Alzheimer's Disease Evaluation Profile, CSF

CPT: 83520(x3)
To be determined. Updates will be made when available.
83520(x3)
Updated on 06/10/2024

Test Includes

ß-Amyloid 1-42 (Abeta42), Total Tau (tTau) and Phospho‑Tau 181 (pTau-181) are measured from CSF. These values are used to calculate the tTau/Abeta42 Ratio and the pTau-181/Abeta42 Ratio.

ß-Amyloid 1-42 (Abeta42), Total Tau (tTau) and Phospho‑Tau 181(pTau-181) are measured from CSF. These values are used to calculate the tTau/Abeta42 Ratio and the pTau-181/Abeta42 Ratio.

ß-Amyloid 1-42 (Abeta42), Total Tau (tTau) and Phospho‑Tau 181 (pTau-181) are measured from CSF. These values are used to calculate the tTau/Abeta42 Ratio and the pTau-181/Abeta42 Ratio.


Expected Turnaround Time

2 - 4 days


Related Documents


Specimen Requirements


Specimen

Cerebrospinal fluid (CSF)


Volume

1 mL


Minimum Volume

0.7 mL (Note: This volume does not allow for repeat testing.)


Container

Sarstedt CSF Tube 63.614.625 (tube provided by Labcorp by request)


Collection

Only the specimen listed below is acceptable for use with this assay. Please follow the steps listed below for CSF sample collection and measurement.

Perform lumbar puncture (LP) using gravity drip collection method.

• Avoid the use of syringes or tubings.

• Perform lumbar puncture (LP) before noon.

Do not use the first 2 mL of CSF for AD Biomarker measurement.

Subsequently, collect at least 2.5 mL of CSF directly into the CSF tube 63.614.625 (Sarstedt) for AD biomarker measurements.

• (Note: 2.5 mL filling volume corresponds to filling up to the mark on the tube.)

• Each sample should be visually inspected for hemolysis.

• Do not use CSF samples that appear reddish for measurement of Elecsys AD biomarkers.

• Instead, collect additional clear (non-hemolytic) CSF in a new CSF tube. Collection of CSF for other purposes can follow thereafter, if required.

Do not process the CSF sample before transport to the measuring site (i.e., no mixing/inverting, no tube transfers, no aliquoting, no freezing and normally no centrifugation) until measurement.

• It is strongly recommended that the sample be kept at 2‑8°C during transport and storage up to the time of measurement.

• Samples can be stored at 2‑8°C for up to 14 days.

• If transport and storage at 2‑8°C is not feasible, the sample can be transported/stored at room temperature (15‑25°C). If this is the case, measurement is to be performed within five days after sample draw.


Storage Instructions

Refrigerate.


Stability Requirements

Temperature

Period

Room temperature

5 days (stability determined by manufacturer or literature reference)

Refrigerated

14 days (stability determined by manufacturer or literature reference)

Frozen

8 weeks (stability determined by manufacturer or literature reference)

Freeze/thaw cycles

Stable x1 (stability determined by manufacturer or literature reference)


Causes for Rejection

Hemolyzed CSF samples that are visibly colored red (samples received in any tube other than the CSF tube 63.614.625 (Sarstedt) will be rejected)


Test Details


Use

Elecsys β-Amyloid (1-42) CSF II assay, Elecsys Total-Tau CSF assay and Elecsys Phospho‑Tau (181P) CSF assay are in vitro electrochemiluminescence immunoassays for the measurement of the β‑Amyloid (1‑42) (Abeta42), total Tau (tTau) and Phospho‑Tau (181P) (pTau-181) protein concentrations in cerebrospinal fluid (CSF) from adult patients aged 55 years and older being evaluated for Alzheimer's disease (AD) and other causes of cognitive impairment to generate a tTau/Abeta42 ratio value1,2 and a pTau-181/Abeta42 ratio value.1,3

The use of AD biomarkers has been included in the new consensus research diagnostic criteria for AD, MCI and preclinical AD, proposed by the National Institute on Aging (NIA) and the Alzheimer’s Association. These new criteria take into account that AD dementia is part of a continuum of clinical and biological phenomena.4,5 The new International Working Group 2 (IWG 2) criteria recommend the use of either CSF biomarker or amyloid PET imaging for evaluation of AD patients.6 In Europe, the Committee for Medicinal Products for Human Use (CHMP) published a number of positive opinions on the use of biomarkers in the context of AD for enrichment of clinical trials in pre‑clinical dementia and mild to moderate AD.7,8


Limitations

The Abeta42, tTau and pTau-181 assays are not intended to be used as standalone tests and should only be used to calculate the tTau/Abeta42 and pTau-181/Abeta42 ratios.

Use of another manufacturer’s pTau-181, tTau and/or Abeta42 CSF assays may result in significantly different calculated ratios because the measured values of these analytes in a given sample, determined with assays from different manufacturers, can vary due to differences in assay methods and reagent. Values determined from samples by different assay methods cannot be used interchangeably.

The performance of the test for African American, Asian and other races had high uncertainty due to the limited number of patients studied.

Due to the sticky properties of the Abeta42 peptide to the test tube, the cutoffs for the tTau/Abeta42 and pTau-181/Abeta42 ratios are only valid if the described preanalytical sampling handling procedure (described in the “Collection” section) is strictly followed.

Positive results for the tTau/Abeta42 and/or pTau-181/Abeta42 ratios in CSF do not establish a diagnosis of Alzheimer's disease (AD) and should always be interpreted in conjunction with clinical information

The performance of the tTau/Abeta42 and pTau-181/Abeta42 ratios have not been established for:

• Predicting development of dementia or other neurologic conditions

• Monitoring responses to therapies


Methodology

Roche Diagnostics Electrochemiluminescence Immunoassay (ECLIA)


Reference Interval

β-Amyloid 1-42 (Abeta42), Total Tau (tTau) and Phospho‑Tau 181(pTau-181) are reported without reference intervals. The results from these three performed tests are used to calculate tTau/Abeta42 and the pTau-181/Abeta42 Ratios.

Elecsys® tTau/Abeta42 ratio

A negative result, defined as tTau/Abeta42 ratio value below cutoff or an Abeta42 value above the measuring range, is consistent with a negative amyloid positron emission tomography (PET) scan result. A negative result reduces the likelihood that a patient’s cognitive impairment is due to AD. A positive result, defined as tTau/Abeta42 ratio value above cutoff, is consistent with a positive amyloid PET scan result.

