CSF Aβ42, Tau and phosphorylated Tau, APOE ɛ4 allele and MCI type in progressive MCI

Herukka, Sanna‐Kaisa; Helisalmi, Seppo; Hallikainen, Merja; Tervo, Susanna; Soininen, Hilkka; Pirttilä, Tuula

doi:10.1016/j.neurobiolaging.2006.02.001

Cited by 102 publications

(52 citation statements)

References 55 publications

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“…As our research and other recent studies indicate (Alladi et al, 2006;Belleville et al, 2007;Herukka et al, 2007), MCI classification criteria based exclusively on the presence of a memory impairment alone exclude a significant number of aging adults with significant decline in other cognitive domains. We found that 35% of our sample with informant-corroborated memory decline did not display an objectively measured impairment to memory but did display impaired attention or working memory functioning.…”

Section: Discussionsupporting

confidence: 65%

Attention and working memory deficits in mild cognitive impairment

Saunders

Summers

2009

Journal of Clinical and Experimental Neuropsychology

146

127

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Mild cognitive impairment (MCI) has emerged as a classification for a prodromal phase of cognitive decline preceding the emergence of Alzheimer's disease (AD). We examined neuropsychological functioning in a sample of 60 adults with amnestic-MCI (a-MCI), 32 with subjective complaints of memory impairment (subjective-MCI, s-MCI), 14 with mild AD, and 25 age-matched controls. Both the a-MCI and s-MCI groups displayed impaired attentional processing, working memory capacity, and semantic language, with a-MCI displaying additional impairments to verbal and/or visual memory. These results indicate that further research is needed to examine cognitive decline in nonamnestic variants of MCI.

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Section: Discussionsupporting

confidence: 65%

Attention and working memory deficits in mild cognitive impairment

Saunders

Summers

2009

Journal of Clinical and Experimental Neuropsychology

146

127

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“…In line with this, these biomarkers were able to predict progression to AD in MCI patients (88)(89)(90)(91)(92). Similarly, marked increases in CSF p-tau levels were found in MCI cases, which at follow-up progressed to AD, compared to stable MCI cases (92,93). Similar results were achieved using the xMAP technology (94).…”

Section: Relation With Disease Severitysupporting

confidence: 72%

“…In agreement with these latter findings, decreased CSF Ab 42 levels and increased t-tau levels were already found very early in progression of AD, and thus trading the correlation with disease progression for better diagnostic sensitivity. In line with this, these biomarkers were able to predict progression to AD in MCI patients (88)(89)(90)(91)(92). Similarly, marked increases in CSF p-tau levels were found in MCI cases, which at follow-up progressed to AD, compared to stable MCI cases (92,93).…”

Section: Relation With Disease Severitysupporting

confidence: 68%

Current state and future directions of neurochemical biomarkers for Alzheimer's disease

Jong¹,

Kremer²,

Rikkert³

et al. 2007

Clinical Chemical Laboratory Medicine

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In this comprehensive review, we summarize the current state-of-the-art of neurochemical biomarkers for Alzheimer's disease. Predominantly, these biomarkers comprise cerebrospinal fluid biomarkers directly related to the pathophysiology of this disorder (such as amyloid beta protein, tau protein). We particularly pay attention to the innovations in this area that have been made in technological aspects during the past 5 years (e.g., multiplex analysis of biomarkers, proteomics), to the discovery of novel, potential biomarkers (e.g., amyloid beta oligomers, isoprostanes), and to the extension of this research towards identification of biomarkers in plasma.

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“…Aβ42 has also been shown to be first amyloid form to accumulate with Aβ40 being deposited later in the process of AD pathogenesis 5. The level of Aβ42 in cerebrospinal fluid (CSF) is reduced in patients with mild cognitive impairment (MCI) and AD,6 7 and a combination test of CSF Aβ42 and τ or phospho-tau has been claimed to be helpful in the early diagnosis of AD 8…”

Section: Introductionmentioning

confidence: 99%

Plasma A 42 and A 40 as markers of cognitive change in follow-up: a prospective, longitudinal, population-based cohort study

Seppälä

Herukka

Hänninen

et al. 2010

Journal of Neurology, Neurosurgery & Psychiatry

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BackgroundSingle measurements of plasma Aβ are not useful in the diagnostics of Alzheimer's disease (AD). However, changes in plasma Aβ levels during repeated testing may be helpful in the prediction and evaluation of progression of the incipient AD or mild cognitive impairment.ObjectiveTo examine the relation of baseline and serial plasma Aβ levels to cognitive change in follow-up.Methods269 subjects (52 cognitively impaired and 217 controls) from a population-based cohort were clinically followed up from 3 to 6 years. Serial plasma samples were available from 70 subjects who were followed up for 3 years and 43 subjects followed for 6 years. The plasma Aβ levels were measured using ELISA.ResultsSubjects who declined cognitively during the follow-up had lower levels of plasma Aβ42 at the baseline. Plasma Aβ42 and the Aβ42/Aβ40 ratio decreased (−2.4 pg/ml for Aβ42 in 6 years) in those who declined in follow-up, whereas Aβ42 and the Aβ42/Aβ40 ratio increased in the subjects who remained cognitively stable or improved in follow-up. Subjects using acetylsalicylic acid, dipyridamole, antidiabetic or anticoagulant drugs as well as subjects with coronary heart disease had higher levels of Aβ40.ConclusionsLow or decreasing plasma Aβ42 during the follow-up is associated with cognitive decline. Serial measurement of plasma Aβ42 may be useful in the detection of the subjects who are at risk for cognitive decline.

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CSF Aβ42, Tau and phosphorylated Tau, APOE ɛ4 allele and MCI type in progressive MCI

Cited by 102 publications

References 55 publications

Attention and working memory deficits in mild cognitive impairment

Attention and working memory deficits in mild cognitive impairment

Current state and future directions of neurochemical biomarkers for Alzheimer's disease

Plasma A 42 and A 40 as markers of cognitive change in follow-up: a prospective, longitudinal, population-based cohort study

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