Cognitive and neurologic deficits in the MRL/lpr mouse: A clinicopathologic study

David C Hess, M. Taormina, J. Thompson, Kapil Dev Sethi, B. Diamond, R. Rao, C. R. Chamberlain, D. S. Feldman

Research output: Contribution to journalArticle

82 Citations (Scopus)

Abstract

Objectives. Determine if the MRL/lpr mouse develops neurological deficits and, if so, the pathologic basis for these deficits. Antiphospholipid antibodies (aPL) are associated with ischemic stroke, multiinfarct dementia, chorea, and cardiac valvular abnormalities. The MRL/lpr mouse develops high titer anticardiolipin antibodies (aCL) suggesting that it may be used as a model for the neurological complications of aPL. Methods. We undertook a prospective clinicopathologic study comparing the MRL/lpr mouse against its congenic strain, the MRL/+ mouse. We studied 15 MRL/lpr and 15 MRL/+ mice at 16 to 20 weeks and a group of 16 mice of each strain at 8 to 10 weeks. aCL and anti-DNA antibodies were measured by ELISA. Cognitive and neurological deficits were assessed by a water maze and a standardized rodent neurological examination. The brains and cardiac valves of the mice were then examined pathologically. Results. The MRL/lpr mice had significantly elevated aCL at both ages. Cognitive and sensorimotor deficits were apparent at 16 weeks but no correlation could be found with aCL or anti-DNA titer. Even at 8 weeks the MRL/lpr mice performed poorer on the water maze when compared to their age matched congenic strain. No evidence of cerebral infarction was found but mononuclear infiltrates were found in the choroid plexus of all the MRL/lpr mice at both 10 and 20 weeks. No evidence of cardiac valve pathology was seen at 20 weeks. Conclusions. (I) The MRL/lpr mouse develops cognitive and neurologic deficits. The etiology of these deficits is not clear but may be related to early infiltration of the central nervous system with mononuclear cells. (2) Despite the elevated aCL, evidence of cerebral infarction or mitral valve abnormalities could not be found.

Original languageEnglish (US)
Pages (from-to)610-617
Number of pages8
JournalJournal of Rheumatology
Volume20
Issue number4
StatePublished - Jan 1 1993

Fingerprint

Inbred MRL lpr Mouse
Neurologic Manifestations
Anticardiolipin Antibodies
Antiphospholipid Antibodies
Heart Valves
Cerebral Infarction
Neurological Models
Multi-Infarct Dementia
Chorea
Choroid Plexus
Water
Antinuclear Antibodies
Neurologic Examination
Mitral Valve
Rodentia
Central Nervous System
Enzyme-Linked Immunosorbent Assay
Stroke
Prospective Studies
Pathology

Keywords

  • animal model
  • anticardiolipin
  • antiphospholipid
  • cognitive testing
  • systemic lupus erythematosus

ASJC Scopus subject areas

  • Rheumatology
  • Immunology and Allergy
  • Immunology

Cite this

Hess, D. C., Taormina, M., Thompson, J., Sethi, K. D., Diamond, B., Rao, R., ... Feldman, D. S. (1993). Cognitive and neurologic deficits in the MRL/lpr mouse: A clinicopathologic study. Journal of Rheumatology, 20(4), 610-617.

Cognitive and neurologic deficits in the MRL/lpr mouse : A clinicopathologic study. / Hess, David C; Taormina, M.; Thompson, J.; Sethi, Kapil Dev; Diamond, B.; Rao, R.; Chamberlain, C. R.; Feldman, D. S.

In: Journal of Rheumatology, Vol. 20, No. 4, 01.01.1993, p. 610-617.

Research output: Contribution to journalArticle

Hess, DC, Taormina, M, Thompson, J, Sethi, KD, Diamond, B, Rao, R, Chamberlain, CR & Feldman, DS 1993, 'Cognitive and neurologic deficits in the MRL/lpr mouse: A clinicopathologic study', Journal of Rheumatology, vol. 20, no. 4, pp. 610-617.
Hess DC, Taormina M, Thompson J, Sethi KD, Diamond B, Rao R et al. Cognitive and neurologic deficits in the MRL/lpr mouse: A clinicopathologic study. Journal of Rheumatology. 1993 Jan 1;20(4):610-617.
Hess, David C ; Taormina, M. ; Thompson, J. ; Sethi, Kapil Dev ; Diamond, B. ; Rao, R. ; Chamberlain, C. R. ; Feldman, D. S. / Cognitive and neurologic deficits in the MRL/lpr mouse : A clinicopathologic study. In: Journal of Rheumatology. 1993 ; Vol. 20, No. 4. pp. 610-617.
@article{f5080c2ad94b4e698ab9d3e649356f0c,
title = "Cognitive and neurologic deficits in the MRL/lpr mouse: A clinicopathologic study",
abstract = "Objectives. Determine if the MRL/lpr mouse develops neurological deficits and, if so, the pathologic basis for these deficits. Antiphospholipid antibodies (aPL) are associated with ischemic stroke, multiinfarct dementia, chorea, and cardiac valvular abnormalities. The MRL/lpr mouse develops high titer anticardiolipin antibodies (aCL) suggesting that it may be used as a model for the neurological complications of aPL. Methods. We undertook a prospective clinicopathologic study comparing the MRL/lpr mouse against its congenic strain, the MRL/+ mouse. We studied 15 MRL/lpr and 15 MRL/+ mice at 16 to 20 weeks and a group of 16 mice of each strain at 8 to 10 weeks. aCL and anti-DNA antibodies were measured by ELISA. Cognitive and neurological deficits were assessed by a water maze and a standardized rodent neurological examination. The brains and cardiac valves of the mice were then examined pathologically. Results. The MRL/lpr mice had significantly elevated aCL at both ages. Cognitive and sensorimotor deficits were apparent at 16 weeks but no correlation could be found with aCL or anti-DNA titer. Even at 8 weeks the MRL/lpr mice performed poorer on the water maze when compared to their age matched congenic strain. No evidence of cerebral infarction was found but mononuclear infiltrates were found in the choroid plexus of all the MRL/lpr mice at both 10 and 20 weeks. No evidence of cardiac valve pathology was seen at 20 weeks. Conclusions. (I) The MRL/lpr mouse develops cognitive and neurologic deficits. The etiology of these deficits is not clear but may be related to early infiltration of the central nervous system with mononuclear cells. (2) Despite the elevated aCL, evidence of cerebral infarction or mitral valve abnormalities could not be found.",
keywords = "animal model, anticardiolipin, antiphospholipid, cognitive testing, systemic lupus erythematosus",
author = "Hess, {David C} and M. Taormina and J. Thompson and Sethi, {Kapil Dev} and B. Diamond and R. Rao and Chamberlain, {C. R.} and Feldman, {D. S.}",
year = "1993",
month = "1",
day = "1",
language = "English (US)",
volume = "20",
pages = "610--617",
journal = "Journal of Rheumatology",
issn = "0315-162X",
publisher = "Journal of Rheumatology",
number = "4",

