The DOI matches its Crossref record; 66 of the 66 references it cites were found in a registry or an index; 27 of the 65 sources its claims cite were checked for support.
National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach
Open accessAbstract
We present a practical guide for the implementation of recently revised National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease (AD). Major revisions from previous consensus criteria are: (1) recognition that AD neuropathologic changes may occur in the apparent absence of cognitive impairment, (2) an "ABC" score for AD neuropathologic change that incorporates histopathologic assessments of amyloid β deposits (A), staging of neurofibrillary tangles (B), and scoring of neuritic plaques (C), and (3) more detailed approaches for assessing commonly co-morbid conditions such as Lewy body disease, vascular brain injury, hippocampal sclerosis, and TAR DNA binding protein (TDP)-43 immunoreactive inclusions. Recommendations also are made for the minimum sampling of brain, preferred staining methods with acceptable alternatives, reporting of results, and clinico-pathologic correlations.
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11 No full text of the sources · 9 Partly supported · 4 Supported · 3 Supported so far · 1 Own interpretation · accuracy not yet measured
Every source the paper cites for this claim was checked and supports it.
In the paper
“recognition that AD neuropathologic changes may occur in the apparent absence of cognitive impairment”
- Also stated in: § CLINICO-PATHOLOGIC CORRELATION · plain
“Similar neuropathologic changes, albeit usually at lower levels, also occur in individuals who did not show cognitive or behavioral impairments during life [54].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > Abstract
What the sources say
- Supportedcites [54] Sperling RA, Aisen PS, Beckett LA et al (2011) Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement 7:280–292 source
Section 6 reports that AD-related biomarker abnormalities can be detected before overt clinical symptoms and that Aβ accumulation occurs in clinically normal older adults. Section 2 also notes that some people have diagnostic AD neuropathological features at autopsy without having developed dementia during life. No page numbers are available in our copy. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § CLINICO-PATHOLOGIC CORRELATION · plain
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“LBs may be detected in neurons of medulla, pons and midbrain with hematoxylin and eosin (H&E)-stained sections; however, greater sensitivity can be achieved with immunohistochemistry for α-synuclein and this approach is strongly preferred [3,4,13].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE > Method
What the sources say
- Partly supportedcites [3] Alafuzoff I, Parkkinen L, Al-Sarraj S et al (2008) Assessment of alpha-synuclein pathology: a study of the BrainNet Europe Consortium. J Neuropathol Exp Neurol 67:125–143 sourceExperimental — accuracy not yet measured
The Introduction (p. 125) says consensus guidelines recommend α-synuclein immunohistochemistry for synucleinopathies, supporting the preference for that approach. The paper’s staining results and Discussion assess variation among immunohistochemical methods, but do not establish that immunohistochemistry detects Lewy bodies more sensitively than H&E; searches for H&E and hematoxylin–eosin found no such comparison. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [4] Alafuzoff I, Pikkarainen M, Al-Sarraj S et al (2006) Interlaboratory comparison of assessments of Alzheimer disease-related lesions: a study of the BrainNet Europe Consortium. J Neuropathol Exp Neurol 65:740–757 source
- Partly supportedcites [13] Beach TG, White CL, Hamilton RL et al (2008) Evaluation of alpha-synuclein immunohistochemical methods used by invited experts. Acta Neuropathol 116:277–288 sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) calls α-synuclein immunohistochemistry the method of choice for diagnosing Lewy body disorders, supporting its preferred use. The paper compares immunohistochemical methods with one another, however, and does not establish that they detect Lewy bodies more sensitively than H&E staining. (LLM, conf=0.84)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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- Partly supported
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In the paper
“one MVL identified in standard sections of brain (Table 1 regions shaded green) is of unclear relationship to cognitive function, while multiple MVLs in these regions are associated with increased likelihood of cognitive impairment or dementia [24,52,62].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > CEREBROVASCULAR DISEASE and VASCULAR BRAIN INJURY > Reporting
What the sources say
- Partly supportedcites [24] Gorelick PB, Scuteri A, Black SE et al (2011) Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 42:2672–2713 sourceExperimental — accuracy not yet measured
Section 3.2 (page not available in our copy) reports that some studies associate multiple microscopic infarcts with dementia, even after accounting for macroscopic infarcts. It does not establish the claim for MVLs generally or specify that the lesions were identified in standard brain sections. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites [52] Sonnen JA, Larson EB, Crane PK et al (2007) Pathological correlates of dementia in a longitudinal, population-based sample of aging. Ann Neurol 62:406–413 source
- Not checked — no full text of the sourcecites [62] White L (2009) Brain lesions at autopsy in older Japanese-American men as related to cognitive impairment and dementia in the final years of life: a summary report from the Honolulu-Asia aging study. J Alzheimers Dis 18:713–725 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Clinico-pathologic correlations for individuals without cognitive impairment should indicate that it is possible for AD neuropathologic change to predate onset of symptoms by years [54].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > AD NEUROPATHOLOGIC CHANGE > Reporting
What the sources say
- Supportedcites [54] Sperling RA, Aisen PS, Beckett LA et al (2011) Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement 7:280–292 source
Section 2, “Redefining the earliest stages of AD,” says the pathological cascade may begin a decade or more before clinically evident impairment. Section 6 also describes AD-related abnormalities in cognitively normal individuals, supporting the claim that neuropathologic change can predate symptoms by years. (LLM, conf=0.94)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“one MVL identified in standard sections of brain (Table 1 regions shaded green) is of unclear relationship to cognitive function, while multiple MVLs in these regions are associated with increased likelihood of cognitive impairment or dementia [24,52,62].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > CEREBROVASCULAR DISEASE and VASCULAR BRAIN INJURY > Reporting
What the sources say
- Partly supportedcites [24] Gorelick PB, Scuteri A, Black SE et al (2011) Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 42:2672–2713 sourceExperimental — accuracy not yet measured
Section 3.2 (page unavailable) says the number of infarcts needed for cognitive impairment is difficult to determine and reports that multiple microscopic infarcts may be related to dementia. It does not specifically assess the cognitive significance of one MVL identified in standard brain sections. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites [52] Sonnen JA, Larson EB, Crane PK et al (2007) Pathological correlates of dementia in a longitudinal, population-based sample of aging. Ann Neurol 62:406–413 source
- Not checked — no full text of the sourcecites [62] White L (2009) Brain lesions at autopsy in older Japanese-American men as related to cognitive impairment and dementia in the final years of life: a summary report from the Honolulu-Asia aging study. J Alzheimers Dis 18:713–725 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“this may represent pre-clinical LBD [12,22,31].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE > Reporting
What the sources say
- Supportedcites [12] Beach TG, Adler CH, Sue LI et al (2008) Reduced striatal tyrosine hydroxylase in incidental Lewy body disease. Acta Neuropathol 115:445–451 source
The Introduction defines incidental Lewy body disease as Lewy bodies without clinically documented parkinsonism or dementia. The Results and discussion report reduced striatal tyrosine hydroxylase in these individuals and say this suggests ILBD is likely a precursor to Parkinson’s disease and/or dementia with Lewy bodies, supporting the citing sentence’s qualified “may represent” claim. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites [22] Dickson DW, Fujishiro H, DelleDonne A et al (2008) Evidence that incidental Lewy body disease is pre-symptomatic Parkinson’s disease. Acta Neuropathol 115:437–444 source
