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Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade
Open accessAbstract
Currently available evidence strongly supports the position that the initiating event in Alzheimer's disease (AD) is related to abnormal processing of beta-amyloid (Abeta) peptide, ultimately leading to formation of Abeta plaques in the brain. This process occurs while individuals are still cognitively normal. Biomarkers of brain beta-amyloidosis are reductions in CSF Abeta(42) and increased amyloid PET tracer retention. After a lag period, which varies from patient to patient, neuronal dysfunction and neurodegeneration become the dominant pathological processes. Biomarkers of neuronal injury and neurodegeneration are increased CSF tau and structural MRI measures of cerebral atrophy. Neurodegeneration is accompanied by synaptic dysfunction, which is indicated by decreased fluorodeoxyglucose uptake on PET. We propose a model that relates disease stage to AD biomarkers in which Abeta biomarkers become abnormal first, before neurodegenerative biomarkers and cognitive symptoms, and neurodegenerative biomarkers become abnormal later, and correlate with clinical symptom severity.
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“Studies of non-demented elderly cohorts overall report approximately 20–40% are PIB-positive [67, 68, 71–78].”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [76]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“These investigations have established that volumetric decline occurs initially in medial temporal lobe grey matter, following tau protein deposition, and is closely correlated to cognitive decline.”
From White matter microstructural abnormality precedes cortical volumetric decline in Alzheimer’s disease: evidence from data-driven disease progression modelling (2022) · cites this paper as Jack Jr. et al 2010
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“On the regional level, abnormality is evident in medial temporal lobe areas first (hippocampus and entorhinal cortex), then in lateral temporal lobe areas (mid-temporal gyrus and fusiform gyrus) and finally in frontal lobe areas (Jack Jr. et al 2010, Young et al 2014).”
From White matter microstructural abnormality precedes cortical volumetric decline in Alzheimer’s disease: evidence from data-driven disease progression modelling (2022) · cites this paper as Jack Jr. et al 2010
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“because measures of all biomarkers studied to date have considerable overlap with those found other types of dementia (as well the cognitively normal elderly population), it remains difficult to determine whether or not cognitive impairment is due to AD or another more dominant and concurrent process.”
From Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer Disease Centers, 2005–2010 (2012) · cites this paper as [1]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“it is Tau pathology and synapse loss that temporally correlate with cognitive impairment and precede overt neurodegeneration (Jack et al., 2010; Scheff et al., 2006; Spires-Jones and Hyman, 2014”
From Changes in the Synaptic Proteome in Tauopathy and Rescue of Tau-Induced Synapse Loss by C1q Antibodies (2018) · cites this paper as Jack et al., 2010
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“Amyloid accumulation probably starts many years before the onset of symptoms,2,26,27 and initiation of anti-amyloid treatment only after dementia develops may be too late to affect the clinical course of the disease.28”
From Two Phase 3 Trials of Bapineuzumab in Mild-to-Moderate Alzheimer's Disease (2014) · cites this paper as [26]
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“Firstly, cognitive decline is more closely correlated to neurodegeneration than tau accumulation (Jack Jr. et al 2010).”
From White matter microstructural abnormality precedes cortical volumetric decline in Alzheimer’s disease: evidence from data-driven disease progression modelling (2022) · cites this paper as Jack Jr. et al 2010
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“Alzheimer’s disease (AD) is characterized by deposition of hallmark pathological peptides and neurodegeneration that progress across partially overlapping neuroanatomical and temporal axes1,2.”
From Integrated multimodal cell atlas of Alzheimer’s disease (2024) · cites this paper as [2]
In the citing paper
“Autosomal dominant mutations to the MAPT (tau) gene lead to neuronal tangle pathology and frontotemporal dementia but not to amyloid plaques 122,123 , suggesting that tau pathology does not induce Aβ pathology.”
From The amyloid hypothesis in Alzheimer disease: new insights from new therapeutics (2022) · cites this paper as [123]
In the citing paper
“Amyloid plaques appear a decade or two before clinical symptoms of AD, but it is tau pathology and synapse loss that correlate best with cognitive impairment during disease progression (Jack et al., 2010).”
