Normal levels of clusterin in cerebrospinal fluid in Alzheimer's disease, and no change after acute ischemic stroke.

The protein clusterin has been suggested to be involved in the pathogenesis of Alzheimer's disease (AD). Its expression is increased in brain regions affected by AD pathology, and to elucidate if there is a concomitant increase of clusterin also in the cerebrospinal fluid (CSF) in different neurological disorders, CSF samples from patients with AD, vascular dementia (VAD), Parkinson's disease (PD), and controls were analysed. Also longitudinal (five occasions) samples from patients with acute stroke were analysed, to follow any degenerative/regenerative phase after acute brain damage. However, there were no changes in CSF-clusterin levels from patients in AD, VAD, PD or acute stroke, as compared to controls. The increase of clusterin in brain tissue is suggested to reflect a regenerative response process, which here is shown not to be followed by a concomitant increase in the CSF. Thus, CSF-clusterin can not be used as an indicator or a diagnostic marker for AD.

[1]  C. Olsson,et al.  Induction of the TRPM-2 gene in cells undergoing programmed death , 1989, Molecular and cellular biology.

[2]  Paul D. Coleman,et al.  Neuron numbers and dendritic extent in normal aging and Alzheimer's disease , 1987, Neurobiology of Aging.

[3]  C. Finch,et al.  Association of apolipoprotein E genotype with brain levels of apolipoprotein E and apolipoprotein J (clusterin) in Alzheimer disease. , 1995, Brain research. Molecular brain research.

[4]  T. Oda,et al.  Relationship between multifunctional protein “clusterin” and Alzheimer disease , 1996, Neurobiology of Aging.

[5]  D. Walker,et al.  Distribution of clusterin in Alzheimer brain tissue , 1992, Brain Research.

[6]  A. Yamaura,et al.  Reactive astrocytes in acute stage after experimental brain injury: relationship to extravasated plasma protein and expression of heat shock protein. , 1996, Journal of Neurotrauma.

[7]  O. Garson,et al.  Regional localization of the gene for clusterin (SP-40,40; gene symbol CLI) to human chromosome 8p12-->p21. , 1992, Cytogenetics and cell genetics.

[8]  L. Agnati,et al.  Increases in sulphated glycoprotein-2 mRNA levels in the rat brain after transient forebrain ischemia or partial mesodiencephalic hemitransection. , 1993, Brain research. Molecular brain research.

[9]  M. Peitsch,et al.  Clusterin (complement lysis inhibitor) forms a high density lipoprotein complex with apolipoprotein A-I in human plasma. , 1991, The Journal of biological chemistry.

[10]  W. Banks,et al.  The putative blood-brain barrier transporter for the beta-amyloid binding protein apolipoprotein j is saturated at physiological concentrations. , 1997, Life sciences.

[11]  D. Brooks,et al.  Core assessment program for intracerebral transplantations (CAPIT) , 1992, Movement disorders : official journal of the Movement Disorder Society.

[12]  A. Delacourte.  General and dramatic glial reaction in Alzheimer brains , 1990, Neurology.

[13]  L. French,et al.  Clusterin: modulation of complement function , 1994, Clinical and experimental immunology.

[14]  K. Blennow,et al.  Cerebrospinal fluid tau protein as a biochemical marker for Alzheimer’s disease: a community based follow up study , 1998, Journal of neurology, neurosurgery, and psychiatry.

[15]  C. Cotman,et al.  The control of glial populations in brain: Changes in astrocyte mitogenic and morphogenic factors in response to injury , 1985, Brain Research.

[16]  Steven A. Johnson,et al.  Dynamics of gene expression for a hippocampal glycoprotein elevated in Alzheimer's disease and in response to experimental lesions in rat , 1990, Neuron.

[17]  G. Hänsch.  The complement attack phase: control of lysis and non-lethal effects of C5b-9. , 1992, Immunopharmacology.

[18]  M. Griswold,et al.  Biosynthesis and molecular cloning of sulfated glycoprotein 2 secreted by rat Sertoli cells. , 1987, Biochemistry.

[19]  P. Gluckman,et al.  Induction of clusterin in the immature brain following a hypoxic-ischemic injury. , 1996, Brain research. Molecular brain research.

[20]  C. Finch,et al.  Sulfated glycoprotein-2 is increased in rat hippocampus following entorhinal cortex lesioning , 1991, Brain Research.

[21]  C. Olsson,et al.  Chromosomal assignment of the human homologue encoding SGP-2. , 1990, Biochemical and biophysical research communications.

[22]  K. Paizis,et al.  Elevation of human cerebrospinal fluid clusterin concentration is associated with acute neuropathology , 1993, Journal of the Neurological Sciences.

[23]  C. Finch,et al.  Purification and characterization of brain clusterin. , 1994, Biochemical and biophysical research communications.

[24]  W. Tourtellotte,et al.  Changes in brain gene expression shared by scrapie and Alzheimer disease. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[25]  M. Lalowski,et al.  Amyloid β binding proteins in vitro and in normal human cerebrospinal fluid , 1995, Neuroscience Letters.

[26]  Steven A. Johnson,et al.  Altered Gene Expression in Alzheimer's Disease Brain Tissue , 1989, Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques.

[27]  E. Matsubara,et al.  Characterization of Apolipoprotein J-Alzheimer's Aβ Interaction (*) , 1995, The Journal of Biological Chemistry.

