Amyloid β protein 42(43) in cerebrospinal fluid of patients with Alzheimer's disease

Tamaoka, Akira; Sawamura, Naoya; Fukushima, Tetsuo; Shoji, Shin’ichi; Matsubara, Etsuro; Shoji, Mikio; Hirai, Shunsaku; Furiya, Yoshiko; Endoh, Riuko; Mori, Hiroshi

doi:10.1016/s0022-510x(96)00314-0

Cited by 129 publications

(84 citation statements)

References 37 publications

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“…An increased ratio of amino-terminally modified A␤x-42: A␤1-42 in CSF samples of AD patients has been suggested previously (65), whereas the ratio of A␤x-40:A␤1-40 did not discriminate between AD and non-AD patients. However, the latter enzyme-linked immunosorbent assay-based study did not further specify the nature of these amino-terminal modifications.…”

Section: Specific Elevation Of An Additional Amino-terminal-truncatedmentioning

confidence: 51%

Elevation of β-Amyloid Peptide 2–42 in Sporadic and Familial Alzheimer's Disease and Its Generation in PS1 Knockout Cells

Wiltfang¹,

Esselmann²,

Cupers³

et al. 2001

Journal of Biological Chemistry

120

123

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show a decrease of all secreted A␤ peptide species, as expected, because this mutant is processed mainly by ␣-secretase. This drop is even more pronounced for the APP-KK construct (APP mutant carrying an endoplasmic reticulum retention motif). Surprisingly, A␤2-42 is significantly less affected in PS1؊/؊ neurons and in neurons transfected with the endocytosis-deficient APP-⌬ct construct. Our data confirm that PS1 is closely involved in the production of A␤1-40/42 and the carboxyl-terminal-truncated A␤1-37, A␤1-38, and A␤1-39, but the amino-terminaltruncated and carboxyl-terminal-elongated A␤2-42 seems to be less affected by PS1 deficiency. Moreover, our results indicate that the latter A␤ peptide species could be generated by a ␤ Asp/Ala -secretase activity.

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Section: Specific Elevation Of An Additional Amino-terminal-truncatedmentioning

confidence: 51%

Elevation of β-Amyloid Peptide 2–42 in Sporadic and Familial Alzheimer's Disease and Its Generation in PS1 Knockout Cells

Wiltfang¹,

Esselmann²,

Cupers³

et al. 2001

Journal of Biological Chemistry

120

123

View full text Add to dashboard Cite

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“…In addition, the concentrations of severe AD patients in this study were similar to those in HC, which is not consistent with most studies on CSF Ab 1-42 published so far. [5][6][7]9,[26][27][28][29] In this individual study, increased CSF Ab 42 was also found in depression, while two other studies have found normal levels of Ab in depressed patients 7,30 Moreover, in the measurement of Ab proteins, the assay used in the study of Jensen et al was different from the assay used to quantitate Ab in the other studies. This may have influenced the concentrations measured in their study group.…”

Section: Discussionmentioning

confidence: 80%

Value of CSF β-amyloid1–42 and tau as predictors of Alzheimer's disease in patients with mild cognitive impairment

Hampel¹,

Teipel²,

Fuchsberger³

et al. 2003

Mol Psychiatry

285

196

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Subjects with mild cognitive impairment (MCI) are at a high risk of developing clinical Alzheimer's disease (AD). We asked to what extent the core biomarker candidates cerebro-spinal fluid (CSF) bamyloid 1-42 (Ab 1-42 ) and CSF tau protein concentrations predict conversion from MCI to AD. We studied 52 patients with MCI, 93 AD patients, and 10 healthy controls (HC). The MCI group was composed of 29 patients who had converted to AD during follow-up, and of 23 patients who showed no cognitive decline. CSF Ab 1-42 and tau protein levels were assessed at baseline in all subjects, using enzyme-linked immunosorbent assays. For assessment of sensitivity and specificity, we used independently established reference values for CSF Ab 1-42 and CSF tau. The levels of CSF tau were increased, whereas levels of Ab 1-42 were decreased in MCI subjects. Ab 1-42 predicted AD in converted MCI with a sensitivity of 59% and a specificity of 100% compared to HC. Tau yielded a greater sensitivity of 83% and a specificity of 90%. In a multiple Cox regression analysis within the MCI group, low baseline levels of Ab 1-42 , but not other predictor variables (tau protein, gender, age, apolipoprotein E e4 carrier status, Mini Mental Status Examination score, observation time, antidementia therapy), correlated with conversion status (Po0.05). Our findings support the notion that CSF tau and Ab 1-42 may be useful biomarkers in the early identification of AD in MCI subjects.

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“…In a large number of studies it has now been demonstrated that Ab 42 concentrations in CSF are decreased in AD patients compared with those in age-matched controls or neurological control groups, 15,18^24 whereas no di¡er-ences were observed in the concentrations of CSF Ab 40 (see Table 1). 18,20,21 Ab 42 concentrations were lower in early onset AD patients compared with late-onset AD patients 19 and slightly lower in probable AD versus possible AD patients, 25 but in either group the concentration was decreased compared with a control group. It should be noted that, biologically relevant as these data are, di¡erences were only evident in group comparisons.…”

Section: Cerebrospinal Uid Ab 42 and Tau In Alzheimer's Diseasementioning

confidence: 73%

Brain-specific proteins in cerebrospinal fluid for the diagnosis of neurodegenerative diseases

Verbeek¹,

Jong²,

Kremer³

2003

Ann Clin Biochem

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Neurodegenerative disorders have traditionally been classi ed according to clinical criteria, e.g. as dementia syndromes (the best known is Alzheimer's disease) or as movement disorders (e.g. Parkinson's disease). Another subdivision is based on recent insights into the respective pathogenetic mechanisms, leading to the recognition of so-called tauopathies and a-synucleinopathies. It is this increased knowledge of the underlying (neuro)pathological mechanisms that has sparked interest in studies aimed at the identi cation of disease-speci c biomarkers in cerebrospinal uid (CSF) for this eld of neurological disorders. This review deals with the recent progress that has been made in identi cation, quanti cation and subsequent validation of brain-speci c proteins in CSF for the diagnosis of various neurodegenerative disorders. Development of disease-speci c CSF biomarkers will undoubtedly add to the process of differential diagnosis early in the course of the disease.

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Amyloid β protein 42(43) in cerebrospinal fluid of patients with Alzheimer's disease

Cited by 129 publications

References 37 publications

Elevation of β-Amyloid Peptide 2–42 in Sporadic and Familial Alzheimer's Disease and Its Generation in PS1 Knockout Cells

Elevation of β-Amyloid Peptide 2–42 in Sporadic and Familial Alzheimer's Disease and Its Generation in PS1 Knockout Cells

Value of CSF β-amyloid1–42 and tau as predictors of Alzheimer's disease in patients with mild cognitive impairment

Brain-specific proteins in cerebrospinal fluid for the diagnosis of neurodegenerative diseases

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