National Institute on Aging–Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease
Open accessAbstract
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 irreversible progressive decline of cognition.
“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
The “Revised Neuropathologic criteria for Alzheimer’s disease” section describes a preclinical phase and says AD processes can be present well before cognitive deficits. It does not establish that this stage is long or that subsequent cognitive decline is irreversible and progressive. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThe 2012 NIA-AA Guidelines use an ABC scoring system requiring amyloid plaques and tau neurofibrillary tangles to describe AD neuropathological change from none to low to intermediate to high.
“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]
The Classification and Reporting sections establish the ABC system and its four levels of AD neuropathologic change. But physical presence of both amyloid plaques and neurofibrillary tangles is not required to assign a score: Classification defines zero scores for absent lesions, and Reporting gives A1, B0, C0 as an example. The system also scores neuritic plaques as its C component. (LLM, conf=0.88)
Experimental — accuracy not yet measuredBoth Aβ and paired helical filament (PHF) tau deposits are required to fulfill neuropathologic criteria for AD.
“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]
The AD Neuropathologic Change section says neurofibrillary tangles and senile plaques are essential for neuropathologic diagnosis; it describes tangles as primarily abnormal tau and plaques as Aβ deposits. It does not specify that the required tau deposits must be paired helical filaments (PHF), so that added specificity is unsupported by our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThe new NIA criteria use the same combination of moderate or frequent neuritic plaques and Braak stage III-VI as the minimum lesion density necessary for attributing the cause of dementia to AD.
“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]
The Classification section defines moderate or frequent neuritic plaques and Braak stages III–VI as scores used by the new criteria. But it requires a third measure, Aβ plaque score, to classify AD neuropathologic change; the Reporting section says an intermediate or high overall level, rather than the stated two-measure combination alone, is an adequate explanation of dementia. Our copy provides no page numbers for these passages. (LLM, conf=0.87)
Experimental — accuracy not yet measuredThe A3B3C3 classification can be interpreted as high, similar to other PSEN1E280A cases.
“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 integration of pathological assessments following NIAA guidelines gives a classification of AD neuropathological changes of A3B3C3.
“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 Braak staging scheme is widely used in neuropathologic criteria for Alzheimer's disease.
“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]
The 2012 NIA-AA Guidelines are based on semi-quantitative measures of Thal Aβ amyloid phase, Braak NFT stage and CERAD neuritic plaque score, and are applicable to patients with or without dementia.
“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]
Higher levels of AD neuropathologic change are typically correlated with greater likelihood of cognitive impairment.
“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]
The shortcomings of the NIA-Reagan criteria have been recognized and a revised set of criteria are currently in press.
“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]
Case #1 autopsy showed high degree AD neuropathology per NIA-AA criteria.
“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]
Case #3 autopsy revealed high level AD neuropathology per NIA-AA criteria.
“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]
Glycolysis pathway genes were maximally expressed at different points in global AD progression for each region (pathology diagnosis by ABC score).
“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]
Neuropathological examination included Braak and Braak staging for plaques and tangles and diagnosis of neuropathological Alzheimer's disease using National Institute on Aging-Reagan criteria.
“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]
Human protein modules M2, M4, and M35 were positively associated with Braak and CERAD neuropathological grades in human AD.
“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]
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.
“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]
Neuropathological criteria for the diagnosis of Alzheimer disease were established by the National Institute on Aging-Alzheimer Association and were updated in 2012.
“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 [ <sup>18</sup> F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [5]
Neuropathological assessment used National Institute on Aging-Alzheimer Association diagnostic scoring guidelines.
“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 [ <sup>18</sup> F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [5]
Isolated tau in mesial temporal regions can represent B1-level NFTs, which are associated with not or low levels of ADNC.
“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 [ <sup>18</sup> F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [5]
Analyses from the National Alzheimer Coordinating Center pathological database 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.
“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 [ <sup>18</sup> F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [5]
Results of this study support the hypothesis that, with high sensitivity and moderate to high specificity, flortaucipir PET 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.
“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 [ <sup>18</sup> F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [5]
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Self-citation
- 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
- Health Sciences › Medicine › Physiology › 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.)
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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