Cerebrospinal fluid {beta}-amyloid 42 and tau proteins as biomarkers of Alzheimer-type pathologic changes in the brain.

By T. Tapiola, I. Alafuzoff, S. Herukka, L. Parkkinen, P. Hartikainen, Hilkka Soininen, T. Pirttilä. Archives of Neurology, 2009

848 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Physiology, Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/63a63fbd1db7ae3faa22e1c0230079d10ba969c5

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Citations in the corpus

Latent feature representation with stacked auto-encoder for AD/MCI diagnosis (2013, background): “…Nordberg et al. 2010; Zhang et al. 2011; Zhang and Shen 2012; Gray et al. 2013), and t -tau, p -tau, and b -amyloid 42 ( A b 42 ) from CSF (Cui et al. 2011; Yuan et al. 2012; Zhang et al. 2011; Zhang and Shen 2012; Walhovd et al. 2010; Westman et al. 2012; Ewers et al. 2012; Tapiola et al. 2009).”
Multi-modal techniques for diagnosis and prognosis of Alzheimer’s disease (2009, result): “In support of this hypothesis, when ante-mortem cerebrospinal-fluid Aβ 42 concentrations are compared with PET PIB scan results or with post-mortem measurements of brain amyloid-β load, virtually all individuals with fibrillar amyloid-β deposits show low concentrations of Aβ 42 in the cerebrospina”
Human apoE isoforms differentially regulate brain amyloid-β peptide clearance (2011, positive): “Given that a CSF Aβ42 concentration lower than 500 pg/ mL has been utilized as a reliable threshold for the presence of cerebral Aβ deposition in humans (7, 19, 22, 26), we determined the proportion of individuals in each genotype with CSF Aβ42 lower than 500 pg/mL.”
Clinical Neurology and Epidemiology of the Major Neurodegenerative Diseases. (2018, methodology): “…181 and 231) in combination with reduced levels of soluble Ab1-42 amyloid distinguish AD patients from controls based on imaging tests (Shaw et al. 2009) and correlate with the presence of AD pathology at autopsy (Tapiola et al. 2009; reviewed in Blennow and Hampel 2003; Blennow et al. 2010).”
Biomarkers for Alzheimer's disease: current status and prospects for the future (2018, methodology): “amyloid (1-42) assay was published (104).”
Preclinical Alzheimer’s disease: Definition, natural history, and diagnostic criteria (2016, background): “This suggests that in AD, CSF tau changes may not only be considered as nonspecific (downstream) markers of neuronal death, as seen in other neurodegenerative diseases [60], but also as a more-specific pathophysiological marker of AD in relation to neurofibrillary tangles [61,62].”