Cutoff

tTau-181/Abeta42 ratio

Interpretation

Cutoff (+)*

>0.28

A positive result consistent with a positive amyloid PET scan result.

Cutoff (-)†

≤0.28

A negative result consistent with a negative amyloid PET scan result.

Invalid result for either or both Elecsys Total‑Tau CSF or Elecsys β‑Amyloid (1-42) CSFII results in tTau-181/Abeta42 ratio being reported with the abbreviation “UPTCAL,” which expands out to state: “Unable to calculate result since non-numeric result obtained for component test.”

A positive result does not establish a diagnosis of AD or other cognitive disorder. The tTau-181/Abeta42 ratio result is used as an adjunct to other clinical diagnostic evaluations.

Elecsys® pTau-181/Abeta42 ratio

The Elecsys® pTau-181/Abeta42 ratio is highly concordant with amyloid PET and provides an alternative solution for detection of amyloid positivity.1,3 The Elecsys® pTau-181/Abeta42 ratio achieves 90% concordance with β-Amyloid PET scan results. A result above the cutoff is consistent with a positive amyloid PET visual read.1,3,9-11

The performance of the Elecsys® AD CSF ratio cutoff vs. amyloid PET visual read has been reported1,3,9 as such:

pTau-181/Abeta42 ratio

Cutoff (+)*

>0.023

Cutoff (-)†

≤0.023

PPA%

88.2 (84.4-91.2)‡

NPA%

92.6 (89.1-95.1)‡

OPA%

90.2(87.7-92.3)‡

• PPA: positive percent agreement

• NPA: negative percent agreement

• OPA: overall percent agreement

*Consistent with positive amyloid PET scan result

†Consistent with negative amyloid PET scan result

‡95% CI are calculated using a Wilson score method for binomial proportions

Invalid result for either or both pTau-181 β‑Amyloid (1-42) results in tTau-181/Abeta42 ratio being reported with the abbreviation “UPTCAL,” which expands out to state: “Unable to calculate result since non-numeric result obtained for component test.”

A negative result, defined as pTau-181/Abeta42 ratio value below cutoff or an Abeta42 value above the measuring range, is consistent with a negative amyloid positron emission tomography (PET) scan result.1,3 A negative result reduces the likelihood that a patient’s cognitive impairment is due to AD. A positive result, defined as pTau-181/Abeta42 ratio value above cutoff, is consistent with a positive amyloid PET scan result. A positive result does not establish a diagnosis of AD or other cognitive disorder. The pTau-181/Abeta42 ratio result is used as an adjunct to other clinical diagnostic evaluations.

β-Amyloid 1-42 (Abeta42), Total Tau (tTau) and Phospho‑Tau 181(pTau-181) are reported without reference intervals. The results from these three performed tests are used to calculate tTau/Abeta42 and the pTau-181/Abeta42 Ratios.

Elecsys® tTau/Abeta42 ratio

A negative result, defined as tTau/Abeta42 ratio value below cutoff or an Abeta42 value above the measuring range, is consistent with a negative amyloid positron emission tomography (PET) scan result. A negative result reduces the likelihood that a patient’s cognitive impairment is due to AD. A positive result, defined as tTau/Abeta42 ratio value above cutoff, is consistent with a positive amyloid PET scan result.

Cutoff

tTau-181/Abeta42 ratio

Interpretation

Cutoff (+)*

>0.28

A positive result consistent with a positive amyloid PET scan result.

Cutoff (-)†

≤0.28

A negative result consistent with a negative amyloid PET scan result.

Invalid result for either or both Elecsys Total‑Tau CSF or Elecsys β‑Amyloid (1-42) CSFII results in tTau-181/Abeta42 ratio being reported with the abbreviation “UPTCAL,” which expands out to state: “Unable to calculate result since non-numeric result obtained for component test.”

A positive result does not establish a diagnosis of AD or other cognitive disorder. The tTau-181/Abeta42 ratio result is used as an adjunct to other clinical diagnostic evaluations.

Elecsys® pTau-181/Abeta42 ratio

The Elecsys® pTau-181/Abeta42 ratio is highly concordant with amyloid PET and provides an alternative solution for detection of amyloid positivity.1,3 The Elecsys® pTau-181/Abeta42 ratio achieves 90% concordance with β-Amyloid PET scan results. A result above the cutoff is consistent with a positive amyloid PET visual read.1,3,9-11

The performance of the Elecsys® AD CSF ratio cutoff vs amyloid PET visual read has been reported1,3,9 as such:

pTau-181/Abeta42 ratio

Cutoff (+)*

>0.023

Cutoff (-)†

≤0.023

PPA%

88.2 (84.4-91.2)‡

NPA%

92.6 (89.1-95.1)‡

OPA%

90.2(87.7-92.3)‡

• PPA: positive percent agreement

• NPA: negative percent agreement

• OPA: overall percent agreement

*Consistent with positive amyloid PET scan result

†Consistent with negative amyloid PET scan result

‡95% CI are calculated using a Wilson score method for binomial proportions

Invalid result for either or both pTau-181 β‑Amyloid (1-42) results in tTau-181/Abeta42 ratio being reported with the abbreviation “UPTCAL,” which expands out to state: “Unable to calculate result since non-numeric result obtained for component test.”

A negative result, defined as pTau-181/Abeta42 ratio value below cutoff or an Abeta42 value above the measuring range, is consistent with a negative amyloid positron emission tomography (PET) scan result.1,3 A negative result reduces the likelihood that a patient’s cognitive impairment is due to AD. A positive result, defined as pTau-181/Abeta42 ratio value above cutoff, is consistent with a positive amyloid PET scan result. A positive result does not establish a diagnosis of AD or other cognitive disorder. The pTau-181/Abeta42 ratio result is used as an adjunct to other clinical diagnostic evaluations.

β-Amyloid 1-42 (Abeta42), Total Tau (tTau) and Phospho‑Tau 181(pTau-181) are reported without reference intervals. The results from these three performed tests are used to calculate tTau/Abeta42 and the pTau-181/Abeta42 Ratios.

Elecsys® tTau/Abeta42 ratio

A negative result, defined as tTau/Abeta42 ratio value below cutoff or an Abeta42 value above the measuring range, is consistent with a negative amyloid positron emission tomography (PET) scan result. A negative result reduces the likelihood that a patient’s cognitive impairment is due to AD. A positive result, defined as tTau/Abeta42 ratio value above cutoff, is consistent with a positive amyloid PET scan result.