[28]  W. Banks,et al.  Interactions of β‐Amyloids with the Blood–Brain Barrier , 1997, Annals of the New York Academy of Sciences.

[29]  K. Haglid,et al.  Determination of S‐100 and Glial Fibrillary Acidic Protein Concentrations in Cerebrospinal Fluid After Brain Infarction , 1991, Stroke.

[30]  K. Blennow,et al.  Protein analyses in cerebrospinal fluid. I. Influence of concentration gradients for proteins on cerebrospinal fluid/serum albumin ratio. , 1993, European neurology.

[31]  M. Folstein,et al.  Clinical diagnosis of Alzheimer's disease , 1984, Neurology.

[32]  K. Blennow,et al.  Clusterin (Apolipoprotein J) Protein Levels Are Increased in Hippocampus and in Frontal Cortex in Alzheimer's Disease , 1998, Experimental Neurology.

[33]  O. Blaschuk,et al.  Ram rete testis fluid contains a protein (clusterin) which influences cell-cell interactions in vitro. , 1983, Biology of reproduction.

[34]  K. Blennow,et al.  Glial fibrillary acidic protein in the cerebrospinal fluid of patients with dementia. , 1996, Dementia.

[35]  C. Finch,et al.  Clusterin (SGP‐2): A multifunctional glycoprotein with regional expression in astrocytes and neurons of the adult rat brain , 1994, The Journal of comparative neurology.

[36]  C. Gillberg,et al.  A sensitive ELISA for glial fibrillary acidic protein: application in CSF of children , 1992, Journal of Neuroscience Methods.

[37]  J. Tschopp,et al.  Molecular structure and functional characterization of a human complement cytolysis inhibitor found in blood and seminal plasma: identity to sulfated glycoprotein 2, a constituent of rat testis fluid. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[38]  R. Balázs,et al.  Neuronal plasticity and astrocytic reaction in Down syndrome and Alzheimer disease , 1990, Journal of the Neurological Sciences.

[39]  K. Blennow,et al.  Tau protein in cerebrospinal fluid: a biochemical marker for axonal degeneration in Alzheimer disease? , 1995, Molecular and chemical neuropathology.

[40]  Steven A. Johnson,et al.  Clusterin (apoJ) Alters the Aggregation of Amyloid β-Peptide (Aβ1-42) and Forms Slowly Sedimenting Aβ Complexes That Cause Oxidative Stress , 1995, Experimental Neurology.

[41]  C. Finch,et al.  Sulfated glycoprotein 2: new relationships of this multifunctional protein to neurodegeneration , 1992, Trends in Neurosciences.

[42]  C. Soto,et al.  Apolipoprotein J and Alzheimer's amyloid beta solubility. , 1996, The Biochemical journal.

[43]  J. Tschopp,et al.  Quantitation of vitronectin and clusterin. Pitfalls and solutions in enzyme immunoassays for adhesive proteins. , 1993, Journal of immunological methods.

[44]  L. Chang,et al.  Elevation of microtubule-associated protein tau in the cerebrospinal fluid of patients with Alzheimer's disease , 1995, Neurology.

[45]  J. Tschopp,et al.  Clusterin: the intriguing guises of a widely expressed glycoprotein. , 1992, Trends in biochemical sciences.

[46]  T. Wisniewski,et al.  The cerebrospinal-fluid soluble form of Alzheimer's amyloid beta is complexed to SP-40,40 (apolipoprotein J), an inhibitor of the complement membrane-attack complex. , 1993, The Biochemical journal.

[47]  Y. Takahashi,et al.  Identification of the disulfide bonds in human plasma protein SP-40,40 (apolipoprotein-J). , 1992, Journal of biochemistry.

[48]  A. Wallin,et al.  Immunoglobulin M in cerebrospinal fluid: reference values derived from 111 healthy individuals 18-88 years of age. , 1996, European neurology.

[49]  Jan Six,et al.  Detection of Proteins in Normal and Alzheimer's Disease Cerebrospinal Fluid with a Sensitive Sandwich Enzyme‐Linked Immunosorbent Assay , 1993 .

[50]  D. G. Ferguson,et al.  A 70-kDa apolipoprotein designated ApoJ is a marker for subclasses of human plasma high density lipoproteins. , 1990, The Journal of biological chemistry.

[51]  P. May,et al.  Clusterin (Apo J) Protects Against In Vitro Amyloid‐β(1–40) Neurotoxicity , 1996 .

[52]  B. Hyman,et al.  Brain Expression of Apolipoproteins E, J, and A‐I in Alzheimer's Disease , 1996, Journal of neurochemistry.

[53]  B. Tycko,et al.  Polymorphisms in the human apolipoprotein-J/clusterin gene: ethnic variation and distribution in Alzheimer’s disease , 1996, Human Genetics.

[54]  G. C. Román,et al.  Vascular dementia , 1993, Neurology.

[55]  M. Dragunow,et al.  Clusterin accumulates in dying neurons following status epilepticus. , 1995, Brain research. Molecular brain research.

[56]  N. Laping,et al.  Castration enhances expression of glial fibrillary acidic protein and sulfated glycoprotein-2 in the intact and lesion-altered hippocampus of the adult male rat. , 1990, Molecular endocrinology.