An examination of a novel multipanel of CSF biomarkers in the Alzheimer's disease clinical and pathological continuum.
An examination of a novel multipanel of CSF biomarkers in the Alzheimer's disease clinical and pathological continuum.
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对阿尔茨海默病临床和病理连续体中一组新的脑脊液生物标记物的研究。
DOI:
10.1002/alz.12204
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发表时间:
2021-03
期刊:
影响因子:
--
通讯作者:
Blennow K
中科院分区:
文献类型:
--
作者:
Van Hulle C;Jonaitis EM;Betthauser TJ;Batrla R;Wild N;Kollmorgen G;Andreasson U;Okonkwo O;Bendlin BB;Asthana S;Carlsson CM;Johnson SC;Zetterberg H;Blennow K
This study examines the utility of a multipanel of cerebrospinal fluid (CSF) biomarkers complementing Alzheimer's disease (AD) biomarkers in a clinical research sample. We compared biomarkers across groups defined by clinical diagnosis and pTau181/Aβ42 status (+/−) and explored their value in predicting cognition. CSF biomarkers amyloid beta (Aβ)42, pTau181, tTau, Aβ40, neurogranin, neurofilament light (NfL), α‐synuclein, glial fibrillary acidic protein (GFAP), chitinase‐3‐like protein 1 (YKL‐40), soluble triggering receptor expressed on myeloid cells 2 (sTREM2), S100 calcium binding protein B (S100B), and interleukin 6 (IL6), were measured with the NeuroToolKit (NTK) for 720 adults ages 40 to 93 years (mean age = 63.9 years, standard deviation [SD] = 9.0; 50 with dementia; 54 with mild cognitive impairment [MCI], 616 unimpaired). Neurodegeneration and glial activation biomarkers were elevated in pTau181/Aβ42+ MCI/dementia participants relative to all pTau181/Aβ42‐ participants. Neurodegeneration biomarkers increased with clinical severity among pTau181/Aβ42+ participants and predicted worse cognitive performance. Glial activation biomarkers were unrelated to cognitive performance. The NTK contains promising markers that improve the pathophysiological characterization of AD. Neurodegeneration biomarkers beyond tTau improved statistical prediction of cognition and disease stages.
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DOI:
10.1016/s1474-4422(12)70227-2
发表时间:
2012-12
期刊:
The Lancet. Neurology
影响因子:
--
作者:
Fleisher AS;Chen K;Quiroz YT;Jakimovich LJ;Gomez MG;Langois CM;Langbaum JB;Ayutyanont N;Roontiva A;Thiyyagura P;Lee W;Mo H;Lopez L;Moreno S;Acosta-Baena N;Giraldo M;Garcia G;Reiman RA;Huentelman MJ;Kosik KS;Tariot PN;Lopera F;Reiman EM
通讯作者:
Reiman EM
影响因子:
29
作者:
Donohue, Michael C.;Sperling, Reisa A.;Salmon, David P.;Rentz, Dorene M.;Raman, Rema;Thomas, Ronald G.;Weiner, Michael;Aisen, Paul S.
通讯作者:
Aisen, Paul S.
影响因子:
9.9
作者:
Kemppainen, N. M.;Aalto, S.;Rinne, J. O.
通讯作者:
Rinne, J. O.
影响因子:
4.2
作者:
Johnson SC;Christian BT;Okonkwo OC;Oh JM;Harding S;Xu G;Hillmer AT;Wooten DW;Murali D;Barnhart TE;Hall LT;Racine AM;Klunk WE;Mathis CA;Bendlin BB;Gallagher CL;Carlsson CM;Rowley HA;Hermann BP;Dowling NM;Asthana S;Sager MA
通讯作者:
Sager MA
DOI:
10.1016/j.jalz.2018.01.010
发表时间:
2018-11
期刊:
Alzheimer's & dementia : the journal of the Alzheimer's Association
影响因子:
--
作者:
Hansson O;Seibyl J;Stomrud E;Zetterberg H;Trojanowski JQ;Bittner T;Lifke V;Corradini V;Eichenlaub U;Batrla R;Buck K;Zink K;Rabe C;Blennow K;Shaw LM;Swedish BioFINDER study group;Alzheimer's Disease Neuroimaging Initiative
通讯作者:
Alzheimer's Disease Neuroimaging Initiative