Rosiglitazone attenuates the age-related changes in astrocytosis and the deficit in LTP.
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Cowley TR, O'Sullivan J, Blau C, Deighan BF, Jones R, Kerskens C, Richardson JC, Virley D, Upton N, Lynch MA, Rosiglitazone attenuates the age-related changes in astrocytosis and the deficit in LTP., Neurobiology of aging, 33, 1, 2012, 162-75Download Item:
Abstract:
Neuroinflammation is a significant and consistent feature of many neurodegenerative disorders, including Alzheimer?s disease (AD) and
Parkinson?s disease (PD). The greatest risk factor for neurodegenerative disorders is age and a proinflammatory phenotype in the aged brain
is believed to contribute to these neurodegenerative conditions. In animal models, neuroinflammatory changes, characterized by increased
microglial activation, have been associated with a loss of synaptic plasticity and here we show that treatment of aged rats with the PPAR
agonist, rosiglitazone, modulates the inflammatory changes and restores synaptic function. The evidence presented highlights an important
role for astrocytes in inducing inflammatory changes and suggests that the age-related astrogliosis and astrocytosis is responsible for the
increase in the proinflammatory cytokine, tumor necrosis factor alpha (TNF- ). Magnetic resonance (MR) imaging revealed an age-related
increase in T1 relaxation time and, importantly, treatment of aged rats with rosiglitazone reversed the age-related increases in astrogliosis
and astrocytosis, TNF- concentration and T1 relaxation time. The evidence indicates that the site of action for rosiglitazone is endothelial
cells, and suggests that its effect on astrocytes is secondary to its effect on endothelial cells.
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http://people.tcd.ie/lynchmahttp://people.tcd.ie/kerskenc
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Neurobiology of aging;33;
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