- Supportedcites [31] Jicha GA, Schmitt FA, Abner E et al (2010) Prodromal clinical manifestations of neuropathologically confirmed Lewy body disease. Neurobiol Aging 31:1805–1813 source
The Introduction (page unavailable) says Lewy body pathology has been found in autopsied people described as normal and suggests that DLB pathology may predate clinical diagnosis. The Discussion (page unavailable) also says the study’s subjects were cognitively and neurologically normal at enrollment. Together, these support the qualified suggestion that LBD without apparent cognitive or motor deficits may be pre-clinical. (LLM, conf=0.91)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“LBs are frequent in the setting of moderate-to-severe levels of AD neuropathologic change [27,59], including some early-onset familial AD cases [32,33].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE
What the sources say
- Supportedcites [32] Leverenz JB, Fishel MA, Peskind ER et al (2006) Lewy body pathology in familial Alzheimer disease: evidence for disease- and mutation-specific pathologic phenotype. Arch Neurol 63:370–376 source
The Results report Lewy body pathology in the amygdala of 24 of 25 familial AD cases with PSEN1 mutations. The section on PSEN1-associated AD reports a mean age at onset of about 43 years in the groups it compares, supporting the early-onset qualifier. The indexed copy provides section labels but no page numbers. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites [33] Lippa CF, Duda JE, Grossman M et al (2007) DLB and PDD boundary issues: diagnosis, treatment, molecular pathology, and biomarkers. Neurology 68:812–819 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Accumulation of Aβ plaques and NFTs follows distinct regional progressions across brain regions as AD advances.”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > AD NEUROPATHOLOGIC CHANGE
What the sources say
- Partly supportedcites [14] Braak H, Alafuzoff I, Arzberger T et al (2006) Staging of Alzheimer disease-associated neurofibrillary pathology using paraffin sections and immunocytochemistry. Acta Neuropathol 112:389–404 sourceExperimental — accuracy not yet measured
The staging-system section describes a predictable regional progression of neurofibrillary pathology, from transentorhinal and entorhinal regions to limbic and then neocortical areas. It does not describe a separate regional progression of Aβ plaques or compare that progression with NFTs. Its references to neuritic plaques occur in the context of tau-immunoreactive pathology, not an Aβ-plaque staging scheme. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [15] Braak H, Braak E (1991) Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol 82:239–259 source
- Not checked — no full text of the sourcecites [57] Thal DR, Rub U, Orantes M, Braak H (2002) Phases of A beta-deposition in the human brain and its relevance for the development of AD. Neurology 58:1791–1800 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“CVD and vascular brain injury (VBI) [50] commonly are encountered in the brains with AD neuropathologic change [25].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > CEREBROVASCULAR DISEASE and VASCULAR BRAIN INJURY
What the sources say
- Partly supportedcites [25] Grinberg LT, Thal DR (2010) Vascular pathology in the aged human brain. Acta Neuropathol 119:277–290 sourceExperimental — accuracy not yet measured
The ‘Cerebral amyloid angiopathy’ section (page unavailable) reports that around 80–100% of AD patients have CAA, supporting the claim that cerebrovascular disease commonly accompanies AD pathology. It identifies infarction and hemorrhage as possible complications of CAA, but does not establish that vascular brain injury itself is commonly found in AD brains. (LLM, conf=0.82)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“LBs are frequent in the setting of moderate-to-severe levels of AD neuropathologic change [27,59], including some early-onset familial AD cases [32,33].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE
What the sources say
- Not checked — no full text of the sourcecites [27] Hamilton RL (2000) Lewy bodies in Alzheimer’s disease: a neuropathological review of 145 cases using alpha-synuclein immunohistochemistry. Brain Pathol 10:378–384 source
- Supportedcites [59] Uchikado H, Lin WL, DeLucia MW, Dickson DW (2006) Alzheimer disease with amygdala Lewy bodies: a distinct form of alpha-synucleinopathy. J Neuropathol Exp Neurol 65:685–697 source
The Materials and Methods section (page unavailable) says all 347 cases met pathologic criteria for AD and had Braak NFT stage IV or greater, indicating advanced AD in almost all cases. The “Frequency of α-Synuclein Pathology in Alzheimer Disease” section (page unavailable) reports Lewy-body pathology in 62 AD/ALB and 149 AD/LBD cases, supporting that Lewy bodies are frequent in this setting. (LLM, conf=0.90)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 2
- Probably not a substantial claim. 1
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Relatively isolated HS may occur in very old individuals, and in this context it is associated with TDP-43-immunoreactive inclusions and with cognitive impairment [45,47].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > HIPPOCAMPAL SCLEROSIS and TAR DNA BINDING PROTEIN (TDP)-43 INCLUSIONS > Reporting
What the sources say
- Partly supportedcites [45] Nelson PT, Abner EL, Schmitt FA et al (2010) Modeling the association between 43 different clinical and pathological variables and the severity of cognitive impairment in a large autopsy cohort of elderly persons. Brain Pathol 20:66–79 sourceExperimental — accuracy not yet measured
The Discussion reports that hippocampal sclerosis (HS) was associated with lower MMSE scores and states that HS is associated with TDP-43 proteinopathy. The Results describe TDP-43-positive inclusions. Neither passage establishes these associations specifically for relatively isolated HS in very old individuals. (LLM, conf=0.86)
- Supportedcites [47] Nelson PT, Schmitt FA, Lin Y et al (2011) Hippocampal sclerosis in advanced age: clinical and pathological features. Brain 134:1506–1518 source
The Introduction describes hippocampal sclerosis in older individuals as unrelated to Alzheimer’s pathology and associated with significant cognitive dysfunction. The Discussion reports aberrant TDP-43 staining in approximately 90% of patients with hippocampal sclerosis, and Table 7 describes HS-Ageing as most prevalent in the oldest-old and associated with dementia. The association is not universal, but the citing sentence does not claim that it is. (LLM, conf=0.92)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
In the paper
“Although not part of this classification scheme, it is important to realize that LBD also occurs frequently in the olfactory bulb in older adults and should be sampled when possible [20].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE > Method
What the sources say
- Not checked — no full text of the sourcecites [20] Del Tredici K, Rub U, De Vos RA et al (2002) Where does Parkinson disease pathology begin in the brain? J Neuropathol Exp Neurol 61:413–426 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“A subset of senile plaques called neuritic plaques appear closely associated with neuronal injury and are characterized by the occurrence of dystrophic neurites that frequently have phospho-tau immunoreactivity [19,36,37,55].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > AD NEUROPATHOLOGIC CHANGE
What the sources say
- Not checked — no full text of the sourcecites [19] DeKosky ST, Scheff SW (1990) Synapse loss in frontal cortex biopsies in Alzheimer’s disease: correlation with cognitive severity. Ann Neurol 27:457–464 source
- Not checked — no full text of the sourcecites [36] Masliah E, Mallory M, Deerinck T et al (1993) Re-evaluation of the structural organization of neuritic plaques in Alzheimer’s disease. J Neuropathol Exp Neurol 52:619–632 source
- Not checked — no full text of the sourcecites [37] Masliah E, Terry RD, Mallory M et al (1990) Diffuse plaques do not accentuate synapse loss in Alzheimer’s disease. Am J Pathol 137:1293–1297
- Not checked — no full text of the sourcecites [55] Terry RD, Masliah E, Salmon DP et al (1991) Physical basis of cognitive alterations in Alzheimer’s disease: synapse loss is the major correlate of cognitive impairment. Ann Neurol 30:572–580 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
Many other neurodegenerative disorders can cause dementia and may be co-morbid with AD neuropathologic change, especially in the elderly.
