Cerebrospinal Fluid Levels ofβ-Amyloid 1-42, but Not of Tau, Are Fully Changed Already 5 to 10 Years Before the Onset of Alzheimer Dementia
Abstract
CONTEXT: Early detection of prodromal Alzheimer disease (AD) is important because new disease-modifying therapies are most likely to be effective when initiated during the early stages of disease. OBJECTIVES: To assess the ability of the cerebrospinal fluid (CSF) biomarkers total tau (T-tau), phosphorylated tau (P-tau), and β-amyloid 1-42 (Aβ42) to predict future development of AD dementia within 9.2 years in patients with mild cognitive impairment (MCI) and to compare CSF biomarkers between early and late converters to AD. DESIGN: A clinical study with a median follow-up of 9.2 years (range, 4.1-11.8 years). SETTING: Memory disorder clinic. Patients A total of 137 patients with MCI who underwent lumbar puncture at baseline. MAIN OUTCOME MEASURE Conversion to AD dementia. RESULTS: During follow-up, 72 patients (53.7%) developed AD and 21 (15.7%) progressed to other forms of dementia. At baseline, CSF Aβ42 levels were reduced and T-tau and P-tau levels were elevated in patients who converted to AD during follow-up compared with nonconverters (P < .001). Baseline CSF Aβ42 levels were equally reduced in patients with MCI who converted to AD within 0 to 5 years (early converters) compared with those who converted between 5 and 10 years (late converters). However, CSF T-tau and P-tau levels were significantly higher in early converters vs late converters. A baseline Aβ42:P-tau ratio predicted the development of AD within 9.2 years with a sensitivity of 88%, specificity of 90%, positive predictive value of 91%, and negative predictive value of 86%. CONCLUSIONS: Approximately 90% of patients with MCI and pathologic CSF biomarker levels at baseline develop AD within 9 to 10 years. Levels of Aβ42 are already fully decreased at least 5 to 10 years before conversion to AD dementia, whereas T-tau and P-tau seem to be later markers. These results provide direct support in humans for the hypothesis that altered Aβ metabolism precedes tau-related pathology and neuronal degeneration.
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AD remains challenging to diagnose early due to the late onset of clinical symptoms such as memory loss and cognitive decline.
“Despite the increasing incidence of AD worldwide, AD remains challenging to diagnose early due to the late onset of clinical symptoms, such as memory loss and cognitive decline.”
From Extracellular vesicles as nanotheranostic platforms for targeted neurological disorder interventions (2024) · cites this paper as [67]
The risk of short-term cognitive decline may also increase continuously with worsening T biomarkers.
“the risk of short-term cognitive decline increases continuously with worsening (N) biomarkers, and this may be true of T biomarkers as well [108,109].”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [108]
The risk of short-term cognitive decline increases continuously with worsening (N) biomarkers.
“the risk of short-term cognitive decline increases continuously with worsening (N) biomarkers, and this may be true of T biomarkers as well [108,109].”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [108]
CSF T-tau likely indicates the intensity of neuronal injury at a given point in time.
“CSF T-tau likely indicates the intensity of neuronal injury at a given point in time [108,114,157,158].”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [108]
Patients with prodromal Alzheimer's disease and elevated cerebrospinal fluid total tau tend to convert to Alzheimer's disease dementia sooner.
“The patients with prodromal AD and increased CSF t-tau levels tended to convert sooner to AD dementia [19, 20].”
From Duration of preclinical, prodromal, and dementia stages of Alzheimer's disease in relation to age, sex, and <i>APOE</i> genotype (2019) · cites this paper as [20]
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Retracted
- Authors
- Buchhave, P.
- Affiliations
- Skåne University Hospital (SE)
- Corresponding author
- Buchhave, Peder
- Venue
- Archives of General Psychiatry
- Publisher
- American Medical Association (AMA)
- Published
- 2012-01-01
- Volume
- 69
- Issue
- 1
- Pages
- 98
- ISSN
- 0003-990X (ISSN-L)
- OpenAlex
- W2060446879
- Cited by
- 664
- References
- 6
- Citations by year
- 2026: 23 · 2025: 41 · 2024: 35 · 2023: 37 · 2022: 35 · 2021: 38 · 2020: 47 · 2019: 35 · 2018: 44 · 2017: 37 · 2016: 48 · 2015: 60 · 2014: 77 · 2013: 66 · 2012: 40
- FWCI
- 55.32
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Archives of General Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Cerebrospinal fluid and hydrocephalus
- Keywords
- Alzheimer's disease, prodromal Alzheimer's disease, mild cognitive impairment, cerebrospinal fluid biomarkers, amyloid-beta 42, phosphorylated tau, total tau, amyloid metabolism, tau pathology, early detection
- MeSH terms
- Aged, Alzheimer Disease, Female, Follow-Up Studies, Humans, Male, Peptide Fragments, Predictive Value of Tests, Time Factors, Biomarkers, Amyloid beta-Peptides, tau Proteins, Cognitive Dysfunction
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