Brain inflammation is induced by co-morbidities and risk factors for stroke
Abstract
Chronic systemic inflammatory conditions, such as atherosclerosis, diabetes and obesity are associated with increased risk of stroke, which suggests that systemic inflammation may contribute to the development of stroke in humans. The hypothesis that systemic inflammation may induce brain pathology can be tested in animals, and this was the key objective of the present study. First, we assessed inflammatory changes in the brain in rodent models of chronic, systemic inflammation. PET imaging revealed increased microglia activation in the brain of JCR-LA (corpulent) rats, which develop atherosclerosis and obesity, compared to the control lean strain. Immunostaining against Iba1 confirmed reactive microgliosis in these animals. An atherogenic diet in apolipoprotein E knock-out (ApoE(-/-)) mice induced microglial activation in the brain parenchyma within 8 weeks and increased expression of vascular adhesion molecules. Focal lipid deposition and neuroinflammation in periventricular and cortical areas and profound recruitment of activated myeloid phagocytes, T cells and granulocytes into the choroid plexus were also observed. In a small, preliminary study, patients at risk of stroke (multiple risk factors for stroke, with chronically elevated C-reactive protein, but negative MRI for brain pathology) exhibited increased inflammation in the brain, as indicated by PET imaging. These findings show that brain inflammation occurs in animals, and tentatively in humans, harbouring risk factors for stroke associated with elevated systemic inflammation. Thus a "primed" inflammatory environment in the brain may exist in individuals at risk of stroke and this can be adequately recapitulated in appropriate co-morbid animal models.
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BibTeX
@article{drake2026brain,
title = {{Brain inflammation is induced by co-morbidities and risk factors for stroke}},
author = {Caroline Drake and Hervé Boutin and Matthew Jones and Adam Denes and Barry Mccoll and Johann Selvarajah and Sharon Hulme and Rachel Georgiou and Rainer Hinz and Alexander Gerhard and Andy Vail and Christian Prenant and Peter Julyan and Renaud Maroy and Gavin Brown and Alison Smigova and Karl Herholz and Michael Kassiou and David Crossman and Sheila Francis and Spencer Proctor and James Russell and Stephen Hopkins and Pippa Tyrrell and Nancy Rothwell and Stuart Allan},
journal = {Brain, Behavior, and Immunity},
year = {2026},
month = oct,
doi = {10.1016/j.bbi.2011.02.008},
url = {https://hal.science/hal-05789918v1},
note = {CC BY},
}
RIS
TY - JOUR
TI - Brain inflammation is induced by co-morbidities and risk factors for stroke
AU - Caroline Drake
AU - Hervé Boutin
AU - Matthew Jones
AU - Adam Denes
AU - Barry Mccoll
AU - Johann Selvarajah
AU - Sharon Hulme
AU - Rachel Georgiou
AU - Rainer Hinz
AU - Alexander Gerhard
AU - Andy Vail
AU - Christian Prenant
AU - Peter Julyan
AU - Renaud Maroy
AU - Gavin Brown
AU - Alison Smigova
AU - Karl Herholz
AU - Michael Kassiou
AU - David Crossman
AU - Sheila Francis
AU - Spencer Proctor
AU - James Russell
AU - Stephen Hopkins
AU - Pippa Tyrrell
AU - Nancy Rothwell
AU - Stuart Allan
PY - 2026
DA - 2026/10/09
JO - Brain, Behavior, and Immunity
DO - 10.1016/j.bbi.2011.02.008
UR - https://hal.science/hal-05789918v1
AB - Chronic systemic inflammatory conditions, such as atherosclerosis, diabetes and obesity are associated with increased risk of stroke, which suggests that systemic inflammation may contribute to the development of stroke in humans. The hypothesis that systemic inflammation may induce brain pathology can be tested in animals, and this was the key objective of the present study. First, we assessed inflammatory changes in the brain in rodent models of chronic, systemic inflammation. PET imaging revealed increased microglia activation in the brain of JCR-LA (corpulent) rats, which develop atherosclerosis and obesity, compared to the control lean strain. Immunostaining against Iba1 confirmed reactive microgliosis in these animals. An atherogenic diet in apolipoprotein E knock-out (ApoE(-/-)) mice induced microglial activation in the brain parenchyma within 8 weeks and increased expression of vascular adhesion molecules. Focal lipid deposition and neuroinflammation in periventricular and cortical areas and profound recruitment of activated myeloid phagocytes, T cells and granulocytes into the choroid plexus were also observed. In a small, preliminary study, patients at risk of stroke (multiple risk factors for stroke, with chronically elevated C-reactive protein, but negative MRI for brain pathology) exhibited increased inflammation in the brain, as indicated by PET imaging. These findings show that brain inflammation occurs in animals, and tentatively in humans, harbouring risk factors for stroke associated with elevated systemic inflammation. Thus a "primed" inflammatory environment in the brain may exist in individuals at risk of stroke and this can be adequately recapitulated in appropriate co-morbid animal models.
SN - 0889-1591
SN - 1090-2139
ER -