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Low cerebrospinal fluid beta-amyloid 42 in patients with acute bacterial meningitis and normalization after treatment

Journal article
Authors Magnus Sjögren
Magnus Gisslén
E. Vanmechelen
Kaj Blennow
Published in Neurosci Lett
Volume 314
Issue 1-2
Pages 33-6
Publication year 2001
Published at Institute of Internal Medicine, Dept of Infectious Diseases
Institute of Clinical Neurosciences, Section of Experimental Neuroscience
Institute of Clinical Neurosciences, Section of Psychiatry
Pages 33-6
Language en
Keywords Acute Disease, Adult, Albumins/cerebrospinal fluid, Amyloid beta-Protein/*cerebrospinal fluid, Anti-Bacterial Agents/therapeutic use, Biological Markers/cerebrospinal fluid, Brain/*metabolism/microbiology/physiopathology, Haemophilus influenzae/metabolism, Humans, Klebsiella pneumoniae/metabolism, Meningitis, Bacterial/*cerebrospinal fluid/diagnosis/drug therapy, Meningitis, Viral/cerebrospinal fluid, Middle Aged, Peptide Fragments/*cerebrospinal fluid, Streptococcus oralis/metabolism, Streptococcus pneumoniae/metabolism, Treatment Outcome
Subject categories Microbiology in the medical area


CSF-A beta 42 may be a marker of Alzheimer's disease (AD). A decreased level of CSF-A beta 42 is consistently found in AD and has been suggested to be related to the deposition of amyloid plaques in the brain. However, low CSF-A beta 42 levels have also been found in disorders devoid of plaques, for instance Creutzfeldt-Jakob disease. To examine if the level of A beta 42 in CSF is related to inflammatory processes, we studied CSF-A beta 42 levels in eight patients with acute purulent bacterial meningitis, 10 patients with acute viral meningitis and 18 age-matched controls. In acute purulent bacterial meningitis, the CSF-A beta 42 level was markedly reduced (28% of that in controls, P<0.0001), whereas no change was found in viral meningitis. After successful treatment of bacterial meningitis, the CSF-A beta 42 level increased (P<0.05 compared to baseline) and did no longer differ from that in controls (ns). The decrease could not be explained by interference with high protein levels, since addition of increasing volumes of serum did not influence the CSF-A beta 42 levels. Our findings suggest that the reduction in CSF-A beta 42 found in bacterial meningitis is not a direct consequence of the inflammatory process. The cause may be disturbance of the clearance of A beta 42 from the brain.

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