TY - JOUR
T1 - CSF markers in Alzheimer disease patients are not related to the different degree of cognitive impairment
AU - Stefani, Alessandro
AU - Martorana, Alessandro
AU - Bernardini, Sergio
AU - Panella, Marta
AU - Mercati, Flavio
AU - Orlacchio, Antonio
AU - Pierantozzi, Mariangela
PY - 2006/12/21
Y1 - 2006/12/21
N2 - Standard markers in cerebrospinal fluid (CSF), as soluble amyloid beta 1-42 (Aβ1-42) and total tau protein (t-tau), may contribute to dementia subtypes diagnostic accuracy. Yet, their sensitivity to assess the different degree of cognitive deficit is not fully clarified. Our study analyses Aβ1-42 and t-tau CSF levels in different cohorts of Alzheimer's disease (AD) patients, distinguished as early AD (mild cognitively impaired subjects recently converted to AD), mild AD (MMSE <23; ≥ 18), and moderately advanced AD (MMSE <18). The control group was represented by age-matched patients affected by depressive pseudo-dementia. Reduced Aβ1-42 and increased t-tau CSF levels were confirmed as hallmarks of AD at any disease stage. In early AD patients, Aβ1-42 levels were already significantly low, if compared to the control group (336 vs 867 ng/L; p <0.0001). On the contrary, Aβ1-42 levels did not differ between AD subgroups, and in particular between mild to moderate AD. A significant progressive increase of t-tau concentration was found when comparing early AD (269 ng/L) to more advanced AD stages (468 ng/L and 495 ng/L for mild and moderate AD, respectively). Our findings confirm that the impairment of amyloidogenic cascade is an early, even pre-clinical process, but suggest that soluble Aβ1-42 concentration has a negligible correlation with the clinical progression. Conversely, t-tau concentration correlates with the transition towards marked cognitive impairment.
AB - Standard markers in cerebrospinal fluid (CSF), as soluble amyloid beta 1-42 (Aβ1-42) and total tau protein (t-tau), may contribute to dementia subtypes diagnostic accuracy. Yet, their sensitivity to assess the different degree of cognitive deficit is not fully clarified. Our study analyses Aβ1-42 and t-tau CSF levels in different cohorts of Alzheimer's disease (AD) patients, distinguished as early AD (mild cognitively impaired subjects recently converted to AD), mild AD (MMSE <23; ≥ 18), and moderately advanced AD (MMSE <18). The control group was represented by age-matched patients affected by depressive pseudo-dementia. Reduced Aβ1-42 and increased t-tau CSF levels were confirmed as hallmarks of AD at any disease stage. In early AD patients, Aβ1-42 levels were already significantly low, if compared to the control group (336 vs 867 ng/L; p <0.0001). On the contrary, Aβ1-42 levels did not differ between AD subgroups, and in particular between mild to moderate AD. A significant progressive increase of t-tau concentration was found when comparing early AD (269 ng/L) to more advanced AD stages (468 ng/L and 495 ng/L for mild and moderate AD, respectively). Our findings confirm that the impairment of amyloidogenic cascade is an early, even pre-clinical process, but suggest that soluble Aβ1-42 concentration has a negligible correlation with the clinical progression. Conversely, t-tau concentration correlates with the transition towards marked cognitive impairment.
KW - Alzheimer's disease
KW - Beta-amyloid
KW - MMSE
KW - Pseudo-dementia
KW - Stage markers
KW - Tau protein
UR - http://www.scopus.com/inward/record.url?scp=33751212726&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33751212726&partnerID=8YFLogxK
U2 - 10.1016/j.jns.2006.09.014
DO - 10.1016/j.jns.2006.09.014
M3 - Article
C2 - 17097109
AN - SCOPUS:33751212726
VL - 251
SP - 124
EP - 128
JO - Journal of the Neurological Sciences
JF - Journal of the Neurological Sciences
SN - 0022-510X
IS - 1-2
ER -