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Cytoskeleton proteins in CSF distinguish frontotemporal dementia from AD

Sjogren, M; Rosengren, L; Minthon, Lennart LU ; Davidsson, P; Blennow, K and Wallin, A (2000) In Neurology 54(10). p.1960-1964
Abstract
OBJECTIVE AND BACKGROUND: To investigate the CSF levels of tau and the light neurofilament protein (NFL) in patients with frontotemporal dementia (FTD) and other common dementia disorders as well as normal control subjects. Both proteins have been implicated in the pathophysiology of FTD. METHODS: CSF levels of tau and NFL were investigated in 18 patients with FTD, 21 patients with early-onset AD (EAD), 21 patients with late-onset AD (LAD), and 18 age-matched control subjects. RESULTS: Mean +/- SD CSF NFL levels were increased in patients with FTD (1442 +/- 1183 pg/mL; p < 0.05) and LAD (1006 +/- 727 pg/mL; p < 0.001) compared with control subjects (241 +/- 166 pg/mL) and in LAD compared with EAD (498 +/- 236 pg/mL; p < 0.05), and... (More)
OBJECTIVE AND BACKGROUND: To investigate the CSF levels of tau and the light neurofilament protein (NFL) in patients with frontotemporal dementia (FTD) and other common dementia disorders as well as normal control subjects. Both proteins have been implicated in the pathophysiology of FTD. METHODS: CSF levels of tau and NFL were investigated in 18 patients with FTD, 21 patients with early-onset AD (EAD), 21 patients with late-onset AD (LAD), and 18 age-matched control subjects. RESULTS: Mean +/- SD CSF NFL levels were increased in patients with FTD (1442 +/- 1183 pg/mL; p < 0.05) and LAD (1006 +/- 727 pg/mL; p < 0.001) compared with control subjects (241 +/- 166 pg/mL) and in LAD compared with EAD (498 +/- 236 pg/mL; p < 0.05), and tended to be increased in FTD compared with EAD. CSF tau levels were increased in EAD (751 +/- 394 pg/mL; p < 0.01) and LAD (699 +/- 319 pg/mL; p < 0.01) compared with control subjects (375 +/- 170 pg/mL), and in EAD (p < 0.001) and LAD (p < 0. 01) compared with FTD (354 +/- 140 pg/mL). CSF NFL correlated positively with degree of cognitive impairment in FTD (r = 0.59; p < 0.05) and LAD (r = 0.61; p < 0.01). No significant differences were found in CSF NFL or CSF tau when comparing patients who did and did not possess the APOE-epsilon4 allele within each diagnostic group. CONCLUSION: The results suggest a differential involvement of these cytoskeleton proteins in FTD and EAD, with NFL primarily involved in the pathophysiology of FTD and tau in that of EAD. The increase in CSF NFL found in LAD might reflect the white-matter degeneration found in a proportion of LAD cases. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Neurology
volume
54
issue
10
pages
1960 - 1964
publisher
American Academy of Neurology
external identifiers
  • wos:000087088000016
  • scopus:0343091321
ISSN
1526-632X
language
English
LU publication?
yes
id
ace16bbe-b6a1-49f6-9016-9f88bded51e3 (old id 1296894)
alternative location
http://www.neurology.org/cgi/content/abstract/54/10/1960
date added to LUP
2009-07-15 15:34:09
date last changed
2017-07-30 04:45:01
@article{ace16bbe-b6a1-49f6-9016-9f88bded51e3,
  abstract     = {OBJECTIVE AND BACKGROUND: To investigate the CSF levels of tau and the light neurofilament protein (NFL) in patients with frontotemporal dementia (FTD) and other common dementia disorders as well as normal control subjects. Both proteins have been implicated in the pathophysiology of FTD. METHODS: CSF levels of tau and NFL were investigated in 18 patients with FTD, 21 patients with early-onset AD (EAD), 21 patients with late-onset AD (LAD), and 18 age-matched control subjects. RESULTS: Mean +/- SD CSF NFL levels were increased in patients with FTD (1442 +/- 1183 pg/mL; p &lt; 0.05) and LAD (1006 +/- 727 pg/mL; p &lt; 0.001) compared with control subjects (241 +/- 166 pg/mL) and in LAD compared with EAD (498 +/- 236 pg/mL; p &lt; 0.05), and tended to be increased in FTD compared with EAD. CSF tau levels were increased in EAD (751 +/- 394 pg/mL; p &lt; 0.01) and LAD (699 +/- 319 pg/mL; p &lt; 0.01) compared with control subjects (375 +/- 170 pg/mL), and in EAD (p &lt; 0.001) and LAD (p &lt; 0. 01) compared with FTD (354 +/- 140 pg/mL). CSF NFL correlated positively with degree of cognitive impairment in FTD (r = 0.59; p &lt; 0.05) and LAD (r = 0.61; p &lt; 0.01). No significant differences were found in CSF NFL or CSF tau when comparing patients who did and did not possess the APOE-epsilon4 allele within each diagnostic group. CONCLUSION: The results suggest a differential involvement of these cytoskeleton proteins in FTD and EAD, with NFL primarily involved in the pathophysiology of FTD and tau in that of EAD. The increase in CSF NFL found in LAD might reflect the white-matter degeneration found in a proportion of LAD cases.},
  author       = {Sjogren, M and Rosengren, L and Minthon, Lennart and Davidsson, P and Blennow, K and Wallin, A},
  issn         = {1526-632X},
  language     = {eng},
  number       = {10},
  pages        = {1960--1964},
  publisher    = {American Academy of Neurology},
  series       = {Neurology},
  title        = {Cytoskeleton proteins in CSF distinguish frontotemporal dementia from AD},
  volume       = {54},
  year         = {2000},
}