From Microglia in Alzheimer’s disease (2018) · cites this paper as Jack et al., 2010
In the citing paper
“Extensive biomarker and imaging studies indicate that amyloid-β aggregation is the earliest pathological event in Alzheimer’s disease, followed at a later stage by pathological changes of tau aggregation extending beyond the limbic system to the neocortex, which correlates with brain atrophy and cognitive decline2,3.”
From Interplay between innate immunity and Alzheimer disease: APOE and TREM2 in the spotlight (2018) · cites this paper as [2]
In the citing paper
“Their timeline states that in individuals who develop AD, Aβ plaque deposition and reduced CSF Aβ occur first. Next, CSF tau levels rise. These changes manifest years before clinical signs or symptoms develop. Later on hippocampal atrophy appears, followed shortly thereafter by memory decline and eventually dementia. Full progression from Aβ changes to clinical decline takes approximately 10 to 20”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [205]
In the citing paper
“Plaque formation rates also vary over time [217]. After a period of rapid accumulation, plaque deposition gradually slows and by the time symptoms manifest plaque deposition is essentially done [20, 205, 218].”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [205]
In the citing paper
“data argue symptoms generally manifest only after plaques stop forming (Figure 5) [205, 216, 217].”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [205]
In the citing paper
“As people meeting preclinical AD criteria may remain cognitively stable for many years [205, 214], these trials will take a long time to complete.”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [205]
In the citing paper
“The new AD biological framework and the model of pathologic AD biomarkers from Jack and colleagues 18 conceptualize a progressive sequence of measurable biochemical, neurophysiological, and neuroanatomical alterations that can be detected years before psychometrically and clinically noticeable deterioration in cognition, behavior, and function.”
From The Alzheimer’s Disease Clinical Spectrum (2019) · cites this paper as [18]
In the citing paper
“The neuropathological changes that are quintessential for AD diagnosis—namely, the development of amyloid plaques and tau tangles—are considered to develop years before onset of the cognitive changes that characterize AD dementia [26].”
From Deep proteomic network analysis of Alzheimer’s disease brain reveals alterations in RNA binding proteins and RNA splicing associated with disease (2018) · cites this paper as [26]
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Metadata
- Authors
- Jack, C. R., Knopman, D. S., Jagust, W. J., Shaw, L. M., Aisen, P. S., Weiner, M. W., Petersen, R. C., & Trojanowski, J. Q.
- Affiliations
- Mayo Clinic (US)
- University of California, Berkeley (US)
- University of Pennsylvania (US)
- University of California San Diego (US)
- University of California, San Francisco (US)
- Corresponding author
- Jack, Clifford R
- ORCID
- Venue
- The Lancet Neurology
- Publisher
- Elsevier BV
- Published
- 2010-01
- Volume
- 9
- Issue
- 1
- Pages
- 119-128
- ISSN
- 1474-4422 (ISSN-L)
- PMC
- PMC2819840
- OpenAlex
- W2167840686
- Cited by
- 4,806
- References
- 119
- Citations by year
- 2026: 273 · 2025: 317 · 2024: 278 · 2023: 259 · 2022: 308 · 2021: 321 · 2020: 359 · 2019: 303 · 2018: 267 · 2017: 283 · 2016: 265 · 2015: 273 · 2014: 335 · 2013: 337 · 2012: 301
- FWCI
- 127.41
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Lancet Neurology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (AG11378)
- National Institute on Aging
- 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
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, amyloid-beta, amyloid PET, tau protein, brain atrophy, FDG-PET, synaptic dysfunction, neurodegeneration, disease stage, biomarkers, cognitive decline
- MeSH terms
- Aging, Alzheimer Disease, Brain, Cognition Disorders, Humans, Magnetic Resonance Imaging, Models, Neurological, Time Factors, Signal Transduction, Biomarkers, Amyloid beta-Peptides, tau Proteins, Disease Progression, Positron-Emission Tomography, Apolipoprotein E4, Plaque, Amyloid
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