title: Follow-up investigations in cerebrospinal fluid of patients with dementia with Lewy bodies and Alzheimer's disease.
abstract: Measuring proteins in cerebrospinal fluid (CSF) has gained wide acceptance for the differential diagnosis of dementia. Some groups have already extended these investigations in Alzheimer's disease (AD) by asking how stable these markers are in follow-up analysis, if they depend on the stage of disease and whether they can be used to monitor the progression and biological effects of treatment. We evaluated 21 patients with dementia with Lewy bodies (DLB) and 19 patients with AD, on two occasions, with regard to levels of tau protein, tau protein phosphorylated at threonine 181 (p-tau), Abeta42, Abeta40 and S-100B protein, using a set of commercially available assays. Tau protein levels were lower in DLB in first and second LP compared to AD and decreased during course of both groups. P-tau levels were increased in AD and DLB and decreased during follow-up. Abeta42 and Abeta40 remained relatively stable during follow-up but we found a slight increase of the median Abeta42 level in DLB, whereas in AD, Abeta42 tends to decrease during follow-up. S-100B protein increased during follow-up in both diseases. The protein dynamics in DLB and AD are relatively similar. S-100B protein may be a useful marker for follow-up in neurodegenerative diseases but has to be analysed in longer follow-up periods. Tau protein may be used to differentiate between DLB and AD. Follow-up CSF analyses are of limited value for the differentiation of AD and DLB. We conclude that more specific markers have to be established for the differentiation and follow-up of these diseases.
authors.affiliation: Department of Neurology, Georg-August University, Goettingen, Germany. bmollenhauer@med.uni-goettingen.de
authors.forename: B
authors.initials: B
authors.lastname: Mollenhauer
authors.forename: M
authors.initials: M
authors.lastname: Bibl
authors.forename: C
authors.initials: C
authors.lastname: Trenkwalder
authors.forename: G
authors.initials: G
authors.lastname: Stiens
authors.forename: L
authors.initials: L
authors.lastname: Cepek
authors.forename: P
authors.initials: P
authors.lastname: Steinacker
authors.forename: B
authors.initials: B
authors.lastname: Ciesielczyk
authors.forename: K
authors.initials: K
authors.lastname: Neubert
authors.forename: J
authors.initials: J
authors.lastname: Wiltfang
authors.forename: H A
authors.initials: HA
authors.lastname: Kretzschmar
authors.forename: S
authors.initials: S
authors.lastname: Poser
authors.forename: M
authors.initials: M
authors.lastname: Otto
mesh_terms: D000110:Acetylcholinesterase / Q000187:drug effects; D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000134:cerebrospinal fluid*; D016229:Amyloid beta-Peptides / Q000134:cerebrospinal fluid* / Q000378:metabolism; D015415:Biomarkers / Q000134:cerebrospinal fluid*; D003937:Diagnosis, Differential; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D006801:Humans; D020961:Lewy Body Disease / Q000134:cerebrospinal fluid*; D008297:Male; D008875:Middle Aged; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors; D016875:tau Proteins / Q000134:cerebrospinal fluid* / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D015415:Biomarkers; D004791:Enzyme Inhibitors; D016194:Receptors, N-Methyl-D-Aspartate; D016875:tau Proteins; D000110:Acetylcholinesterase