“There are many other neurodegenerative disorders that can cause dementia in addition to those discussed here, and any may be co-morbid with AD neuropathologic change, especially in the elderly.”
The paper relies on this without support.
Multiple diseases in the cerebrum can conspire to worsen cognitive symptoms.
“Multiple diseases in cerebrum can conspire to worsen cognitive symptoms; however, it often is difficult to judge the extent to which each disease observed at autopsy may have contributed to a given patient’s cognitive state.”
The paper relies on this without support.
Abnormal neuropil and neuronal cytoplasmic α-synuclein immunoreactivity are usually present with Lewy bodies but will not be apparent by H&E; in some instances, these changes occur in the absence of Lewy bodies.
“Abnormal neuropil and neuronal cytoplasmic α-synuclein immunoreactivity are usually present with LBs but will not be apparent by H&E; in some instances, these changes occur in the absence of LBs.”
The paper relies on this without support.
Diffuse white matter injury is a form of VBI but it is more difficult to judge objectively and is not specific to VBI.
“Diffuse white matter injury is a form of VBI but it is more difficult to judge objectively and is not specific to VBI.”
The paper relies on this without support.
Hippocampal sclerosis can be observed in the context of AD neuropathologic change, FTLD, and VBI, likely reflecting a heterogeneous etiology.
“HS can be observed in the context of AD neuropathologic change, frontotemporal lobar degeneration (FTLD), and VBI, likely reflecting a heterogeneous etiology.”
The paper relies on this without support.
Hippocampal sclerosis can be focal, so its absence in the recommended screening section does not rule out the possibility of HS elsewhere in the hippocampal formation.
“HS can be focal, thus its absence in the recommended screening section does not rule out the possibility of HS elsewhere in the hippocampal formation.”
The paper relies on this without support.
Hippocampal sclerosis can occur in several different diseases and has varying clinical implications in different settings.
“Clinico-pathological correlations need to recognize that HS can occur in several different diseases and has varying clinical implications in different settings.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The 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 [40]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The definitive diagnosis of AD requires microscopic examination of multiple brain regions employing staining methods that can detect Alzheimer type neuropathologic change [24], with diagnosis based upon the morphology and density of lesions and their topographic distribution.”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [24]
The cited source says what the claim attributes to it.
In the citing paper
“This finding is highlighted by the fact that nearly one third of patients with pathological findings of high likelihood Alzheimer’s disease [24] were thought to other disorders, and 3% were considered clinically normal at the time of their last clinical exam (Table 2).”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [24]
The cited source says what the claim attributes to it.
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 [105]
The cited source says what the claim attributes to it.
In the citing paper
“Autopsy analyses classified the level of ADNC from “none” to “high” using an established scoring system when available.”
From Automatic classification of AD pathology in FTD phenotypes using natural speech (2024) · cites this paper as [30]
The cited source says what the claim attributes to it.
In the citing paper
“Participants in the Confirmed-AD group (n ¼ 1854) were diagnosed with primary or contributing ADdementia at their last UDS visit before death and met our criteria for ADNC: moderate to frequent neuritic plaques and Braak stages III through VI, which loosely aligns with NIA-AA criteria for intermediate or high ADNC (13).”
From Concordance of Clinical Alzheimer Diagnosis and Neuropathological Features at Autopsy (2020) · cites this paper as [13]
The cited source says what the claim attributes to it.
In the citing paper
“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 [40]
The cited source says what the claim attributes to it.
In the citing paper
“In the revision of the 1997 criteria, combinations of plaque and tangle pathologies considered sufficient to cause dementia and qualify for the neuropathological diagnosis of AD are explicitly stated (40, 41).”
From Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer Disease Centers, 2005–2010 (2012) · cites this paper as [40]
The cited source says what the claim attributes to it.
In the citing paper
“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 Montine et al., 2012
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 [40]
In the citing paper
“Additional changes that may also occur in the brains of AD patients include amyloid angiopathy, age-related brain atrophy, synaptic pathology, white matter rarefaction, granulovacuolar degeneration, neuron loss, TDP-43 proteinopathy, and neuroinflammation (20-26), which may contribute to cognitive impairment; however, these are not considered pathognomonic features of AD (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“In contrast, dense and extensive neocortical NFTs are very consistently associated with dementia and thus, according to new diagnostic criteria, these are required to constitute high burden of AD neuropathologic change (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“The current revision of the National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of AD stipulate that subjects with moderately dense neuritic AβPs may be regarded as having an intermediate level of AD neuropathologic change and that other potential contributors to cognitive impairment and dementia should be sought (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“There is no universally applied rubric for CVD pathologic diagnosis, although the recent National Institute on Aging–Alzheimer’s Association criteria attempted to systematize neuropathologic assessment of this complex form of brain injury (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“Alzheimer's disease cases met criteria for a high likelihood of AD (Montine et al., 2012).”
From Alzheimer's amyloid‐β and tau protein accumulation is associated with decreased expression of the LDL receptor‐associated protein in human brain tissue (2020) · cites this paper as Montine et al., 2012
Citations
Cites
McKhann, G. M., Knopman, D. S., Chertkow, H., Hyman, B. T., Jack, C. R., Kawas, C. H., Klunk, W. E., Koroshetz, W. J., Manly, J. J., Mayeux, R., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.005 · Cited by 18,657 · cited 1×
“‘‘Alzheimer’s disease’’ refers to a constellation of cognitive and behavioral changes that are typical for patients who have substantial amounts of its hallmark lesions [6, 39].”
Self-citationNeuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123 · cited 8×
“‘‘Intermediate’’ or ‘‘High’’ AD neuropathologic change (italicized) is considered sufficient explanation for dementia a NFT stage should be determined by the method of Braak [14, 15] b Ab/amyloid plaque score should be determined by the method of Thal et al.”
