Circulating autoantibodies against the NR2 peptide of the NMDA receptor are associated with subclinical brain damage in hypertensive patients with other pre-existing conditions for vascular risk.
Arterial hypertension (HT) and other vascular pre-existing conditions (PEC) generate asymptomatic brain damage which increases the occurrence of stroke and cognitive decline. The aim of this work was to explore if serum antibodies against the NR2 subunit of the NMDA receptor (NR2Ab) could predict subclinical brain damage (SBD) in hypertensive patients with PEC. Forty seven neurologically asymptomatic hypertensive subjects were classified according to the number of PEC (retinopathy, overweight/obesity, diabetes mellitus and dyslipidemia). NR2A/B Ab were measured in serum employing an ELISA method. 3.0-T Brain MRI imaging was performed, and visual ratings of white matter hyperintensities (WMH) and counts of dilated Virchow-Robin spaces (DVRS) and lacunes were obtained. Brain atrophy was evaluated with cortical thickness measurements and linear measures. Higher levels of NR2Ab were associated with more severe periventricular WMH (PWMH), more DVRS and more severe SBD; while greater frontal interhemispheric fissure width (IHFW), as a linear measure of frontal atrophy, was inversely related with NR2Ab. Overall and regional cortical thickness were not significantly associated with NR2 Ab. A multivariate analyses showed that IHFW and PWMH were the only variables independently associated with serum NR2Ab concentration. ROC analysis revealed that NR2Ab (cutoff: 1.7ng/ml) predicted PWMH with a sensitivity and specificity of 65% and 87% respectively.


CONCLUSIONS
Serum NR2Ab levels may reflect SBD in HT subjects with PEC, especially in younger populations at risk, where age-related cortical atrophy has not yet been fully established.
Neurobiology Department, Institute of Neurology and Neurosurgery, Havana, Cuba. Electronic address: sergiogg@infomed.sld.cu.
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S
González-García
Neurobiology Department, Institute of Neurology and Neurosurgery, Havana, Cuba. Electronic address: aglez@infomed.sld.cu.
A
A
González-Quevedo
Radiology Department, Institute of Neurology and Neurosurgery, Havana, Cuba. Electronic address: zmhernandez@infomed.sld.cu.
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Z
Hernandez-Diaz
Policlinic "19 de Abril", Havana, Cuba.
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L
Alvarez Camino
Neurobiology Department, Institute of Neurology and Neurosurgery, Havana, Cuba. Electronic address: marisol.pena@infomed.sld.cu.
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M
Peña-Sanchez
Neurobiology Department, Institute of Neurology and Neurosurgery, Havana, Cuba. Electronic address: aceiriz@infomed.sld.cu.
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A
Cordero-Eiriz
Clinical Neurosciences, Neuroscience Center, Havana, Cuba. Electronic address: martabr@infomed.sld.cu.
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Brown
Clinical Neurosciences, Neuroscience Center, Havana, Cuba. Electronic address: gaya@cneuro.edu.cu.
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JA
Gaya
Neurobiology Department, Institute of Neurology and Neurosurgery, Havana, Cuba.
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M
Betancourt-Losa
Neurobiology Department, Institute of Neurology and Neurosurgery, Havana, Cuba.
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Fernandez-Almirall
Neurobiology Department, Institute of Neurology and Neurosurgery, Havana, Cuba. Electronic address: cary@infomed.sld.cu.
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MC
Menendez-Sainz
Neurobiology Department, Institute of Neurology and Neurosurgery, Havana, Cuba. Electronic address: rebeca@infomed.sld.cu.
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Fernandez-Carriera
D000328:Adult; D000368:Aged; D001284:Atrophy / Q000209:etiology / Q000473:pathology; D001323:Autoantibodies / Q000097:blood*; D001794:Blood Pressure / Q000502:physiology; D001930:Brain Injuries / Q000097:blood* / Q000000981:diagnostic imaging / Q000209:etiology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications*; D007091:Image Processing, Computer-Assisted; D016014:Linear Models; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D064266:Preexisting Condition Coverage / Q000706:statistics & numerical data*; D012372:ROC Curve; D016194:Receptors, N-Methyl-D-Aspartate / Q000276:immunology*; D018709:Statistics, Nonparametric
D001323:Autoantibodies; C120997:NR2A NMDA receptor; D016194:Receptors, N-Methyl-D-Aspartate
Brain atrophy; Hypertension; NR2 antibodies; Subclinical brain damage, vascular pre-existing conditions; White matter hyperintensities