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Cerebrospinal fluid analysis detects cerebral amyloid-β accumulation earlier than positron emission tomography
Open accessAbstract
See Rabinovici (doi: 10.1093/brain/aww025 ) for a scientific commentary on this article. Cerebral accumulation of amyloid-β is thought to be the starting mechanism in Alzheimer’s disease. Amyloid-β can be detected by analysis of cerebrospinal fluid amyloid-β 42 or amyloid positron emission tomography, but it is unknown if any of the methods can identify an abnormal amyloid accumulation prior to the other. Our aim was to determine whether cerebrospinal fluid amyloid-β 42 change before amyloid PET during preclinical stages of Alzheimer’s disease. We included 437 non-demented subjects from the prospective, longitudinal Alzheimer’s Disease Neuroimaging Initiative (ADNI) study. All underwent 18 F-florbetapir positron emission tomography and cerebrospinal fluid amyloid-β 42 analysis at baseline and at least one additional positron emission tomography after a mean follow-up of 2.1 years (range 1.1–4.4 years). Group classifications were based on normal and abnormal cerebrospinal fluid and positron emission tomography results at baseline. We found that cases with isolated abnormal cerebrospinal fluid amyloid-β and normal positron emission tomography at baseline accumulated amyloid with a mean rate of 1.2%/year, which was similar to the rate in cases with both abnormal cerebrospinal fluid and positron emission tomography (1.2%/year, P = 0.86). The mean accumulation rate of those with isolated abnormal cerebrospinal fluid was more than three times that of those with both normal cerebrospinal fluid and positron emission tomography (0.35%/year, P = 0.018). The group differences were similar when analysing yearly change in standardized uptake value ratio of florbetapir instead of percentage change. Those with both abnormal cerebrospinal fluid and positron emission tomography deteriorated more in memory and hippocampal volume compared with the other groups ( P < 0.001), indicating that they were closer to Alzheimer’s disease dementia. The results were replicated after adjustments of different factors and when using different cut-offs for amyloid-β abnormality including a positron emission tomography classification based on the florbetapir uptake in regions where the initial amyloid-β accumulation occurs in Alzheimer’s disease. This is the first study to show that individuals who have abnormal cerebrospinal amyloid-β 42 but normal amyloid-β positron emission tomography have an increased cortical amyloid-β accumulation rate similar to those with both abnormal cerebrospinal fluid and positron emission tomography and higher rate than subjects where both modalities are normal. The results indicate that cerebrospinal fluid amyloid-β 42 becomes abnormal in the earliest stages of Alzheimer’s disease, before amyloid positron emission tomography and before neurodegeneration starts. See Rabinovici (doi: 10.1093/brain/aww025 ) for a scientific commentary on this article. The success of disease-modifying therapies in Alzheimer’s disease may depend on detecting the earliest signs of abnormal amyloid-β load. Palmqvist et al . show that CSF amyloid-β 42 becomes abnormal before amyloid PET and before neurodegeneration onset in preclinical Alzheimer’s disease. This may have implications for risk factor interventions and future therapies.
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“This may be due to a temporal offset between these two measures [121–123].”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [122]
In the citing paper
“This indicates that individuals with AD may first be defined as being CSF+/PET−, and then progress to CSF+/PET+.”
From Earliest accumulation of β-amyloid occurs within the default-mode network and concurrently affects brain connectivity (2017) · cites this paper as [12]
In the citing paper
“those with abnormally low CSF levels of Aβ42, but with still normal Aβ levels detected by PET (CSF+/PET−), accumulated Aβ fibrils longitudinally at a similar rate as those who had both abnormal CSF levels of Aβ42 and abnormal levels of Aβ detected by PET (CSF+/PET+) and four times higher than those with normal biomarker results on both parameters (CSF−/PET−)12.”
From Earliest accumulation of β-amyloid occurs within the default-mode network and concurrently affects brain connectivity (2017) · cites this paper as [12]
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“In a recent study, we also showed that CSF+/PET− subjects accumulated Aβ at a similar rate as CSF+/PET+ subjects and about four times higher than CSF−/PET− subjects12.”
From Earliest accumulation of β-amyloid occurs within the default-mode network and concurrently affects brain connectivity (2017) · cites this paper as [12]
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“Mixture modeling statistics provide an unbiased threshold for abnormality (i.e., the diagnosis or status is not used in analysis) and it is a well-established method for defining Aβ PET cut-offs12, 17, 60, 61.”
From Earliest accumulation of β-amyloid occurs within the default-mode network and concurrently affects brain connectivity (2017) · cites this paper as [12]
In the citing paper
“reduced concentrations of Aβ42 in CSF and increased retention of Aβ tracers in the brain have been considered as early biomarkers of AD.255–258”
From Amyloid β-based therapy for Alzheimer’s disease: Challenges, successes and future (2023) · cites this paper as [258]
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Self-citation
Metadata
- Authors
- Palmqvist, S., Mattsson, N., Hansson, O., & Initiative, F. T. A. D. N.
- Affiliations
- Lund University (SE)
- Corresponding author
- Palmqvist, Sebastian
- Hansson, Oskar
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2016-03-02
- Volume
- 139
- Issue
- 4
- Pages
- 1226-1236
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- PMC
- PMC4806222
- OpenAlex
- W2302528231
- Cited by
- 400
- References
- 59
- Citations by year
- 2026: 32 · 2025: 41 · 2024: 33 · 2023: 31 · 2022: 36 · 2021: 58 · 2020: 50 · 2019: 43 · 2018: 38 · 2017: 25 · 2016: 11
- FWCI
- 34.64
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- Brain (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- HighWire Press Open Archive (submittedVersion)
- Funders
- Lunds Universitet
- National Institutes of Health (5u01ag024904-10)
- Canadian Institutes of Health Research
- National Institute on Aging (U01-AG-024904)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Clinical Neurology › Cerebrospinal fluid and hydrocephalus
- Keywords
- cerebrospinal fluid amyloid-beta 42, amyloid PET, florbetapir, preclinical Alzheimer's disease, standardized uptake value ratio, memory decline, hippocampal volume, Alzheimer's dementia, biomarker comparison, ADNI cohort, longitudinal follow-up
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Cerebral Cortex, Cross-Sectional Studies, Female, Humans, Male, Middle Aged, Peptide Fragments, Prospective Studies, Amyloid beta-Peptides, Early Diagnosis, Positron-Emission Tomography
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