Cutoff

tTau-181/Abeta42 ratio

Interpretation

Cutoff (+)*

>0.28

A positive result consistent with a positive amyloid PET scan result.

Cutoff (-)†

≤0.28

A negative result consistent with a negative amyloid PET scan result.

Invalid result for either or both Elecsys Total‑Tau CSF or Elecsys β‑Amyloid (1-42) CSFII results in tTau-181/Abeta42 ratio being reported with the abbreviation “UPTCAL,” which expands out to state: “Unable to calculate result since non-numeric result obtained for component test.”

A positive result does not establish a diagnosis of AD or other cognitive disorder. The tTau-181/Abeta42 ratio result is used as an adjunct to other clinical diagnostic evaluations.

Elecsys® pTau-181/Abeta42 ratio

The Elecsys® pTau-181/Abeta42 ratio is highly concordant with amyloid PET and provides an alternative solution for detection of amyloid positivity.1,3 The Elecsys® pTau-181/Abeta42 ratio achieves 90% concordance with β-Amyloid PET scan results. A result above the cutoff is consistent with a positive amyloid PET visual read.1,3,9-11

The performance of the Elecsys® AD CSF ratio cutoff vs. amyloid PET visual read has been reported1,3,9 as such:

pTau-181/Abeta42 ratio

Cutoff (+)*

>0.023

Cutoff (-)†

≤0.023

PPA%

88.2 (84.4-91.2)‡

NPA%

92.6 (89.1-95.1)‡

OPA%

90.2(87.7-92.3)‡

• PPA: positive percent agreement

• NPA: negative percent agreement

• OPA: overall percent agreement

*Consistent with positive amyloid PET scan result

†Consistent with negative amyloid PET scan result

‡95% CI are calculated using a Wilson score method for binomial proportions

Invalid result for either or both pTau-181 β‑Amyloid (1-42) results in tTau-181/Abeta42 ratio being reported with the abbreviation “UPTCAL,” which expands out to state: “Unable to calculate result since non-numeric result obtained for component test.”

A negative result, defined as pTau-181/Abeta42 ratio value below cutoff or an Abeta42 value above the measuring range, is consistent with a negative amyloid positron emission tomography (PET) scan result.1,3 A negative result reduces the likelihood that a patient’s cognitive impairment is due to AD. A positive result, defined as pTau-181/Abeta42 ratio value above cutoff, is consistent with a positive amyloid PET scan result. A positive result does not establish a diagnosis of AD or other cognitive disorder. The pTau-181/Abeta42 ratio result is used as an adjunct to other clinical diagnostic evaluations.


Additional Information

The use of AD biomarkers has been included in the new consensus research diagnostic criteria for AD, MCI and preclinical AD, proposed by the National Institute on Aging (NIA) and the Alzheimer’s Association. These new criteria take into account that AD dementia is part of a continuum of clinical and biological phenomena.4,5 The new International Working Group 2 (IWG2) criteria recommend the use of either CSF biomarker or amyloid PET imaging for evaluation of AD patients.6 In Europe, the Committee for Medicinal Products for Human Use (CHMP) published a number of positive opinions on the use of biomarkers in the context of AD for enrichment of clinical trials in pre‑dementia and mild to moderate AD.

Clinical relevance of Abeta42

The Elecsys β-Amyloid (1-42) CSF II assay is designed to quantify the concentration of Abeta42 in CSF. The Abeta42 peptide is a small, 4 kDa protein of about 40 amino acids that is formed following proteolytic cleavage of a transmembrane protein known as amyloid precursor protein (APP). Cleavage of APP occurs via two events: cleavage by β‑secretase within the extracellular domain and cleavage by γ‑secretase in the transmembrane region. Due to its hydrophobic nature, the Abeta42 peptide has the propensity to form aggregates and oligomers. Oligomers of higher order form fibrils that accumulate into β‑Amyloid plaques.12

Abeta42 peptide deposition in the brain is considered as one of the two hallmarks of AD, besides neurofibrillary tangles. It can be detected by several methods: (a) histopathological staining of Abeta42 deposits in post mortem brain tissue; (b) use of radiolabeled tracers that bind to β-Amyloid deposits in the brain and can then be detected in vivo using amyloid PET scan; (c) measuring the Abeta42 level in CSF because lower titers in CSF are believed to reflect accumulation of this molecule in the brain.13,14

Pathological changes in the β-Amyloid metabolism are the earliest alterations during AD development known so far that can be utilized diagnostically. They are reflected by the decrease in the CSF concentration of Abeta42 as well as by the increase in the brain uptake of the specific tracers on the amyloid PET.15 Current clinical diagnostic criteria for AD require a patient to have dementia before a diagnosis of AD can be made and are largely based on the exclusion of other disorders. No clinical method is available for identifying prodromal AD in patients with mild cognitive impairment (MCI), as such individuals have only mild disturbances in episodic memory.16

Numerous studies show that while Abeta42 levels in CSF decrease to around half the level in controls, pTau-181 levels in CSF increase around two-to-three-fold in mild to moderate AD patients compared to age-matched controls.17,18 The pTau-181 levels in CSF are also associated with a faster progression from MCI to AD with more rapid cognitive decline in AD patients19 as well as in very mild AD dementia cases. The pTau-181 biomarker in CSF has the highest power when used in combination with Abeta42 in CSF for detecting the likely progression of subjects with MCI to AD.20

Clinical relevance of tTau

Tau (tubulin‑associated unit) protein is found as six molecular isoforms in the human brain. These isoforms are coded by a single gene on chromosome 17 and generated by alternative splicing of its pre‑mRNA. The Tau from all these isoforms is called total Tau (tTau). The Elecsys Total‑Tau CSF assay is designed to detect the six human brain Tau isoforms or soluble aggregates and fragments thereof in human CSF.

