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National Institute on Aging–Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease
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A consensus panel from the United States and Europe was convened recently to update and revise the 1997 consensus guidelines for the neuropathologic evaluation of Alzheimer's disease (AD) and other diseases of brain that are common in the elderly. The new guidelines recognize the pre‐clinical stage of AD, enhance the assessment of AD to include amyloid accumulation as well as neurofibrillary change and neuritic plaques, establish protocols for the neuropathologic assessment of Lewy body disease, vascular brain injury, hippocampal sclerosis, and TDP‐43 inclusions, and recommend standard approaches for the workup of cases and their clinico‐pathologic correlation.
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“Clinically, there is a long, prodromal stage in AD prior to the irreversibly progressive decline of cognition (Hyman et al., 2012).”
From Deep Multilayer Brain Proteomics Identifies Molecular Networks in Alzheimer’s Disease Progression (2020) · cites this paper as Hyman et al., 2012
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
“The current criteria use an ABC scoring system that requires the presence of amyloid plaques and tau neurofibrillary tangles to describe the amount of AD neuropathological change ranging from none to low to intermediate to high amounts of change.”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [69]
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
“However, both Aβ and paired helical filament (PHF) tau deposits are required to fulfill neuropathologic criteria for AD [105,106]”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [106]
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
“The new NIA criteria use the same combination of NPs and Braak stage as the minimum lesion density necessary for attributing the cause of dementia to AD (39, 40).”
From Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer Disease Centers, 2005–2010 (2012) · cites this paper as [39]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Furthermore, the integration of these pathological assessments following the NIAA guidelines gives a classification of AD neuropathological changes of A3B3C3 [16], that can be interpreted as high, similar to other PSEN1E280A cases.”
From Distinct tau neuropathology and cellular profiles of an APOE3 Christchurch homozygote protected against autosomal dominant Alzheimer’s dementia (2022) · cites this paper as [16]
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“Furthermore, the integration of these pathological assessments following the NIAA guidelines gives a classification of AD neuropathological changes of A3B3C3 [16], that can be interpreted as high, similar to other PSEN1E280A cases.”
From Distinct tau neuropathology and cellular profiles of an APOE3 Christchurch homozygote protected against autosomal dominant Alzheimer’s dementia (2022) · cites this paper as [16]
The cited source says what the claim attributes to it.
In the citing paper
“The staging scheme is widely used in neuropathologic criteria for AD [69, 70].”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [69]
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“The most current set of criteria for the neuropathological assessment of Alzheimer’s disease termed the 2012 National Institute on Aging-Alzheimer’s Association Guidelines are based on the semi-quantitative measure of Thal Aβ amyloid phase, Braak NFT stage and CERAD neuritic plaque score, and they are applicable to patients with or without dementia [69].”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [69]
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“For cases with incomplete clinical history, higher levels of AD neuropathologic change typically are correlated with greater likelihood of cognitive impairment [29].”
From National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach (2012) · cites this paper as [29]
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“The shortcomings of the NIA-Reagan criteria have been recognized and a revised set of criteria are currently in press (39, 40).”
From Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer Disease Centers, 2005–2010 (2012) · cites this paper as [39]
The cited source says what the claim attributes to it.
In the citing paper
“these findings were consistent with a high degree of AD neuropathology per the National Institute on Aging-Alzheimer’s Association (NIA-AA) criteria [3–7].”
From Diagnosing the frontal variant of Alzheimer’s disease: a clinician’s yellow brick road (2017) · cites this paper as [4]
The cited source says what the claim attributes to it.
In the citing paper
“By NIA-AA criteria, the findings met criteria for “high level” AD neuropathology [3–7].”
From Diagnosing the frontal variant of Alzheimer’s disease: a clinician’s yellow brick road (2017) · cites this paper as [4]
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“Finally, we noticed that the glycolysis pathway genes were maximally expressed at different points in global AD progression for each region (pathology diagnosis by ABC score)29,30.”
From Single-cell multiregion dissection of Alzheimer’s disease (2024) · cites this paper as [30]
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“Neuropathologic diagnosis of AD was in accordance with current NIA-AA guidelines (Hyman et al., 2012; Montine et al., 2012).”
From Cholesterol and matrisome pathways dysregulated in astrocytes and microglia (2022) · cites this paper as Hyman et al., 2012
In the citing paper
“Neuropathological examination included Braak and Braak staging for plaques and tangles and diagnosis of neuropathological AD using National Institute on Aging-Reagan criteria [47].”
From Microglia facilitate loss of perineuronal nets in the Alzheimer's disease brain (2020) · cites this paper as [47]
In the citing paper
“Anti-inflammatory DAM and pro-inflammatory DAM module members overlapped (FDR < 10%) with human protein modules (M2, M4, M35, unadjusted p-values < 0.01) that were also positively associated with Braak and CERAD neuropathological grades in human AD (Fig. 9e) [58].”