InfluentialStaging of brain pathology related to sporadic Parkinson’s disease
Braak, H., Tredici, K. D., Rüb, U., de Vos, R. A. I., Jansen Steur, E. N. H., & Braak, E. (2003) · Neurobiology of Aging · doi:10.1016/s0197-4580(02)00065-9 · Cited by 10,777 · cited 2×
“Given our focus on cognitive impairment and dementia rather than movement disorders [16], we recommend a modification of Fig.”
Albert, M. S., DeKosky, S. T., Dickson, D., Dubois, B., Feldman, H. H., Fox, N. C., Gamst, A., Holtzman, D. M., Jagust, W. J., Petersen, R. C., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.008 · Cited by 10,152 · cited 1×
“‘‘Alzheimer’s disease’’ refers to a constellation of cognitive and behavioral changes that are typical for patients who have substantial amounts of its hallmark lesions [6, 39].”
Self-citationSperling, R. A., Aisen, P. S., Beckett, L. A., Bennett, D. A., Craft, S., Fagan, A. M., Iwatsubo, T., Jack, C. R., Kaye, J., Montine, T. J., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.003 · Cited by 7,155 · cited 2×
“Similar neuropathologic changes, albeit usually at lower levels, also occur in individuals who did not show cognitive or behavioral impairments during life [54].”
Self-citationDiagnosis and management of dementia with Lewy bodies: Third report of the DLB consortium
McKeith, I. G., Dickson, D. W., Lowe, J., Emre, M., O'Brien, J. T., Feldman, H., Cummings, J., Duda, J. E., Lippa, C., Perry, E. K., et al. (2005) · Neurology · doi:10.1212/01.wnl.0000187889.17253.b1 · Cited by 5,069
Self-citationMirra, S. S., Heyman, A., McKeel, D., Sumi, S. M., Crain, B. J., Brownlee, L. M., Vogel, F. S., Hughes, J. P., Belle, G. V., Berg, L., et al. (1991) · Neurology · doi:10.1212/wnl.41.4.479 · Cited by 4,961 · cited 11×
“Region Stain for A /amyloid plaques [57] Stain for NFTs [14,15] Stain for NPs [41] Stain for LBs H&E”
InfluentialSelf-citationDeJesus-Hernandez, M., Mackenzie, I. R., Boeve, B. F., Boxer, A. L., Baker, M., Rutherford, N. J., Nicholson, A. M., Finch, N. A., Flynn, H., Adamson, J., et al. (2011) · Neuron · doi:10.1016/j.neuron.2011.09.011 · Cited by 4,936 · cited 1×
“With the exception of individuals with mutations in TARDBP, GRN, VCP or c9ORF72 [10, 18], it is not clear whether TDP-43 proteinopathy in these other neurodegenerative diseases is”
Self-citationTerry, R. D., Masliah, E., Salmon, D. P., Butters, N., DeTeresa, R., Hill, R., Hansen, L. A., & Katzman, R. (1991) · Annals of Neurology · doi:10.1002/ana.410300410 · Cited by 4,397 · cited 1×
“frequently have phospho-tau immunoreactivity [19, 36, 37, 55].”
Self-citationGorelick, P. B., Scuteri, A., Black, S. E., DeCarli, C., Greenberg, S. M., Iadecola, C., Launer, L. J., Laurent, S., Lopez, O. L., Nyenhuis, D., et al. (2011) · Stroke · doi:10.1161/str.0b013e3182299496 · Cited by 3,811
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Items 2,201–2,300 of 2,854
Feyzbakhsh, H. (2025) · Tissue Barriers · doi:10.1080/21688370.2025.2599564 · Cited by 5
“19,29 Prominent theories of its pathogenesis implicate the toxic accumulation of Aβ plaques and tau tangles, and synaptic malfunction, calcium dysregulation, autophagy failure, microgliosis-astrogliosis, and demyelination of neurons as central players in disease progression.”
Association of cancer with neuropathological markers of Alzheimer's disease and related dementias
Teipel, S. J., Akmatov, M. K., Michalowsky, B., Junghanß, C., Holstiege, J., & Bohlken, J. (2025) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.70222 · Cited by 3
AD‐related plasma biomarkers in centenarians: links to cognition and neuropathology
Lorenz, L. M. C., Rohde, S. K., Luimes, M. C., Rozemüller, A. J. M., Bank, N. B., Hulsman, M., Graat, M. J. I., van der Hoorn, M. E., Daatselaar, D. A. H., Gouda, M., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70969 · Cited by 4
Musacchio, J. B., Martuscello, R. T., Betzios, S. I., Hernandez, R. S., Kuo, S., Cosentino, S., Fujita, H., Louis, E. D., & Faust, P. L. (2026) · Acta Neuropathologica · doi:10.1007/s00401-025-02974-4 · Cited by 2
“…interval (PMI = hours between death and placement of brain in a cold room), Braak and Braak AD staging for neurofibrillary tangles [15], Consortium to Establish a Registry for AD (CERAD) ratings for neuritic plaques [69], Thal beta-amyloid staging [70] and Braak staging for Lewy pathology [16].”
InfluentialThe enigma of vascular dementia: current state and emerging perspectives
Jellinger, K. A. (2026) · Journal of Neural Transmission · doi:10.1007/s00702-026-03104-4 · Cited by 3
Cerebral amyloid angiopathy and Alzheimer's and related pathologies across APOE genotypes
Mehta, R. I., Wang, T., Leurgans, S. E., Bennett, D. A. A., & Schneider, J. A. (2026) · Brain · doi:10.1093/brain/awag025 · Cited by 3
Self-citationCastellani, R. J., Bharadwaj, R. A., Fisher‐Hubbard, A., Deep‐Soboslay, A., Hyde, T. M., Kleinman, J. E., Hazrati, L., & Iverson, G. L. (2026) · Journal of Alzheimer s Disease · doi:10.1177/13872877251411332 · Cited by 2
Associations between structural neuroimaging markers and neuropathology of Alzheimer’s Disease
Frenzel, S., Teipel, S. J., & Grabe, H. J. (2026) · NeuroImage · doi:10.1016/j.neuroimage.2026.121841 · Cited by 2
Mastrangelo, A., Caldera, S., Baiardi, S., et al. (2026) · Alzheimer s Research & Therapy · doi:10.1186/s13195-026-02004-9 · Cited by 2
“In all cases, the presence of AD neuro-pathological changes and LB pathology was assessed by an experienced neuropathologist (P.P.), and staging was performed according to international criteria [34–35].”
Ubiquitin-specific peptidase-19 links TDP-43 aggregation to ER stress
Yan, Y., Wang, X., Jeon, H., Kee, T. R., Tran, K. D., Lee, H., Zhao, X., Liu, T., Wing, S. S., Woo, J. A., et al. (2026) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2514355123 · Cited by 2
Garcia, D., Sharma, S. R. R., Saito, N., Beckett, L. A., Sevilla, L. N. C., Vasquez, L. R., DeCarli, C. S., Gutman, D., Vizcarra, J. C., Coughlin, D. G., et al. (2025) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlaf152 · Cited by 2
“8 13–15 Although these evaluation methods have their advantages, 16 the advent of digital pathology has presented an opportunity to achieve scalable deeper phenotyping by quantifying pathology burden in brain tissues.”