In AD, numerous studies show that while CSF β‑Amyloid (1‑42) levels decrease to around half the level in controls, CSF tTau levels increase around two-to-three-fold in mild to moderate AD patients compared to age‑matched controls.17,18 CSF tTau has been shown to reflect the intensity of the neuronal and axonal damage and degeneration. High CSF tTau is also associated with a faster progression from mild cognitive impairment (MCI) to AD.21 CSF tTau biomarker might be useful in detecting the likely progression of MCI to AD6 and has most power when used in combination with CSF β‑Amyloid (1‑42).22

Clinical relevance of pTau-181

The most common post‑translational modification of Tau proteins is phosphorylation. Phosphorylation changes the shape of the Tau molecule and regulates its biological activity. During neurodegeneration, abnormal phosphorylation leads to formation of intracellular neurofibrillary tangles (NFTs) composed of the Tau protein that has undergone hyper‑phosphorylation and developed aggregates of hyper‑phosphorylated Tau proteins called Phospho‑Tau (pTau).22,23

In AD, numerous studies show that while Abeta42 levels in CSF decrease to around half the level in controls, CSF pTau-181 levels increase around two-to-three-fold in mild‑moderate AD patients compared to age‑matched controls.17,18 High CSF pTau-181 levels are also associated with a faster progression from mild cognitive impairment (MCI) to AD with more rapid cognitive decline in AD patients20 and in mild AD dementia cases.24 6 pTau-181 as a biomarker in CSF might be useful in detecting the likely progression of MCI to AD25 and has most power when used in combination with Abeta42 in CSF.