From Identification and therapeutic modulation of a pro-inflammatory subset of disease-associated-microglia in Alzheimer’s disease (2018) · cites this paper as [58]
In the citing paper
“Neuropathology criteria for Alzheimer’s disease provide no cutoff for establishing Alzheimer’s disease diagnosis, but only define low, intermediate, or high levels of Alzheimer’s disease neuropathological change.14”
From Clinical diagnosis of Alzheimer’s disease: Recommendations of the International Working Group (2021) · cites this paper as [14]
In the citing paper
“Neuropathological criteria for the diagnosis of AD were established by the National Institute on Aging–Alzheimer Association (NIA–AA)4 and were updated in 2012 to reflect the current thinking on AD pathological assessment.5,6”
From Positron Emission Tomography Imaging With [ 18 F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [5]
In the citing paper
“Neuropathological assessment was performed by 2 authors (T.G.B. and T.J.M.) blinded to clinical and imaging results and using NIA–AA diagnostic scoring guidelines.5,40”
From Positron Emission Tomography Imaging With [ 18 F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [5]
In the citing paper
“Furthermore, although these areas are key in early NFT accumulation in AD, isolated tau in these regions can represent B1-level NFTs, which are associated with not or low levels of ADNC.5”
From Positron Emission Tomography Imaging With [ 18 F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [5]
In the citing paper
“Analyses from the National Alzheimer Coordinating Center pathological database have indicated that individuals with a B2 score had clinically normal result at a rate of 25.3% (34 of 134), and 41 (37.6%) of 109 people with Aβ at autopsy had a B2 score.5”
From Positron Emission Tomography Imaging With [ 18 F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [5]
In the citing paper
“Results of this study support the hypothesis that, with a high sensitivity and moderate to high specificity, PET imaging with [18F]flortaucipir is able to identify the underlying presence of NFTs at the B3 level and a high level of ADNC per the NIA–AA criteria, consistent with a neuropathological diagnosis of AD.5”
From Positron Emission Tomography Imaging With [ 18 F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [5]
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Metadata
- Authors
- Hyman, B. T., Phelps, C. H., Beach, T. G., Bigio, E. H., Cairns, N. J., Carrillo, M. C., Dickson, D. W., Duyckaerts, C., Frosch, M. P., Masliah, E., Mirra, S. S., Nelson, P. T., Schneider, J. A., Thal, D. R., Thies, B., Trojanowski, J. Q., Vinters, H. V., & Montine, T. J.
- Affiliations
- Harvard University (US)
- National Institutes of Health (US)
- Banner Sun Health Research Institute (US)
- Northwestern University (US)
- Washington University in St. Louis (US)
- Alzheimer's Association Chicago IL USA
- Mayo Clinic (US)
- Service de Neuropathologie Raymond Escourolle Hôpital de la Salpêtriére Paris France
- University of California San Diego (US)
- SUNY Downstate Health Sciences University (US)
- University of Kentucky (US)
- Rush University Medical Center (US)
- Universität Ulm (DE)
- Alzheimer's Association (US)
- University of Pennsylvania (US)
- University of California, Los Angeles (US)
- University of Washington (US)
- Corresponding author
- Montine, Thomas J.
- ORCID
- Venue
- Alzheimer's & Dementia
- Publisher
- Wiley
- Published
- 2012-01
- Volume
- 8
- Issue
- 1
- Pages
- 1-13
- ISSN
- 1552-5260 (ISSN-L)
- 1552-5279
- PMC
- PMC3266529
- OpenAlex
- W2143461767
- Cited by
- 3,092
- References
- 114
- Citations by year
- 2026: 214 · 2025: 285 · 2024: 286 · 2023: 233 · 2022: 260 · 2021: 327 · 2020: 247 · 2019: 228 · 2018: 206 · 2017: 190 · 2016: 170 · 2015: 161 · 2014: 118 · 2013: 115 · 2012: 46
- FWCI
- 98.94
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Alzheimer s & Dementia (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Alzheimer's Association
- Arizona Department of Health Services (211002)
- Arizona Alzheimer’s Consortium
- Deutsche Forschungsgemeinschaft (DFG TH‐624‐4‐1)
- Alzheimer Forschung Initiative (AFI #10810)
- Nancy and Buster Alvord Endowment
- 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
- MeSH terms
- Alzheimer Disease, Brain, Humans, Societies, Medical, United States, Consensus Development Conferences, NIH as Topic, Practice Guidelines as Topic, National Institute on Aging (U.S.)
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