Trautwig, A. N., Shantaraman, A., Chung, M., Dammer, E. B., Ping, L., Duong, D. M., Watson, C. M., Petrucelli, L., Ward, M. E., Glass, J. D., et al. (2026) · Cell Reports · doi:10.1016/j.celrep.2026.117142 · Cited by 10
Self-citationLocus coeruleus TDP-43 pathology in a community-based cohort: Clinical and pathological correlates
Neltner, A. M., Shahidehpour, R. K., Hall, M. E., Ning, X., Fister, S. X., Kang, H., Anderson, S., Jicha, G. A., Lee, T., Abner, E. L., et al. (2026) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlag035 · Cited by 1
“47,48 Briefly, after autopsy, tissue was fixed in 10% buffered formalin for approximately a month.”
Self-citationShahidehpour, R. K., Neltner, A. M., Klusty, M. A., Corbett, W. C., Gonzalez, A. D., Gutman, D. A., Fardo, D. W., Bachstetter, A. D., Bumgardner, C., Flanagan, M. E., et al. (2026) · Brain Pathology · doi:10.1111/bpa.70102 · Cited by 1
“…neuropathologic change (ADNC) are β -amyloid peptide (A β ) deposition, neuritic amyloid plaques, and neurofibrillary tangles (NFTs), each categorized using semiquantitative metrics, according to the National Institute on Aging – Alzheimer ’ s Association (NIA-AA) consensus-based guidelines [1, 2].”
Self-citationAlzheimer's Disease Co‐Pathology and Cognitive Impairment in Amyotrophic Lateral Sclerosis
Kasper, E., Lehto, A., Jürs, A. V., Nordmann, N., Peters, O., Hellmann, J., Priller, J., Spruth, E. J., Petzold, G. C., Voigt, I., et al. (2026) · Annals of Neurology · doi:10.1002/ana.78227 · Cited by 2
Lin, M., Chiotis, K., Maiti, P., Zhang, J., Blazhenets, G., Rocha, S., Shankar, R. P., Amuiri, A. N., Hammers, D. B., Eloyan, A., et al. (2026) · Brain Communications · doi:10.1093/braincomms/fcag176 · Cited by 2
Richardson, T. E., Cherry, J. D., Kandoi, S., Rohde, S. K., Uretsky, M., Tuz‐Zahra, F., Bieniek, K. F., Farrell, K. W., Hefti, M. M., Miller, M. B., et al. (2026) · Acta Neuropathologica · doi:10.1007/s00401-026-03031-4 · Cited by 3
“As noted by Montine et al., however, significant levels of ADNC may precede symptom onset by years [41].”
InfluentialSelf-citationCavero, I., & Holzgrefe, H. H. (2015) · Journal of Pharmacological and Toxicological Methods · doi:10.1016/j.vascn.2015.08.155 · Cited by 2
de Oliveira, F. H., Neto, E. R., Fonseca, M. K., Costa, A. S. R., Rockenbach, M. A. B. C., Padilha, R. D. S., Fernandez, L. L., & Hilbig, A. (2015) · Arquivos de Neuro-Psiquiatria · doi:10.1590/0004-282x20150066 · Cited by 2
Compta, Y., Ramos‐Campoy, O., Grau‐Rivera, O., Colom‐Cadena, M., Clarimón, J., Martí, M. J., & Gelpí, E. (2016) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12340 · Cited by 2
Anforderungen des Neurologen an Obduktionen
Schulz‐Schaeffer, W., Dillmann, U., Fassbender, K. C., et al. (2017) · Der Pathologe · doi:10.1007/s00292-017-0336-3 · Cited by 2
Tanaka, H., Hird, M. A., Tang‐Wai, D. F., & Kovács, G. G. (2022) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlac117 · Cited by 2
Watanabe, M., Nakamura, K., Saito, R., et al. (2023) · Neuropathology · doi:10.1111/neup.12908 · Cited by 2
Alteration of metabolic profile during the progression of Alzheimer’s disease
Yu, W., Li, X., Han, T.-L., Lü, Y., Long, F., Hu, C., Yu, W., & Lü, Y. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.061193 · Cited by 2
Korvatska, O., Bucks, S. A., Yoda, R. A., Nolan, A., Dorschner, M. O., Tsuang, D. W., Jayadev, S., Raskind, W. H., & Bird, T. D. (2023) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2023.120763 · Cited by 2
Robinson, A., Rizwan, T. B., Davidson, Y. S., Minshull, J., Tinkler, P., Payton, A., Mann, D. M. A., & Roncaroli, F. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-231429 · Cited by 2
“Two experienced neuropathologists (DM and FR) conducted the neuropathological evaluation using the consensus criteria and staging of neurodegenerative diseases [31–43].”
Hongo, S., Shimizu, H., Saji, E., Nakajima, A., Okamoto, K., Kawachi, I., Onodera, O., & Kakita, A. (2024) · Neuropathology · doi:10.1111/neup.12976 · Cited by 2
“9 There were no pathological features suggestive of complications arising from Alzheimer ’ s disease (Braak and Braak stage, III/A; ABC score, A1B2C0 8 ) or Parkinson ’ s disease (Lewy body disease: none 10 ).”
Matsubara, T., Ishii, K., Saito, Y., Tokumaru, A. M., Arakawa, A., Kurihara, M., Kurihara, M., Sengoku, R., Kanemaru, K., Iwata, A., et al. (2024) · Acta Neuropathologica Communications · doi:10.1186/s40478-024-01815-x · Cited by 2
“…the brain condition at autopsy was categorized as intermediate AD according to the National Institute on Aging-Alzheimer’s Association criteria [7] and did not meet the NFTD/PART criteria [3, 10], the longitudinal PET findings suggest that the pathological findings would have met the criteria…”
MethodMohammadzadeh, N., Wu, C., Donahue, J. E., & Friedman, J. H. (2024) · Movement Disorders Clinical Practice · doi:10.1002/mdc3.14149 · Cited by 2
Murakami, A., Koga, S., Fujioka, S., White, A. E., Bieniek, K. F., Sekiya, H., DeJesus‐Hernandez, M., Finch, N. A., van Blitterswijk, M., Nakamura, M., et al. (2024) · Brain Pathology · doi:10.1111/bpa.13286 · Cited by 2
Self-citationAlcohol consumers with liver pathology rarely display α-synuclein pathology
Libard, S., Tamsen, F., & Alafuzoff, I. I. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02772-4 · Cited by 2
“Excessive levels of these two proteins together are considered causative factors for Alzheimer’s Disease (AD), and the pathology is referred to as AD Neuropathologic Change (ADNC) [11, 20, 38].”