Footnotes

1. Elecsys β-Amyloid (1-42) CSF II [instructions for use]. Roche Diagnostics, 2022-12, V 1.0 English.
2. Elecsys Total-Tau (tTau) CSF [instructions for use]. Roche Diagnostics, 2023-08, V 1.0 English.
3. Elecsys Phospho-Tau (181P) CSF [instructions for use]. Roche Diagnostics, 2022-12, V 1.0 English.
4. Jack CR Jr, Albert MS, Knopman DS, et al. Introduction to the recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011 May;7(3):257-262.21514247
5. Albert MS, DeKosky ST, Dickson D, et al. The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011 May;7(3):270-279.21514249
6. Dubois B, Feldman HH, Jacova C, et al. Advancing research diagnostic criteria for Alzheimer's disease: the IWG-2 criteria. Lancet Neurol. 2014 Jun;13(6):614-629.24849862
7. European Medicines Agency (ESA). Qualification opinion of Alzheimer’s disease novel methodologies/biomarkers for the use of CSF AB 1-42 and t-tau signature and/or PET-amyloid imaging (positive/negative) as a biomarkers for enrichment, for use in regulatory clinical trials in mild and moderate of Alzheimer's disease. ESA website: https://www.ema.europa.eu/en/documents/regulatory-procedural-guideline/qualification-opinion-alzheimers-disease-novel-methodologies-biomarkers-use-cerebrospinal-fluid-amyloid-beta-1-42-and-t-tau-and-or-positron-emission-tomography-amyloid-imaging-positive-negative_en.pdf. Accessed May 2024.
8. European Medicines Agency (ESA). Draft guideline on the clinical investigation of medicines for the treatment of Alzheimer’s disease and other dementias. ESA website: https://www.ema.europa.eu/en/documents/scientific-guideline/draft-guideline-clinical-investigation-medicines-treatment-alzheimers-disease-and-other-dementias_en.pdf. Accessed May 2024.
9. Hansson O, Seibyl J, Stomrud E, et al. CSF biomarkers of Alzheimer's disease concord with amyloid-β PET and predict clinical progression: A study of fully automated immunoassays in Bio FINDER and ADNI cohorts. Alzheimer’sDement. 2018 Nov;14(11):1470-1481.29499171
10. Willemse EAJ, van Maurik IS, Tijms BM, et al. Diagnostic performance of Elecsys immunoassays for cerebrospinal fluid Alzheimer's disease biomarkers in a nonacademic, multicenter memory clinic cohort: The ABIDE project. Alzheimer’s Dement (Amst). 2018 Sep 12;10:563-572.30406175
11. Bittner T, Zetterberg H, Teunissen CE, et al. Technical performance of a novel, fully automated electrochemiluminescence immunoassay for the quantitation of β-amyloid (1-42) in human cerebrospinal fluid. Alzheimer’s Dement. 2016 May;12(5):517-526.26555316
12. Vandenberghe R, Adamczuk K, Dupont P, Van Laere K, Chételat G. Amyloid PET in clinical practice: Its place in the multidimensional space of Alzheimer's disease. Neuroimage Clin. 2013 Apr 6:2:497-511.24179802
13. Blennow K, Zetterberg H, Fagan AM. Fluid Biomarkers in Alzheimer Disease. Cold Spring Harb Perspect Med. 2012 Sep 1;2(9):a006221.22951438
14. Bates KA, Verdile G, Li Q-X, et al. Clearance mechanisms of Alzheimer's amyloid-β peptide: implications for therapeutic design and diagnostic tests. Mol Psychiatry. 2009 May;14(5):469-486.18794889
15. Lewczuk P, Mroczko B, Fagan A, Kornhuber J. Biomarkers of Alzheimer's disease and mild cognitive impairment: a current perspective. Adv Med Sci. 2015 Mar;60(1):76-82.25579841
16. Blennow K, Hampel H, Weiner M, Zetterberg H. Cerebrospinal fluid and plasma biomarkers in Alzheimer disease. Nat Rev Neurol. 2010 Mar;6(3):131-144.20157306
17. Mattsson N, Zetterberg H, Hansson O, et al. CSF biomarkers and incipient Alzheimer disease in patients with mild cognitive impairment. JAMA. 2009 Jul 22;302(4):385-393.19622817
18. Hampel H, Blennow K. CSF tau and β-amyloid as biomarkers for mild cognitive impairment. Dialogues Clin Neurosci. 2004 Dec;6(4):379-390.22034251
19. Snider BJ, Fagan AM, Roe C, et al. Cerebrospinal fluid biomarkers and rate of cognitive decline in very mild dementia of the Alzheimer type. Arch Neurol. 2009 May;66(5):638-645.19433664
20. Li J-Q, Tan L, Wang H-F, et al. Risk factors for predicting progression from mild cognitive impairment to Alzheimer’s disease: a systematic review and meta-analysis of cohort studies. J Neurol Neurosurg Psychiatry. 2016 May;87(5):476-484.26001840
21. Blom ES, Giedraitis V, Zetterberg H, et al. Rapid progression from mild cognitive impairment to Alzheimer's disease in subjects with elevated levels of tau in cerebrospinal fluid and the APOE epsilon4/epsilon4 genotype. DementGeriatr Cogn Disord. 2009;27(5):458-464.19420940
22. Wang Y, Mandelkow E. Tau in physiology and pathology. Nat Rev Neurosci. 2016 Jan;17(1):5-21.26631930
23. Iqbal K, Liu F, Gong C-X. Tau and neurodegenerative disease: the story so far. Nat Rev Neurol. 2016 Jan;12(1):15-27.26635213
24. Snider BJ, Fagan AM, Roe C, et al. Cerebrospinal fluid biomarkers and rate of cognitive decline in very mild dementia of the Alzheimer’s type. Arch Neurol. 2009 May;66(5):638-645.19433664
25. Andreasen N, Vanmechelen E, Vanderstichele H, Davidson P, Blennow K. Cerebrospinal fluid levels of total-tau, phospho-tau and A beta 42 predicts development of Alzheimer's disease inpatients with mild cognitive impairment. Acta Neurol ScandSuppl. 2003;179:47-51.12603251
1. Elecsys β-Amyloid (1-42) CSF II [instructions for use]. Roche Diagnostics, 2022-12, V 1.0 English.
2. Elecsys Total-Tau (tTau) CSF [instructions for use]. Roche Diagnostics, 2023-08, V 1.0 English.
3. Elecsys Phospho-Tau (181P) CSF [instructions for use]. Roche Diagnostics, 2022-12, V 1.0 English.
4. Jack CR Jr, Albert MS, Knopman DS, et al. Introduction to the recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011 May;7(3):257-262.21514247
5. Albert MS, DeKosky ST, Dickson D, et al. The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011 May;7(3):270-279.21514249
6. Dubois B, Feldman HH, Jacova C, et al. Advancing research diagnostic criteria for Alzheimer's disease: the IWG-2 criteria. Lancet Neurol. 2014 Jun;13(6):614-629.24849862
7. European Medicines Agency (ESA). Qualification opinion of Alzheimer’s disease novel methodologies/biomarkers for the use of CSF AB 1-42 and t-tau signature and/or PET-amyloid imaging (positive/negative) as a biomarkers for enrichment, for use in regulatory clinical trials in mild and moderate of Alzheimer's disease. ESA website: https://www.ema.europa.eu/en/documents/regulatory-procedural-guideline/qualification-opinion-alzheimers-disease-novel-methodologies-biomarkers-use-cerebrospinal-fluid-amyloid-beta-1-42-and-t-tau-and-or-positron-emission-tomography-amyloid-imaging-positive-negative_en.pdf. Accessed May 2024.