}

TY - JOUR

T1 - Cognitive and neurologic deficits in the MRL/lpr mouse

T2 - A clinicopathologic study

AU - Hess, David C

AU - Taormina, M.

AU - Thompson, J.

AU - Sethi, Kapil Dev

AU - Diamond, B.

AU - Rao, R.

AU - Chamberlain, C. R.

AU - Feldman, D. S.

PY - 1993/1/1

Y1 - 1993/1/1

N2 - Objectives. Determine if the MRL/lpr mouse develops neurological deficits and, if so, the pathologic basis for these deficits. Antiphospholipid antibodies (aPL) are associated with ischemic stroke, multiinfarct dementia, chorea, and cardiac valvular abnormalities. The MRL/lpr mouse develops high titer anticardiolipin antibodies (aCL) suggesting that it may be used as a model for the neurological complications of aPL. Methods. We undertook a prospective clinicopathologic study comparing the MRL/lpr mouse against its congenic strain, the MRL/+ mouse. We studied 15 MRL/lpr and 15 MRL/+ mice at 16 to 20 weeks and a group of 16 mice of each strain at 8 to 10 weeks. aCL and anti-DNA antibodies were measured by ELISA. Cognitive and neurological deficits were assessed by a water maze and a standardized rodent neurological examination. The brains and cardiac valves of the mice were then examined pathologically. Results. The MRL/lpr mice had significantly elevated aCL at both ages. Cognitive and sensorimotor deficits were apparent at 16 weeks but no correlation could be found with aCL or anti-DNA titer. Even at 8 weeks the MRL/lpr mice performed poorer on the water maze when compared to their age matched congenic strain. No evidence of cerebral infarction was found but mononuclear infiltrates were found in the choroid plexus of all the MRL/lpr mice at both 10 and 20 weeks. No evidence of cardiac valve pathology was seen at 20 weeks. Conclusions. (I) The MRL/lpr mouse develops cognitive and neurologic deficits. The etiology of these deficits is not clear but may be related to early infiltration of the central nervous system with mononuclear cells. (2) Despite the elevated aCL, evidence of cerebral infarction or mitral valve abnormalities could not be found.

AB - Objectives. Determine if the MRL/lpr mouse develops neurological deficits and, if so, the pathologic basis for these deficits. Antiphospholipid antibodies (aPL) are associated with ischemic stroke, multiinfarct dementia, chorea, and cardiac valvular abnormalities. The MRL/lpr mouse develops high titer anticardiolipin antibodies (aCL) suggesting that it may be used as a model for the neurological complications of aPL. Methods. We undertook a prospective clinicopathologic study comparing the MRL/lpr mouse against its congenic strain, the MRL/+ mouse. We studied 15 MRL/lpr and 15 MRL/+ mice at 16 to 20 weeks and a group of 16 mice of each strain at 8 to 10 weeks. aCL and anti-DNA antibodies were measured by ELISA. Cognitive and neurological deficits were assessed by a water maze and a standardized rodent neurological examination. The brains and cardiac valves of the mice were then examined pathologically. Results. The MRL/lpr mice had significantly elevated aCL at both ages. Cognitive and sensorimotor deficits were apparent at 16 weeks but no correlation could be found with aCL or anti-DNA titer. Even at 8 weeks the MRL/lpr mice performed poorer on the water maze when compared to their age matched congenic strain. No evidence of cerebral infarction was found but mononuclear infiltrates were found in the choroid plexus of all the MRL/lpr mice at both 10 and 20 weeks. No evidence of cardiac valve pathology was seen at 20 weeks. Conclusions. (I) The MRL/lpr mouse develops cognitive and neurologic deficits. The etiology of these deficits is not clear but may be related to early infiltration of the central nervous system with mononuclear cells. (2) Despite the elevated aCL, evidence of cerebral infarction or mitral valve abnormalities could not be found.

KW - animal model

KW - anticardiolipin

KW - antiphospholipid

KW - cognitive testing

KW - systemic lupus erythematosus

UR - http://www.scopus.com/inward/record.url?scp=0027288802&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027288802&partnerID=8YFLogxK

M3 - Article

C2 - 8496852

AN - SCOPUS:0027288802

VL - 20

SP - 610

EP - 617

JO - Journal of Rheumatology

JF - Journal of Rheumatology

SN - 0315-162X

IS - 4

ER -