrier structure and function in schizophrenia and related psychoses. We consider how blood–brain barrier dysfunction could relate to glutamatergic and inflammatory abnormalities, which are increasingly understood to play a part in the pathogenesis of psychosis. Mechanisms by which the blood–brain barrier and its associated solute transporters moderate CNS availability of antipsychotic drugs are summarised. We conclude that the complex nature of blood–brain barrier dysfunction in psychosis might be relevant to many aspects of disrupted neuronal and synaptic function, increased permeability to inflammatory molecules, disrupted glutamate homoeostasis, impaired action of antipsychotics, and development of antipsychotic resistance. Future research should address the longitudinal course of blood–brain barrier alterations in psychosis, to determine whether blood–brain barrier dysfunction is a cause or consequence of the pathology associated with the disorder.

U2 - 10.1016/S2215-0366(17)30293-6

DO - 10.1016/S2215-0366(17)30293-6

M3 - Article

SN - 2215-0366

JO - The Lancet Psychiatry

JF - The Lancet Psychiatry

ER -

The blood–brain barrier in psychosis

Abstract

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