8. European Medicines Agency (ESA). Draft guideline on the clinical investigation of medicines for the treatment of Alzheimer’s disease and other dementias. ESA website: https://www.ema.europa.eu/en/documents/scientific-guideline/draft-guideline-clinical-investigation-medicines-treatment-alzheimers-disease-and-other-dementias_en.pdf. Accessed May 2024.
9. Hansson O, Seibyl J, Stomrud E, et al. CSF biomarkers of Alzheimer's disease concord with amyloid-β PET and predict clinical progression: A study of fully automated immunoassays in Bio FINDER and ADNI cohorts. Alzheimer’sDement. 2018 Nov;14(11):1470-1481.29499171
10. Willemse EAJ, van Maurik IS, Tijms BM, et al. Diagnostic performance of Elecsys immunoassays for cerebrospinal fluid Alzheimer's disease biomarkers in a nonacademic, multicenter memory clinic cohort: The ABIDE project. Alzheimer’s Dement (Amst). 2018 Sep 12;10:563-572.30406175
11. Bittner T, Zetterberg H, Teunissen CE, et al. Technical performance of a novel, fully automated electrochemiluminescence immunoassay for the quantitation of β-amyloid (1-42) in human cerebrospinal fluid. Alzheimer’s Dement. 2016 May;12(5):517-526.26555316
12. Vandenberghe R, Adamczuk K, Dupont P, Van Laere K, Chételat G. Amyloid PET in clinical practice: Its place in the multidimensional space of Alzheimer's disease. Neuroimage Clin. 2013 Apr 6:2:497-511.24179802
13. Blennow K, Zetterberg H, Fagan AM. Fluid Biomarkers in Alzheimer Disease. Cold Spring Harb Perspect Med. 2012 Sep 1;2(9):a006221.22951438
14. Bates KA, Verdile G, Li Q-X, et al. Clearance mechanisms of Alzheimer's amyloid-β peptide: implications for therapeutic design and diagnostic tests. Mol Psychiatry. 2009 May;14(5):469-486.18794889
15. Lewczuk P, Mroczko B, Fagan A, Kornhuber J. Biomarkers of Alzheimer's disease and mild cognitive impairment: a current perspective. Adv Med Sci. 2015 Mar;60(1):76-82.25579841
16. Blennow K, Hampel H, Weiner M, Zetterberg H. Cerebrospinal fluid and plasma biomarkers in Alzheimer disease. Nat Rev Neurol. 2010 Mar;6(3):131-144.20157306
17. Mattsson N, Zetterberg H, Hansson O, et al. CSF biomarkers and incipient Alzheimer disease in patients with mild cognitive impairment. JAMA. 2009 Jul 22;302(4):385-393.19622817
18. Hampel H, Blennow K. CSF tau and β-amyloid as biomarkers for mild cognitive impairment. Dialogues Clin Neurosci. 2004 Dec;6(4):379-390.22034251
19. Snider BJ, Fagan AM, Roe C, et al. Cerebrospinal fluid biomarkers and rate of cognitive decline in very mild dementia of the Alzheimer type. Arch Neurol. 2009 May;66(5):638-645.19433664
20. Li J-Q, Tan L, Wang H-F, et al. Risk factors for predicting progression from mild cognitive impairment to Alzheimer’s disease: a systematic review and meta-analysis of cohort studies. J Neurol Neurosurg Psychiatry. 2016 May;87(5):476-484.26001840
21. Blom ES, Giedraitis V, Zetterberg H, et al. Rapid progression from mild cognitive impairment to Alzheimer's disease in subjects with elevated levels of tau in cerebrospinal fluid and the APOE epsilon4/epsilon4 genotype. DementGeriatr Cogn Disord. 2009;27(5):458-464.19420940
22. Wang Y, Mandelkow E. Tau in physiology and pathology. Nat Rev Neurosci. 2016 Jan;17(1):5-21.26631930
23. Iqbal K, Liu F, Gong C-X. Tau and neurodegenerative disease: the story so far. Nat Rev Neurol. 2016 Jan;12(1):15-27.26635213
24. Snider BJ, Fagan AM, Roe C, et al. Cerebrospinal fluid biomarkers and rate of cognitive decline in very mild dementia of the Alzheimer’s type. Arch Neurol. 2009 May;66(5):638-645.19433664
25. Andreasen N, Vanmechelen E, Vanderstichele H, Davidson P, Blennow K. Cerebrospinal fluid levels of total-tau, phospho-tau and A beta 42 predicts development of Alzheimer's disease inpatients with mild cognitive impairment. Acta Neurol ScandSuppl. 2003;179:47-51.12603251
1. Elecsys β-Amyloid (1-42) CSF II [instructions for use]. Roche Diagnostics, 2022-12, V 1.0 English.
2. Elecsys Total-Tau (tTau) CSF [instructions for use]. Roche Diagnostics, 2023-08, V 1.0 English.
3. Elecsys Phospho-Tau (181P) CSF [instructions for use]. Roche Diagnostics, 2022-12, V 1.0 English.
4. Jack CR Jr, Albert MS, Knopman DS, et al. Introduction to the recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011 May;7(3):257-262.21514247
5. Albert MS, DeKosky ST, Dickson D, et al. The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011 May;7(3):270-279.21514249
6. Dubois B, Feldman HH, Jacova C, et al. Advancing research diagnostic criteria for Alzheimer's disease: the IWG-2 criteria. Lancet Neurol. 2014 Jun;13(6):614-629.24849862
7. European Medicines Agency (ESA). Qualification opinion of Alzheimer’s disease novel methodologies/biomarkers for the use of CSF AB 1-42 and t-tau signature and/or PET-amyloid imaging (positive/negative) as a biomarkers for enrichment, for use in regulatory clinical trials in mild and moderate of Alzheimer's disease. ESA website: https://www.ema.europa.eu/en/documents/regulatory-procedural-guideline/qualification-opinion-alzheimers-disease-novel-methodologies-biomarkers-use-cerebrospinal-fluid-amyloid-beta-1-42-and-t-tau-and-or-positron-emission-tomography-amyloid-imaging-positive-negative_en.pdf. Accessed May 2024.
8. European Medicines Agency (ESA). Draft guideline on the clinical investigation of medicines for the treatment of Alzheimer’s disease and other dementias. ESA website: https://www.ema.europa.eu/en/documents/scientific-guideline/draft-guideline-clinical-investigation-medicines-treatment-alzheimers-disease-and-other-dementias_en.pdf. Accessed May 2024.
9. Hansson O, Seibyl J, Stomrud E, et al. CSF biomarkers of Alzheimer's disease concord with amyloid-β PET and predict clinical progression: A study of fully automated immunoassays in Bio FINDER and ADNI cohorts. Alzheimer’sDement. 2018 Nov;14(11):1470-1481.29499171
10. Willemse EAJ, van Maurik IS, Tijms BM, et al. Diagnostic performance of Elecsys immunoassays for cerebrospinal fluid Alzheimer's disease biomarkers in a nonacademic, multicenter memory clinic cohort: The ABIDE project. Alzheimer’s Dement (Amst). 2018 Sep 12;10:563-572.30406175
11. Bittner T, Zetterberg H, Teunissen CE, et al. Technical performance of a novel, fully automated electrochemiluminescence immunoassay for the quantitation of β-amyloid (1-42) in human cerebrospinal fluid. Alzheimer’s Dement. 2016 May;12(5):517-526.26555316
