P3-232: Correlations between cognitive tests and CSF biomarkers in Alzheimer's disease

2010 ◽  
Vol 6 ◽  
pp. S519-S520
Author(s):  
Claire Paquet ◽  
Julien Dumurgier ◽  
Sarah Benisty ◽  
Pauline Lapalus ◽  
Francois Mouton Liger ◽  
...  
2016 ◽  
Vol 22 (10) ◽  
pp. 968-977 ◽  
Author(s):  
Anja Soldan ◽  
Corinne Pettigrew ◽  
Abhay Moghekar ◽  
Marilyn Albert ◽  

AbstractObjectives: Evidence suggests that Alzheimer’s disease (AD) biomarkers become abnormal many years before the emergence of clinical symptoms of AD, raising the possibility that biomarker levels measured in cognitively normal individuals would be associated with cognitive performance many years later. This study examined whether performance on computerized cognitive tests is associated with levels of cerebrospinal fluid (CSF) biomarkers of amyloid, tau, and phosphorylated tau (p-tau) obtained approximately 10 years earlier, when individuals were cognitively normal and primarily middle-aged. Methods: Individuals from the BIOCARD cohort (mean age at testing=69 years) were tested on two computerized tasks hypothesized to rely on brain regions affected by the early accumulation of AD pathology: (1) a Paired Associates Learning (PAL) task (n=67) and (2) a visual search task (n=86). Results: In regression analyses, poorer performance on the PAL task was associated with higher levels of CSF p-tau obtained years earlier, whereas worse performance in the visual search task was associated with lower levels of CSF Aβ1-42. Conclusions: These findings suggest that AD biomarker levels may be differentially predictive of specific cognitive functions many years later. In line with the pattern of early accumulation of AD pathology, the PAL task, hypothesized to rely on medial temporal lobe function, was associated with CSF p-tau, whereas the visual search task, hypothesized to rely on frontoparietal function, was associated with CSF amyloid. Studies using amyloid and tau PET imaging will be useful in examining these hypothesized relationships further. (JINS, 2016, 22, 968–977)


PLoS ONE ◽  
2012 ◽  
Vol 7 (6) ◽  
pp. e38639 ◽  
Author(s):  
Sebastian Palmqvist ◽  
Joakim Hertze ◽  
Lennart Minthon ◽  
Carina Wattmo ◽  
Henrik Zetterberg ◽  
...  

2021 ◽  
pp. 1-13
Author(s):  
Jonathan D. Drake ◽  
Alison B. Chambers ◽  
Brian R. Ott ◽  
Lori A. Daiello ◽  

Background: Cerebrovascular dysfunction confers risk for functional decline in Alzheimer’s disease (AD), yet the clinical interplay of these two pathogenic processes is not well understood. Objective: We utilized Alzheimer’s Disease Neuroimaging Initiative (ADNI) data to examine associations between peripherally derived soluble cell adhesion molecules (CAMs) and clinical diagnostic indicators of AD. Methods: Using generalized linear regression models, we examined cross-sectional relationships of soluble plasma vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-Selectin to baseline diagnosis and functional impairment (clinical dementia rating sum-of-boxes, CDR-SB) in the ADNI cohort (n = 112 AD, n = 396 mild cognitive impairment (MCI), n = 58 cognitively normal). We further analyzed associations of these biomarkers with brain-based AD biomarkers in a subset with available cerebrospinal fluid (CSF) data (n = 351). p-values derived from main effects and interaction terms from the linear regressions were used to assess the relationship between independent and dependent variables for significance (significance level was set at 0.05 a priori for all analysis). Results: Higher mean VCAM-1 (p = 0.0026) and ICAM-1 (p = 0.0189) levels were found in AD versus MCI groups; however, not in MCI versus cognitively normal groups. Only VCAM-1 was linked with CDR-SB scores (p = 0.0157), and APOE ɛ4 genotype modified this effect. We observed independent, additive associations when VCAM-1 and CSF amyloid-β (Aβ 42), total tau, phosphorylated tau (P-tau), or P-tau/Aβ 42 (all <  p = 0.01) were combined in a CDR-SB model; ICAM-1 showed a similar pattern, but to a lesser extent. Conclusion: Our findings indicate independent associations of plasma-based vascular biomarkers and CSF biomarkers with AD-related clinical impairment.