BackgroundAstrocytic centrin‐2 expression in entorhinal cortex correlates with Alzheimer's disease severity
Degl’Innocenti, E., Poloni, T. E., Medici, V., Olimpico, F., Finamore, F., Profka, X., Bascarane, K., Morrone, C., Pastore, A., Escartin, C., et al. (2024) · Glia · doi:10.1002/glia.24603 · Cited by 2
“…pTAU ( B raak stages), and NPs ( C ERAD — Consortium to Establish a Registry for AD) represent the ABC criteria to define AD diagnosis and pathological severity (i.e., no AD, low AD, intermediate AD, high AD) (Braak et al., 2006; Mirra et al., 1991; Montine et al., 2012; Thal et al., 2002).”
Marmor, A., Vakil, E., Merhavi, S. K., & Meiner, Z. (2024) · Journal of Clinical and Experimental Neuropsychology · doi:10.1080/13803395.2024.2400109 · Cited by 2
“…diagnosis was based on a significant decline in cognitive abilities and daily function, as reported by the patient or a caregiver, and as manifest in cognitive tests (mainly the MMSE (Statsenko et al., 2023)), the NINCDS-ADRDA (McKhann et al., 1984), and the AA-NIA criteria (Montine et al., 2012).”
Lee, K.-H., Kim, S., Shim, Y., Kim, E., Yoo, S., Won, J.-K., & Park, S. (2024) · Experimental Neurobiology · doi:10.5607/en24027 · Cited by 2
Salman, Y., Huyghe, L., Quenon, L., Ghysens, O., Malotaux, V., Tomé, S. O., Thal, D. R., & Hanseeuw, B. J. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251314199 · Cited by 2
Self-citationShahidehpour, R. K., Nelson, P. T., Srinivasan, S., Zhong, Y., & Bachstetter, A. D. (2025) · Neuropathology · doi:10.1111/neup.70003 · Cited by 2
Self-citationHeylen, A., Vermeiren, Y., Deyn, P. P. D., & Dam, D. V. (2025) · Journal of Neurochemistry · doi:10.1111/jnc.70046 · Cited by 2
Braun, A. S., Satoh, R., Pham, N. T. T., Singh, N. A., Ali, F., Dickson, D. W., Lowe, V. J., Whitwell, J. L., & Josephs, K. A. (2025) · Annals of Neurology · doi:10.1002/ana.27265 · Cited by 2
Self-citationAzizzadeh, A., Najafi, M., Nafar, Z., Salehzehi, S., Jahromi, S. A., Fallah, H., Ghoshouni, H., & Initiative, A. D. N. (2025) · Neurological Sciences · doi:10.1007/s10072-025-08268-7 · Cited by 2
“Following the National Institute on Aging-Alzheimer’s Association standards for the neuropathological assessment of AD, pathology exami - nations explored a wide spectrum of AD neuropathologic lesions and prevalent non-AD diseases [18 ].”
Beamon, Q., Zhu, A., Leverenz, J. B., & Pillai, J. A. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70360 · Cited by 3
Iverson, G. L., Jamshidi, P., Deep‐Soboslay, A., Hyde, T. M., Kleinman, J. E., Hazrati, L., & Castellani, R. J. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251351524 · Cited by 2
Tsering, W., Philips, J. L., Golde, T. E., Villareal, J. A. B., & Prokop, S. (2025) · Molecular Neurobiology · doi:10.1007/s12035-025-05231-7 · Cited by 2
“ADNC staging was based on the NIH-AA guideline [31, 37] and has been described previously for the cohort used in this study [19, 34].”
Dendritic location of dystrophic neurites in FTLD ‐ TDP type C with annexinopathy
Kawles, A., Zouridakis, A., Nelson, C., Keszycki, R. M., Minogue, G., Macomber, A. J., Jamshidi, P., Castellani, R. J., Geula, C., Gefen, T. D., et al. (2025) · Brain Pathology · doi:10.1111/bpa.70032 · Cited by 2
“No cases had an extent of AD pathology (ADNC) above “ low ” according to Hyman et al. and Montine et al. [26, 27], with Braak staging ranging from 0 to 1.”
Hypometabolic subtypes of AD are linked to comorbid hippocampal sclerosis and Lewy body pathology
Levin, F., Dyrba, M., Teipel, S. J., & Grothe, M. J. (2025) · Alzheimer s Research & Therapy · doi:10.1186/s13195-025-01796-6 · Cited by 2
“Presence of pathologic AD required at least moderate levels of AD neuropathologic change (i.e., ADNC ≥ 2) [28].”
Cockell, S. M., Wang, H., Benke, K. S., Ware, E. B., & Bakulski, K. M. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251365283 · Cited by 2
Almeida, F., Santos, A. C., Jesus, T., Gauthreaux, K. M., Mock, C., Kukull, W. A., Crary, J. F., & Oliveira, T. G. (2025) · Journal of Neurology · doi:10.1007/s00415-025-13360-1 · Cited by 7
“Classification of LB pathology into these groups has been previously detailed [26].”
InfluentialMartinez, N., Bharani, K., Hasan, S., & Hayes, C. A. (2025) · Alzheimer s Research & Therapy · doi:10.1186/s13195-025-01863-y · Cited by 3
“ADRC uploaded data to NACC using neuropathology forms 9 and 10 per consensus guidelines [8, 22].”
Duyckaerts, C. J. (2014) · Cambridge University Press eBooks · doi:10.1017/cbo9781107588660.007 · Cited by 2
Self-citationTo Stage Alzheimer’s Disease Related Neurodegeneration Using one Section of Hippocampus
Popova, S. N., Pesälä, S., & Alafuzoff, I. I. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-150494 · Cited by 2
Kepe, V. (2013) · PET Clinics · doi:10.1016/j.cpet.2013.08.002 · Cited by 2
Same Ages, Same Genes: Same Brains, Same Pathologies?