12. Vandenberghe R, Adamczuk K, Dupont P, Van Laere K, Chételat G. Amyloid PET in clinical practice: Its place in the multidimensional space of Alzheimer's disease. Neuroimage Clin. 2013 Apr 6:2:497-511.24179802
13. Blennow K, Zetterberg H, Fagan AM. Fluid Biomarkers in Alzheimer Disease. Cold Spring Harb Perspect Med. 2012 Sep 1;2(9):a006221.22951438
14. Bates KA, Verdile G, Li Q-X, et al. Clearance mechanisms of Alzheimer's amyloid-β peptide: implications for therapeutic design and diagnostic tests. Mol Psychiatry. 2009 May;14(5):469-486.18794889
15. Lewczuk P, Mroczko B, Fagan A, Kornhuber J. Biomarkers of Alzheimer's disease and mild cognitive impairment: a current perspective. Adv Med Sci. 2015 Mar;60(1):76-82.25579841
16. Blennow K, Hampel H, Weiner M, Zetterberg H. Cerebrospinal fluid and plasma biomarkers in Alzheimer disease. Nat Rev Neurol. 2010 Mar;6(3):131-144.20157306
17. Mattsson N, Zetterberg H, Hansson O, et al. CSF biomarkers and incipient Alzheimer disease in patients with mild cognitive impairment. JAMA. 2009 Jul 22;302(4):385-393.19622817
18. Hampel H, Blennow K. CSF tau and β-amyloid as biomarkers for mild cognitive impairment. Dialogues Clin Neurosci. 2004 Dec;6(4):379-390.22034251
19. Snider BJ, Fagan AM, Roe C, et al. Cerebrospinal fluid biomarkers and rate of cognitive decline in very mild dementia of the Alzheimer type. Arch Neurol. 2009 May;66(5):638-645.19433664
20. Li J-Q, Tan L, Wang H-F, et al. Risk factors for predicting progression from mild cognitive impairment to Alzheimer’s disease: a systematic review and meta-analysis of cohort studies. J Neurol Neurosurg Psychiatry. 2016 May;87(5):476-484.26001840
21. Blom ES, Giedraitis V, Zetterberg H, et al. Rapid progression from mild cognitive impairment to Alzheimer's disease in subjects with elevated levels of tau in cerebrospinal fluid and the APOE epsilon4/epsilon4 genotype. DementGeriatr Cogn Disord. 2009;27(5):458-464.19420940
22. Wang Y, Mandelkow E. Tau in physiology and pathology. Nat Rev Neurosci. 2016 Jan;17(1):5-21.26631930
23. Iqbal K, Liu F, Gong C-X. Tau and neurodegenerative disease: the story so far. Nat Rev Neurol. 2016 Jan;12(1):15-27.26635213
24. Snider BJ, Fagan AM, Roe C, et al. Cerebrospinal fluid biomarkers and rate of cognitive decline in very mild dementia of the Alzheimer’s type. Arch Neurol. 2009 May;66(5):638-645.19433664
25. Andreasen N, Vanmechelen E, Vanderstichele H, Davidson P, Blennow K. Cerebrospinal fluid levels of total-tau, phospho-tau and A beta 42 predicts development of Alzheimer's disease inpatients with mild cognitive impairment. Acta Neurol ScandSuppl. 2003;179:47-51.12603251
1. Elecsys β-Amyloid (1-42) CSF II [instructions for use]. Roche Diagnostics, 2022-12, V 1.0 English.
2. Elecsys Total-Tau (tTau) CSF [instructions for use]. Roche Diagnostics, 2023-08, V 1.0 English.
3. Elecsys Phospho-Tau (181P) CSF [instructions for use]. Roche Diagnostics, 2022-12, V 1.0 English.
4. Jack CR Jr, Albert MS, Knopman DS, et al. Introduction to the recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011 May;7(3):257-262.21514247
5. Albert MS, DeKosky ST, Dickson D, et al. The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011 May;7(3):270-279.21514249
6. Dubois B, Feldman HH, Jacova C, et al. Advancing research diagnostic criteria for Alzheimer's disease: the IWG-2 criteria. Lancet Neurol. 2014 Jun;13(6):614-629.24849862
7. European Medicines Agency (ESA). Qualification opinion of Alzheimer’s disease novel methodologies/biomarkers for the use of CSF AB 1-42 and t-tau signature and/or PET-amyloid imaging (positive/negative) as a biomarkers for enrichment, for use in regulatory clinical trials in mild and moderate of Alzheimer's disease. ESA website: https://www.ema.europa.eu/en/documents/regulatory-procedural-guideline/qualification-opinion-alzheimers-disease-novel-methodologies-biomarkers-use-cerebrospinal-fluid-amyloid-beta-1-42-and-t-tau-and-or-positron-emission-tomography-amyloid-imaging-positive-negative_en.pdf. Accessed May 2024.
8. European Medicines Agency (ESA). Draft guideline on the clinical investigation of medicines for the treatment of Alzheimer’s disease and other dementias. ESA website: https://www.ema.europa.eu/en/documents/scientific-guideline/draft-guideline-clinical-investigation-medicines-treatment-alzheimers-disease-and-other-dementias_en.pdf. Accessed May 2024.
9. Hansson O, Seibyl J, Stomrud E, et al. CSF biomarkers of Alzheimer's disease concord with amyloid-β PET and predict clinical progression: A study of fully automated immunoassays in Bio FINDER and ADNI cohorts. Alzheimer’sDement. 2018 Nov;14(11):1470-1481.29499171
10. Willemse EAJ, van Maurik IS, Tijms BM, et al. Diagnostic performance of Elecsys immunoassays for cerebrospinal fluid Alzheimer's disease biomarkers in a nonacademic, multicenter memory clinic cohort: The ABIDE project. Alzheimer’s Dement (Amst). 2018 Sep 12;10:563-572.30406175
11. Bittner T, Zetterberg H, Teunissen CE, et al. Technical performance of a novel, fully automated electrochemiluminescence immunoassay for the quantitation of β-amyloid (1-42) in human cerebrospinal fluid. Alzheimer’s Dement. 2016 May;12(5):517-526.26555316
12. Vandenberghe R, Adamczuk K, Dupont P, Van Laere K, Chételat G. Amyloid PET in clinical practice: Its place in the multidimensional space of Alzheimer's disease. Neuroimage Clin. 2013 Apr 6:2:497-511.24179802
13. Blennow K, Zetterberg H, Fagan AM. Fluid Biomarkers in Alzheimer Disease. Cold Spring Harb Perspect Med. 2012 Sep 1;2(9):a006221.22951438
14. Bates KA, Verdile G, Li Q-X, et al. Clearance mechanisms of Alzheimer's amyloid-β peptide: implications for therapeutic design and diagnostic tests. Mol Psychiatry. 2009 May;14(5):469-486.18794889
15. Lewczuk P, Mroczko B, Fagan A, Kornhuber J. Biomarkers of Alzheimer's disease and mild cognitive impairment: a current perspective. Adv Med Sci. 2015 Mar;60(1):76-82.25579841
16. Blennow K, Hampel H, Weiner M, Zetterberg H. Cerebrospinal fluid and plasma biomarkers in Alzheimer disease. Nat Rev Neurol. 2010 Mar;6(3):131-144.20157306
17. Mattsson N, Zetterberg H, Hansson O, et al. CSF biomarkers and incipient Alzheimer disease in patients with mild cognitive impairment. JAMA. 2009 Jul 22;302(4):385-393.19622817
18. Hampel H, Blennow K. CSF tau and β-amyloid as biomarkers for mild cognitive impairment. Dialogues Clin Neurosci. 2004 Dec;6(4):379-390.22034251
19. Snider BJ, Fagan AM, Roe C, et al. Cerebrospinal fluid biomarkers and rate of cognitive decline in very mild dementia of the Alzheimer type. Arch Neurol. 2009 May;66(5):638-645.19433664
