TY - JOUR
AU1 - Gonzales, Mitzi M.
AU2 - Wiedner, Crystal
AU3 - Wang, Chen‐Pin
AU4 - Liu, Qianqian
AU5 - Bis, Joshua C.
AU6 - Li, Zhiguang
AU7 - Himali, Jayandra J.
AU8 - Ghosh, Saptaparni
AU9 - Thomas, Emy A.
AU1 - Parent, Danielle M.
AU1 - Kautz, Tiffany F.
AU1 - Pase, Matthew P.
AU1 - Aparicio, Hugo J.
AU1 - Djoussé, Luc
AU1 - Mukamal, Kenneth J.
AU1 - Psaty, Bruce M.
AU1 - Longstreth, William T.
AU1 - Mosley, Thomas H.
AU1 - Gudnason, Vilmundur
AU2 - Mbangdadji, Djass
AU2 - Lopez, Oscar L.
AU2 - Yaffe, Kristine
AU2 - Sidney, Stephen
AU2 - Bryan, R. Nick
AU2 - Nasrallah, Ilya M.
AU2 - DeCarli, Charles S.
AU2 - Beiser, Alexa S.
AU2 - Launer, Lenore J.
AU2 - Fornage, Myriam
AU3 - Tracy, Russell P.
AU3 - Seshadri, Sudha
AU3 - Satizabal, Claudia L.
AB - IntroductionThe past decade has seen tremendous progress in the validation of biological markers for Alzheimer's disease and related dementias (ADRD), even extending into the pre‐symptomatic stage.1,2 Amyloid and tau positron emission tomography (PET) imaging have the capacity to detect abnormal protein deposition 15 to 20 years prior to clinical diagnosis.3 While PET imaging has provided major advances within clinical and research settings, a need still exists for inexpensive, minimally invasive, and broadly available screening tools.4 With the use of ultrasensitive assays, the hallmark biological features of Alzheimer's disease (AD), including amyloid beta 40 and 42 and phosphorylated tau 217 and 181, can be reliably detected in blood.5,6Blood‐based assays also afford the opportunity to simultaneously evaluate proteins reflecting diverse pathophysiological processes underlying ADRD, which may facilitate identification of new drug targets and precision medicine approaches.7 Even as a singular diagnostic entity, AD is highly heterogenous with numerous pathways implicated beyond amyloid beta and tau deposition.8 Furthermore, individuals with dementia often present with multiple co‐pathologies at autopsy,9 highlighting the need for broader screening approaches. While the combination of elevated cerebral amyloid beta and tau is considered specific for AD, glial dysfunction and neuroinflammation manifest across dementia subtypes.10 Growing research supports the fundamental 
TI - A population‐based meta‐analysis of circulating GFAP for cognition and dementia risk
JF - Annals of Clinical and Translational Neurology
DO - 10.1002/acn3.51652
DA - 2022-10-01
UR - https://www.deepdyve.com/lp/wiley/a-population-based-meta-analysis-of-circulating-gfap-for-cognition-and-7cMqItKYLi
SP - 1574
EP - 1585
VL - 9
IS - 10
DP - DeepDyve
ER -