Iacono, D., Volkmann, I., Nennesmo, I., Pedersen, N. L., Fratiglioni, L., Johansson, B. E. A., Karlsson, D., Winblad, B. G., & Gatz, M. (2015) · Alzheimer Disease & Associated Disorders · doi:10.1097/wad.0000000000000114 · Cited by 2
Protocols for Monitoring the Development of Tau Pathology in Alzheimer’s Disease
Rábano, A., Cuadros, R., Merino‐Serrais, P., Rodal, I., Benavides‐Piccione, R., Góméz, E., Medina, M., DeFelipe, J., & Ávila, J. (2015) · Methods in molecular biology · doi:10.1007/978-1-4939-2627-5_7 · Cited by 2
Protein Microarrays in Neurodegenerative Diseases
Segundo‐Acosta, P. S., Garranzo‐Asensio, M., Montero‐Calle, A., Oeo‐Santos, C., Villalba, M., Guzmán‐Aránguez, A., & Barderas, R. (2017) · Neuromethods · doi:10.1007/978-1-4939-7119-0_4 · Cited by 2
A Cytomic Approach Towards Genomic Individuality of Neurons
Arendt, T., Belter, B., Brückner, M. K., Ueberham, U., Morawski, M., & Tárnok, A. (2017) · Neuromethods · doi:10.1007/978-1-4939-7280-7_5 · Cited by 2
The Pattern of Cortical Lesions in Preclinical Stages
Braak, H., & Tredici, K. D. (2014) · Advances in anatomy, embryology and cell biology · doi:10.1007/978-3-319-12679-1_7 · Cited by 3
Mahía, A., Conde-Giménez, M., Salillas, S., et al. (2018) · Analytical and Bioanalytical Chemistry · doi:10.1007/s00216-018-1433-8 · Cited by 2
Cerebral Multimorbidity in Aging
Jellinger, K. A. (2016) · Journal of Neurology and Neuromedicine · doi:10.29245/2572.942x/2017/1.1001 · Cited by 2
Biomarqueurs du liquide cérébrospinal dans la maladie d’Alzheimer
Hugon, J., Dumurgier, J., Cognat, E., & Paquet, C. (2018) · Bulletin de l Académie Nationale de Médecine · doi:10.1016/s0001-4079(19)30359-0 · Cited by 2
Verwey, N. A., Teunissen, C. E., Hoozemans, J. J. M., Rozemüller, A. J. M., Scheltens, P., & Pijnenburg, Y. A. L. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-190344 · Cited by 2
Ikeda, T., Iwasaki, Y., Sakurai, K., et al. (2019) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2019.116515 · Cited by 2
Advances in Retinal Imaging: Retinal Amyloid Imaging
Koronyo‐Hamaoui, M., Doustar, J., Oviatt, M., Black, K. L., & Koronyo, Y. (2020) · Springer eBooks · doi:10.1007/978-3-030-26269-3_6 · Cited by 4
Corticobasal syndrome-Pick's disease: A clinicopathological study
Uchida, Y., Yoshida, M., Takada, K., Tsugu, Y., Ueki, Y., & Matsukawa, N. (2020) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2020.116752 · Cited by 2
Tanprasertsuk, J., Scott, T. M., Johnson, M. A., Poon, L. W., Nelson, P. T., Davey, A., Woodard, J. L., Vishwanathan, R., Barbey, A. K., Barger, K., et al. (2021) · Journal of Aging Research and Lifestyle · doi:10.14283/jarlife.2021.2 · Cited by 2
“Braak staging is one of the criteria for the neuropathological diagnosis of AD from the National Institute on Aging-Reagan Institute (NIARI) (28), along with Aβ loads and Consortium to Establish a Registry for AD’s scoring of NP.”
MethodInfluentialSelf-citationAmyloid in the ageing brain: New frameworks and perspectives
Hunter, S., & Brayne, C. (2021) · Aging Brain · doi:10.1016/j.nbas.2021.100008 · Cited by 2
“In the quest to understand AD and find efficient therapeutic interventions, the dominant amyloid cascade hypothesis [1,2] has been driven by several lines of evidence including: 1) genetic evidence from familial forms of AD (FAD), where fully penetrant mutations in the presenilins (PSEN1 and 2) and the amyloid b precu…”
BackgroundThe Complex and Integral Roles of Pericytes Within the Neurovascular Unit in Health and Disease
Sutherland, B. A. (2021) · Stem cell biology and regenerative medicine · doi:10.1007/978-3-030-62129-2_2 · Cited by 2
Zebhauser, P. T., Berthele, A., Franz, M., Goldhardt, O., Diehl‐Schmid, J., Priller, J., Ortner, M., & Grimmer, T. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210286 · Cited by 2
“A (cid:2) peptides derive from the membrane-bound amyloid-(cid:2) protein precursor (A (cid:2) PP) and, when deposited in extracellular plaques, constitute a pathological hallmark of AD [19].”
Kubo, S., Matsubara, T., Taguchi, T., Sengoku, R., Takeuchi, A., & Saito, Y. (2021) · BMC Neurology · doi:10.1186/s12883-021-02504-1 · Cited by 2
“The level of Alzheimer’s disease-related neuropathological changes corresponded to “low” according to the National Institute on Aging-Alzheimer’s Association classification [11] (Thal phase for amyloid β plaques: 3 [12], Consortium to Establish a Registry for Alzheimer’s Disease score: B [13], Braak NFT stage: II [14]…”
BackgroundAltuna, M., Larumbe, R., Zelaya, M. V., Moreno, S., García-Solaesa, V., Mendióroz, M., Ramos, M. A., & Erro, M. E. (2022) · Journal of Neurology · doi:10.1007/s00415-022-11125-8 · Cited by 2
“The patient’s final neuropathological diagnosis met the criteria for EOAD, based on the actual consensus criteria [32].”
MethodAlzheimer's Disease: An Overview☆
Castellani, R., Zhu, X., Perry, G., & Moreira, P. I. (2014) · Elsevier eBooks · doi:10.1016/b978-0-12-801238-3.04491-3 · Cited by 2
Epilepsy - Seizures without Triggers
Shad, K. F. (2022) · IntechOpen eBooks · doi:10.5772/intechopen.100833 · Cited by 2
Characterization of memory profile in idiopathic REM sleep behavior disorder
Wenke, Š., Mana, J., Havlík, F., Cohn, M., Nikolai, T., Herman Buschke, L., Nepožitek, J., Peřinová, P., Dostálová, S., y Losada, V. I. L., et al. (2022) · Journal of Clinical and Experimental Neuropsychology · doi:10.1080/13803395.2022.2107182 · Cited by 2
“Third, only a prospective longitudinal follow-up could exclude that iRBD converting into the symptomatic phase of neurodegeneration will not develop associative deficit in memory, possibly those who can convert to concomitant PD + AD pathology (Irwin et al., 2012; Montine et al., 2012).”
BackgroundSasaki, R., Morimoto, S., Ozawa, F., Okano, H., Yoshida, M., Ishiura, H., Tsuji, S., Kuzuhara, S., & Kokubo, Y. (2022) · Neurology · doi:10.1212/wnl.0000000000201156 · Cited by 2
“Lewy body pathology was assessed by modified previous consensus guidelines.(9,10) TDP-43 pathology in ALS was assessed by staging, as suggested by Brettschneider et al.”
MethodYang, D., Masurkar, A. V., Khasiyev, F., Rundek, T., Wright, C. B., Elkind, M. S. V., Sacco, R. L., & Gutierrez, J. (2022) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2022.120533 · Cited by 2
A Possible Explanation For Neurodegenerative Disease
Armstrong, R. A. (2019) · EMJ Neurology · doi:10.33590/emjneurol/10314063 · Cited by 2
Matchett, B. J., Lincoln, S., Baker, M. C., Tamvaka, N., Labuzan, S. A., Sirmans, T. N. H., Moloney, C. M., Helminger, J., Hinkle, K. M., Cabrera-Rodriguez, J. N., et al. (2023) · Medicine · doi:10.1097/md.0000000000034017 · Cited by 2
“[1] As the hippocampus can be differentially affected in AD, [2] it is important to understand what mechanisms contribute to this selective vulnerability.”