20. Li J-Q, Tan L, Wang H-F, et al. Risk factors for predicting progression from mild cognitive impairment to Alzheimer’s disease: a systematic review and meta-analysis of cohort studies. J Neurol Neurosurg Psychiatry. 2016 May;87(5):476-484.26001840
21. Blom ES, Giedraitis V, Zetterberg H, et al. Rapid progression from mild cognitive impairment to Alzheimer's disease in subjects with elevated levels of tau in cerebrospinal fluid and the APOE epsilon4/epsilon4 genotype. DementGeriatr Cogn Disord. 2009;27(5):458-464.19420940
22. Wang Y, Mandelkow E. Tau in physiology and pathology. Nat Rev Neurosci. 2016 Jan;17(1):5-21.26631930
23. Iqbal K, Liu F, Gong C-X. Tau and neurodegenerative disease: the story so far. Nat Rev Neurol. 2016 Jan;12(1):15-27.26635213
24. Snider BJ, Fagan AM, Roe C, et al. Cerebrospinal fluid biomarkers and rate of cognitive decline in very mild dementia of the Alzheimer’s type. Arch Neurol. 2009 May;66(5):638-645.19433664
25. Andreasen N, Vanmechelen E, Vanderstichele H, Davidson P, Blennow K. Cerebrospinal fluid levels of total-tau, phospho-tau and A beta 42 predicts development of Alzheimer's disease inpatients with mild cognitive impairment. Acta Neurol ScandSuppl. 2003;179:47-51.12603251
1. Elecsys β-Amyloid (1-42) CSF II [instructions for use]. Roche Diagnostics, 2022-12, V 1.0 English.
2. Elecsys Total-Tau (tTau) CSF [instructions for use]. Roche Diagnostics, 2023-08, V 1.0 English.
3. Elecsys Phospho-Tau (181P) CSF [instructions for use]. Roche Diagnostics, 2022-12, V 1.0 English.
4. Jack CR Jr, Albert MS, Knopman DS, et al. Introduction to the recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011 May;7(3):257-262.21514247
5. Albert MS, DeKosky ST, Dickson D, et al. The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011 May;7(3):270-279.21514249
6. Dubois B, Feldman HH, Jacova C, et al. Advancing research diagnostic criteria for Alzheimer's disease: the IWG-2 criteria. Lancet Neurol. 2014 Jun;13(6):614-629.24849862
7. European Medicines Agency (ESA). Qualification opinion of Alzheimer’s disease novel methodologies/biomarkers for the use of CSF AB 1-42 and t-tau signature and/or PET-amyloid imaging (positive/negative) as a biomarkers for enrichment, for use in regulatory clinical trials in mild and moderate of Alzheimer's disease. ESA website: https://www.ema.europa.eu/en/documents/regulatory-procedural-guideline/qualification-opinion-alzheimers-disease-novel-methodologies-biomarkers-use-cerebrospinal-fluid-amyloid-beta-1-42-and-t-tau-and-or-positron-emission-tomography-amyloid-imaging-positive-negative_en.pdf. Accessed May 2024.
8. European Medicines Agency (ESA). Draft guideline on the clinical investigation of medicines for the treatment of Alzheimer’s disease and other dementias. ESA website: https://www.ema.europa.eu/en/documents/scientific-guideline/draft-guideline-clinical-investigation-medicines-treatment-alzheimers-disease-and-other-dementias_en.pdf. Accessed May 2024.
9. Hansson O, Seibyl J, Stomrud E, et al. CSF biomarkers of Alzheimer's disease concord with amyloid-β PET and predict clinical progression: A study of fully automated immunoassays in Bio FINDER and ADNI cohorts. Alzheimer’sDement. 2018 Nov;14(11):1470-1481.29499171
10. Willemse EAJ, van Maurik IS, Tijms BM, et al. Diagnostic performance of Elecsys immunoassays for cerebrospinal fluid Alzheimer's disease biomarkers in a nonacademic, multicenter memory clinic cohort: The ABIDE project. Alzheimer’s Dement (Amst). 2018 Sep 12;10:563-572.30406175
11. Bittner T, Zetterberg H, Teunissen CE, et al. Technical performance of a novel, fully automated electrochemiluminescence immunoassay for the quantitation of β-amyloid (1-42) in human cerebrospinal fluid. Alzheimer’s Dement. 2016 May;12(5):517-526.26555316
12. Vandenberghe R, Adamczuk K, Dupont P, Van Laere K, Chételat G. Amyloid PET in clinical practice: Its place in the multidimensional space of Alzheimer's disease. Neuroimage Clin. 2013 Apr 6:2:497-511.24179802
13. Blennow K, Zetterberg H, Fagan AM. Fluid Biomarkers in Alzheimer Disease. Cold Spring Harb Perspect Med. 2012 Sep 1;2(9):a006221.22951438
14. Bates KA, Verdile G, Li Q-X, et al. Clearance mechanisms of Alzheimer's amyloid-β peptide: implications for therapeutic design and diagnostic tests. Mol Psychiatry. 2009 May;14(5):469-486.18794889
15. Lewczuk P, Mroczko B, Fagan A, Kornhuber J. Biomarkers of Alzheimer's disease and mild cognitive impairment: a current perspective. Adv Med Sci. 2015 Mar;60(1):76-82.25579841
16. Blennow K, Hampel H, Weiner M, Zetterberg H. Cerebrospinal fluid and plasma biomarkers in Alzheimer disease. Nat Rev Neurol. 2010 Mar;6(3):131-144.20157306
17. Mattsson N, Zetterberg H, Hansson O, et al. CSF biomarkers and incipient Alzheimer disease in patients with mild cognitive impairment. JAMA. 2009 Jul 22;302(4):385-393.19622817
18. Hampel H, Blennow K. CSF tau and β-amyloid as biomarkers for mild cognitive impairment. Dialogues Clin Neurosci. 2004 Dec;6(4):379-390.22034251
19. Snider BJ, Fagan AM, Roe C, et al. Cerebrospinal fluid biomarkers and rate of cognitive decline in very mild dementia of the Alzheimer type. Arch Neurol. 2009 May;66(5):638-645.19433664
20. Li J-Q, Tan L, Wang H-F, et al. Risk factors for predicting progression from mild cognitive impairment to Alzheimer’s disease: a systematic review and meta-analysis of cohort studies. J Neurol Neurosurg Psychiatry. 2016 May;87(5):476-484.26001840
21. Blom ES, Giedraitis V, Zetterberg H, et al. Rapid progression from mild cognitive impairment to Alzheimer's disease in subjects with elevated levels of tau in cerebrospinal fluid and the APOE epsilon4/epsilon4 genotype. DementGeriatr Cogn Disord. 2009;27(5):458-464.19420940
22. Wang Y, Mandelkow E. Tau in physiology and pathology. Nat Rev Neurosci. 2016 Jan;17(1):5-21.26631930
23. Iqbal K, Liu F, Gong C-X. Tau and neurodegenerative disease: the story so far. Nat Rev Neurol. 2016 Jan;12(1):15-27.26635213
24. Snider BJ, Fagan AM, Roe C, et al. Cerebrospinal fluid biomarkers and rate of cognitive decline in very mild dementia of the Alzheimer’s type. Arch Neurol. 2009 May;66(5):638-645.19433664
25. Andreasen N, Vanmechelen E, Vanderstichele H, Davidson P, Blennow K. Cerebrospinal fluid levels of total-tau, phospho-tau and A beta 42 predicts development of Alzheimer's disease inpatients with mild cognitive impairment. Acta Neurol ScandSuppl. 2003;179:47-51.12603251

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