Hippocampal alterations of apolipoprotein E and D mRNA levels in vivo and in vitro following kainate excitotoxicity

Montpied, Pascale; Bock, Frédéric de; Lerner‐Natoli, Mireille; Bockaert, Joël; Rondouin, G.

doi:10.1016/s0920-1211(99)00003-0

Cited by 40 publications

(35 citation statements)

References 56 publications

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“…The increase of apoD expression that has been observed in response to diverse neuropathologies may represent a nonspecific response to cellular injury. However, given the distinct sites of apoD upregulation observed after CNS insult in the rodent studies and the regional specificity of apoD induction observed in human disease, [8][9][10][11][13][14][15] we hypothesize that apoD represents a response to a pathological process in affected brain regions. Given its role as a lipidbinding protein and member of the lipocalin family of transport proteins, apoD may be involved in the binding of steroids or fatty acids released upon CNS insult, or the transport of lipid molecules necessary for dendritic or synaptic remodeling in response to neuropathology.…”

Section: Discussionmentioning

confidence: 91%

“…Its expression is increased under pathological conditions and, in many cases, these increases occur in distinct brain regions. For example, in the rat, increased apoD immunoreactivity and mRNA levels have been observed in the hippocampus after kainic acid or entorhinal cortex lesioning 8,9 and in the cortex after traumatic brain injury. 10 ApoD mRNA and protein levels were elevated in the cerebellum of a mouse strain considered to be a model of NiemannPick disease, a human condition characterized by abnormal lysosomal cholesterol storage and chronic progressive neurodegeneration.…”

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confidence: 99%

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Differences in neuroanatomical sites of apoD elevation discriminate between schizophrenia and bipolar disorder

et al. 2003

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We previously demonstrated that apolipoprotein D (apoD) levels are elevated in the dorsolateral prefrontal cortex and caudate obtained postmortem from subjects with schizophrenia and bipolar disorder compared to controls, suggesting a focal compensatory response to neuropathology associated with psychiatric disorders. We have now extended those studies by measuring apoD protein levels in additional brain regions from post-mortem samples of schizophrenic and bipolar disorder subjects using an enzyme-linked immunosorbent assay. Increased apoD levels were observed in the lateral prefrontal cortex (Brodmann Area 46) in both schizophrenia (46%) and bipolar disorder (111%), and in the orbitofrontal cortex (Brodmann Area 11) (44.3 and 37.9% for schizophrenia and bipolar disorder, respectively). However, differences between the disease groups were observed in other brain regions. In subjects with schizophrenia, but not bipolar disorder, apoD levels were significantly elevated in the amygdala (42.8%) and thalamus (31.7%), while in bipolar disorder, but not schizophrenia, additional increases were detected in the parietal cortex (Brodmann Area 40; 123%) and the cingulate cortex (Brodmann Area 24; 57.7%). These data demonstrate that there is anatomical overlap in the pathophysiologies of schizophrenia and bipolar disorder, as well as areas of pathology that distinguish the two disorders.

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Section: Discussionmentioning

confidence: 91%

mentioning

confidence: 99%

Differences in neuroanatomical sites of apoD elevation discriminate between schizophrenia and bipolar disorder

et al. 2003

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“…Several studies in rodents have implicated apoD in neuronal degeneration after CNS injury. For example, increased apoD immunoreactivity and mRNA levels have been observed in glial cells and neurons of the hippocampus and͞or cortex after kainic acid lesioning and traumatic brain injury, two experimental insults that result in massive excitotoxic damage (35)(36)(37). In addition, apoD mRNA and protein levels were found to be elevated in the cerebellum of a mouse strain considered to be a model of Niemann-Pick disease, a human condition that is characterized by abnormal lysosomal cholesterol storage and chronic progressive neurodegeneration (38,39).…”

Section: Discussionmentioning

confidence: 99%

Increased CNS levels of apolipoprotein D in schizophrenic and bipolar subjects: Implications for the pathophysiology of psychiatric disorders

Thomas

Dean

Pavey

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

119

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Chronic administration of the atypical antipsychotic drug, clozapine, to rodents has been shown to increase the concentration of apolipoprotein D (apoD) in several area of the brain, suggesting that apoD could be involved in the therapeutic effects of antipsychotic drugs and͞or the pathology of psychotic illnesses. Here, we measured a significant decrease in the concentration of apoD in serum samples from schizophrenic patients. In contrast, apoD levels were significantly increased (92-287%) in dorsolateral prefrontal cortex (Brodmann's area 9) of schizophrenic and bipolar subjects. Elevated levels of apoD expression were also observed in the caudate of schizophrenic and bipolar subjects (68 -89%). No differences in apoD immunoreactivity were detected in occipital cortex (Brodmann's area 18) in either group, or in the hippocampus, substantia nigra, or cerebellum of the schizophrenic group. The low serum concentrations of apoD observed in these patients supports recent hypotheses involving systemic insufficiencies in lipid metabolism͞signaling in schizophrenia. Elevation of apoD expression selectively within central nervous system regions implicated in the pathology of these neuropsychiatric disorders suggests a focal compensatory response that neuroleptic drug regimens may augment.

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“…Apolipoprotein D levels have been shown to be elevated in old age and in a number of other neuropathologic disorders such as Alzheimer's disease (Kalman et al 2000) and excitotoxic damage (Montpied et al 1999) in regionally specific patterns. This suggests that upregulation of apolipoprotein D may be a localized response to regional brain lipid pathology (for review see Rassart et al 2000).…”

Section: Therapeutic Interventions To Improve Myelinationmentioning

confidence: 99%

Schizophrenia Breakdown in the Well-regulated Lifelong Process of Brain Development and Maturation

Bartzokis

2002

Neuropsychopharmacology

173

133

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Hippocampal alterations of apolipoprotein E and D mRNA levels in vivo and in vitro following kainate excitotoxicity

Cited by 40 publications

References 56 publications

Differences in neuroanatomical sites of apoD elevation discriminate between schizophrenia and bipolar disorder

Differences in neuroanatomical sites of apoD elevation discriminate between schizophrenia and bipolar disorder

Increased CNS levels of apolipoprotein D in schizophrenic and bipolar subjects: Implications for the pathophysiology of psychiatric disorders

Schizophrenia Breakdown in the Well-regulated Lifelong Process of Brain Development and Maturation

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