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Cerebrospinal fluid biomarkers of white matter lesions – cross‐sectional results from the LADIS study
Author(s) -
Jonsson M.,
Zetterberg H.,
Van Straaten E.,
Lind K.,
Syversen S.,
Edman Å.,
Blennow K.,
Rosengren L.,
Pantoni L.,
Inzitari D.,
Wallin A.
Publication year - 2010
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/j.1468-1331.2009.02808.x
Subject(s) - hyperintensity , cerebrospinal fluid , medicine , dementia , pathology , magnetic resonance imaging , white matter , amyloid (mycology) , alzheimer's disease , disease , radiology
Background and purpose: White matter lesions (WMLs) caused by small vessel disease are common in elderly people and contribute to cognitive impairment. There are no established biochemical markers for WMLs. We aimed to study the relation between degree of WMLs rated on magnetic resonance imaging of the brain and cerebrospinal fluid (CSF) levels of structural biomarkers associated with Alzheimer’s disease (AD) and subcortical vascular dementia. Methods: Fifty‐three non‐demented elderly individuals with WMLs were subjected to lumbar puncture. Degree of WMLs was rated using the Fazekas scale. Volumetric assessment of WMLs was performed. CSF samples were analyzed for the 40 and 42 amino acid fragments of amyloid β, α‐ and β‐cleaved soluble amyloid precursor protein, total tau (T‐tau), hyperphosphorylated tau (P‐tau 181 ), neurofilament light protein (NFL), sulfatide and CSF/Serum‐albumin ratio. Results: Fifteen subjects had mild, 23 had moderate and 15 had severe degree of WMLs . CSF‐NFL levels differed between the groups ( P < 0.001) and correlated with the volume of WMLs ( r = 0.477, P < 0.001). CSF sulfatide concentration displayed similar changes but less strongly. T‐tau, P‐tau 181 and the different amyloid markers as well as CSF/S‐albumin ratio did not differ significantly between the groups. Conclusions: The association of increased CSF‐NFL levels with increasing severity of WMLs in non‐demented subjects suggests that NFL is a marker for axonal damage in response to small vessel disease in the brain. This manifestation may be distinct from or earlier than the neurodegenerative process seen in AD, as reflected by the lack of association between WMLs and AD biomarkers.