2021 ◽  
pp. 102804
Author(s):  
José Contador ◽  
Agnès Pérez-Millán ◽  
Adrià Tort-Merino ◽  
Mircea Balasa ◽  
Neus Falgàs ◽  
...  

2021 ◽  
Vol 11 (2) ◽  
pp. 215
Author(s):  
Donovan A. McGrowder ◽  
Fabian Miller ◽  
Kurt Vaz ◽  
Chukwuemeka Nwokocha ◽  
Cameil Wilson-Clarke ◽  
...  

Alzheimer’s disease is a progressive, clinically heterogeneous, and particularly complex neurodegenerative disease characterized by a decline in cognition. Over the last two decades, there has been significant growth in the investigation of cerebrospinal fluid (CSF) biomarkers for Alzheimer’s disease. This review presents current evidence from many clinical neurochemical studies, with findings that attest to the efficacy of existing core CSF biomarkers such as total tau, phosphorylated tau, and amyloid-β (Aβ42), which diagnose Alzheimer’s disease in the early and dementia stages of the disorder. The heterogeneity of the pathophysiology of the late-onset disease warrants the growth of the Alzheimer’s disease CSF biomarker toolbox; more biomarkers showing other aspects of the disease mechanism are needed. This review focuses on new biomarkers that track Alzheimer’s disease pathology, such as those that assess neuronal injury (VILIP-1 and neurofilament light), neuroinflammation (sTREM2, YKL-40, osteopontin, GFAP, progranulin, and MCP-1), synaptic dysfunction (SNAP-25 and GAP-43), vascular dysregulation (hFABP), as well as CSF α-synuclein levels and TDP-43 pathology. Some of these biomarkers are promising candidates as they are specific and predict future rates of cognitive decline. Findings from the combinations of subclasses of new Alzheimer’s disease biomarkers that improve their diagnostic efficacy in detecting associated pathological changes are also presented.


Author(s):  
Claudio Liguori ◽  
Mariangela Pierantozzi ◽  
Agostino Chiaravalloti ◽  
Giulia M. Sancesario ◽  
Nicola B. Mercuri ◽  
...  

2021 ◽  
Vol 429 ◽  
pp. 119059
Author(s):  
Edoardo Barvas ◽  
Chiara Monaldini ◽  
Roberto Frusciante ◽  
Mirco Volpini ◽  
Beatrice Viti ◽  
...  

Author(s):  
Rosha Babapour Mofrad ◽  
Niki S.M. Schoonenboom ◽  
Betty M. Tijms ◽  
Philip Scheltens ◽  
Pieter Jelle Visser ◽  
...  

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Ezra Mulugeta ◽  
Elisabet Londos ◽  
Oskar Hansson ◽  
Clive Ballard ◽  
Ragnhild Skogseth ◽  
...  

We measured cerebrospinal fluid (CSF) levels of the soluble isoforms of amyloid precursor protein (APP; sAPPαsAPPβ) and other CSF biomarkers in 107 patients with Alzheimer's disease (AD), dementia with Lewy body dementia (DLB), Parkinson's disease dementia (PDD), and normal controls (NC) using commercial kits. DLB and PDD were combined in a Lewy body dementia group (LBD). No differences were observed in sAPPαand sAPPβlevels between the groups. Significant correlations were observed between sAPPαand sAPPβand between sAPPβand Mini-Mental State Examination scores in the total group analysis as well as when LBD and AD groups were analyzed separately. sAPPαand sAPPβlevels correlated with Aβ38, Aβ40, Aβ42, and Tau in the LBD group. In AD, sAPPαcorrelated with p-Tau and sAPPβwith Aβ40. The differential association between sAPPαand sAPPβwith Aβand Tau species between LBD and AD groups suggests a possible relationship with the underlying pathologies in LBD and AD.


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