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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Volumetric decline occurs initially in medial temporal lobe grey matter, following tau protein deposition, and is closely correlated to cognitive decline.
“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
In “Use of biomarkers to stage AD,” the paper says cerebral atrophy begins in medial temporal limbic areas. “Biomarkers of neurodegeneration” reports a strong correlation between atrophy and cognitive decline. The temporal-ordering section places abnormal CSF tau before MRI atrophy, but does not establish that tau protein deposition itself precedes the volumetric decline. (LLM, conf=0.85)
Experimental — accuracy not yet measuredOn 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.
“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
In “Biomarker abnormalities precede clinical symptoms” (page unavailable), the paper says neurofibrillary tangles in asymptomatic individuals tend to be confined to the entorhinal cortex, whereas they are more widespread in symptomatic individuals. “Biomarkers of neurodegeneration” (page unavailable) says the distribution of MRI atrophy maps onto Braak staging. These passages support an early entorhinal abnormality and later wider involvement, but do not establish the claimed sequence through the mid-temporal and fusiform gyri and finally the frontal lobe. (LLM, conf=0.83)
Experimental — accuracy not yet measuredMeasures of all biomarkers studied to date have considerable overlap with those found in other types of dementia and cognitively normal elderly, making it difficult to determine whether cognitive impairment is due to AD or another process.
“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]
The section ‘Biomarker abnormalities precede clinical symptoms’ (page not provided) reports amyloid-biomarker abnormalities in 20–40% of cognitively normal elderly people, and ‘AD clinical features and pathological changes’ notes that dementia in older patients often has multiple underlying pathologies. The ‘Biomarkers of neurodegeneration’ section also says CSF tau is not specific to AD. These passages support diagnostic ambiguity, but not the broader assertion that all biomarkers studied have considerable overlap with both other dementias and cognitively normal elderly people. (LLM, conf=0.84)
Experimental — accuracy not yet measuredCognitive decline is more closely correlated to neurodegeneration than tau accumulation.
“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
Alzheimer's disease is characterized by deposition of hallmark pathological peptides and neurodegeneration that progress across partially overlapping neuroanatomical and temporal axes.
“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]
Autosomal dominant mutations in MAPT lead to neuronal tangle pathology and frontotemporal dementia but not amyloid plaques, suggesting that tau pathology does not induce Aβ pathology.
“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]
Amyloid plaques appear a decade or two before clinical symptoms of Alzheimer's disease, but tau pathology and synapse loss correlate best with cognitive impairment during disease progression.
“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
Amyloid accumulation probably begins many years before the onset of symptoms.
“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]
Amyloid-β aggregation is the earliest pathological event in Alzheimer's disease, followed at a later stage by tau aggregation extending beyond the limbic system to the neocortex, which correlates with brain atrophy and cognitive decline.
“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 individuals who develop AD, Aβ plaque deposition and reduced CSF Aβ occur first, followed by CSF tau rise, years before clinical signs; later hippocampal atrophy, memory decline, and dementia occur; full progression takes approximately 10 to 20 years.
“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]
Plaque formation rates vary over time; after rapid accumulation, plaque deposition gradually slows and by symptom manifestation is essentially done.
“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]
Symptoms generally manifest only after plaques stop forming.
“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]
People meeting preclinical AD criteria may remain cognitively stable for many years.
“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]
The new AD biological framework and the model of pathologic AD biomarkers from Jack and colleagues 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.
“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]
Studies of non-demented elderly cohorts overall report approximately 20-40% are PIB-positive.
“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]
Neuropathological changes (amyloid plaques and tau tangles) are considered to develop years before onset of the cognitive changes that characterize AD dementia.
“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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Self-citationFDG PET imaging in patients with pathologically verified dementia.
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Self-citationβ‐amyloid burden is not associated with rates of brain atrophy
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Self-citationCSF biomarkers in frontotemporal lobar degeneration with known pathology
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The clinical use of structural MRI in Alzheimer disease
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“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).”
BackgroundTwo Phase 3 Trials of Bapineuzumab in Mild-to-Moderate Alzheimer's Disease
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Disease-Associated Microglia: A Universal Immune Sensor of Neurodegeneration
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“The emergence of new biomarkers may have a major impact on clinical diagnostic practice (1); however, because measures of all biomarkers studied to date have considerable overlap with those found in other types of dementia (as well the cognitively normal elderly population), it remains difficult to determine whether c…”
BackgroundAssociation of plasma neurofilament light with neurodegeneration in patients with Alzheimer disease
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- 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
- 107
- 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
- Health Sciences › Medicine › Physiology › 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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