Self-citationA Pragmatic Approach to the Postmortem Neuropathological Diagnosis of Dementia
Reichard, R. R., & Parisi, J. E. (2012) · Academic Forensic Pathology · doi:10.23907/2012.001 · Cited by 2
Fukasawa, N., Fukuda, T., Nagaoka, M., Harada, T., Takahashi, H., & Ikegami, M. (2017) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12422 · Cited by 2
Marcum, Z. A., Keene, C. D., & Larson, E. B. (2020) · Pharmacoepidemiology and Drug Safety · doi:10.1002/pds.5068 · Cited by 2
“This important work has led to the creation of consensus guidelines for the neuropathological evaluation of various neurodegenerative disorders, such as Alzheimer’s disease (AD).(5) However, current staging criteria have limitations due to their ordinal”
BackgroundButyrylcholinesterase as a biomarker in Alzheimer’s disease
DeBay, D. R., & Darvesh, S. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-815854-8.00017-3 · Cited by 2
Cerebral pathological findings in long‐lived patient with Werner syndrome and dementia
Kuzuya, M., Shi, R. Q., Yanagawa, M., Watanabe, K., Samizo, S., Ando, R., Miyahara, H., Iwasaki, Y., & Yoshida, M. (2021) · Geriatrics and gerontology international/Geriatrics & gerontology international · doi:10.1111/ggi.14206 · Cited by 2
Fathy, Y. Y., de Jong, F. J., van Dam, A., Rozemüller, A. J. M., & van de Berg, W. D. J. (2017) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/156984 · Cited by 1
“Confirmation of either iLBD, PD or DLB and concommitant AD pathology was based on guidelines using Braak staging for neurofibrillary tangles (Braak NFT 0-6), Braak α -synuclein (Braak α-syn 0-6), Thal phase for β-amyloid (0-5), and ABC scoring system [10, 12, 29, 39, 51] .”
MethodPasquini, L., Nana, A. L., Toller, G., Brown, J., Deng, J., Staffaroni, A., Kim, E.-J., Hwang, J.-H. L., Li, L., Park, Y., et al. (2019) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/691212 · Cited by 2
The Alzheimer risk factor CD2AP causes dysfunction of the brain vascular networkPreprint
Vandal, M., Institóris, Á., Korin, B., Gunn, C., Lee, S., Lee, J. Y., Bourassa, P., Mishra, R. C., Peringod, G., Jiang, Y., et al. (2020) · Research Square · doi:10.1101/2020.12.10.419598 · Cited by 2
Stefanovski, L., Meier, J. M., Pai, R. K., Triebkorn, P., Lett, T. A. P., Martin, L., Bülau, K., Hofmann‐Apitius, M., Solodkin, A., McIntosh, A. R., et al. (2020) · PsyArXiv (OSF Preprints) · doi:10.31234/osf.io/4t5qa · Cited by 2
Frigerio, I., Boon, B. D. C., Lin, C.-P., Graaf, Y. G.-D., Bol, J. G. J. M., Preziosa, P., Twisk, J. W. R., Barkhof, F., Hoozemans, J. J. M., Bouwman, F. H., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.06.16.448650 · Cited by 2
Michno, W., Bowman, A. P., Jha, D., Minta, K., Ge, J., Koutarapu, S., Zetterberg, H., Blennow, K., Lashley, T., Heeren, R. M. A., et al. (2023) · ChemRxiv · doi:10.26434/chemrxiv-2023-zt864 · Cited by 2
Ramanan, S., Akarca, D., Henderson, S., Rouse, M., Allinson, K., Patterson, K., Rowe, J., & Ralph, M. L. (2023) · medRxiv · doi:10.1101/2023.10.11.23296861 · Cited by 1
“the NIA-AA Alzheimer’s disease neuropathologic change score (NPADNC variable) to categorise low, intermediate and high Alzheimer’s disease neuropathologic change.(71) • Primary cerebrovascular disease (primary vascular pathology) was coded using the NPPVASC variable.”
MethodJohnson, A. S., Ziaggi, G., Smith, A. C., Houlihan, H. M., Heuer, L. B., Guzmán, D. S., Okafor, A., Huey, E. D., Talmasov, D., Provenzano, F. A., et al. (2024) · medRxiv · doi:10.1101/2024.01.12.24301221 · Cited by 2
MU-BRAIN: MUltiethnic Brain Rna-seq for Alzheimer INitiativePreprint
Yang, Z., Cieza, B., Reyes‐Dumeyer, D., Lee, A., Ma, Y., Yılmaz, E., Lantigua, R., Miller, G. W., Brown, L. M., Honig, L. S., et al. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.02.20.581250 · Cited by 2
Self-citationBarsoum, S., Latimer, C. S., Nolan, A., Barrett, A., Chang, K., Troncoso, J. C., Keene, C. D., & Benjamini, D. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.05.06.592719 · Cited by 2
A Neuropathology Case Report of a Woman with Down Syndrome who Remained Cognitively StablePreprint
Liou, J., Lou, J. J., Nakagiri, J., Yong, W. H., Hom, C. L., Doran, E. W., Totoiu, M. O., Lott, I. T., Mapstone, M. E., Keator, D. B., et al. (2024) · medRxiv · doi:10.1101/2024.06.01.24308050 · Cited by 2
“Tissue sampling and staining included all brain regions of the left hemisphere recommended by the 2012 National Institutes of Aging – Alzheimer’s Association consensus criteria for the neuropathological evaluation of Alzheimer’s disease [40, 41].”
MethodGawor, K., Tomé, S. O., Vandenberghe, R. R., Damme, P. V., Vandenbulcke, M., Otto, M., Arnim, C. A. F. V., Ghebremedhin, E., Ronisz, A., Ospitalieri, S., et al. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.06.21.599515 · Cited by 2
Self-citationMammel, A., Hsiung, G. R., Mousavi, A., Hallett, K., Mackenzie, I. R., Hirsch‐Reinshagen, V., Biehl, D., Gill, P. S., Encarnacion, M. J., & Frykman, H. (2024) · medRxiv · doi:10.1101/2024.07.27.24310872 · Cited by 2
Epigenetic signatures of regional tau pathology and cognition in the aging and pathological brainPreprint
Goldberg, D. C., Wadhwani, A. R., Dehghani, N., Sreepada, L. P., Fu, H., Jager, P. L. D., Bennett, D. A., Wolk, D. A., Lee, E. B., White, C. L., et al. (2024) · medRxiv · doi:10.1101/2024.11.07.24316933 · Cited by 2
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Zhang, N., Adler, C. H., Atri, A., Aslam, S., Serrano, G. E., Beach, T. G., & Chen, K. (2025) · medRxiv · doi:10.1101/2025.04.23.25326286 · Cited by 2
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“This included scoring of Thal phase, Braak and Braak staging system for neurofibrillary tangles (NFT Braak), and Consortium to Establish a Registry for AD (CERAD) scale for neuritic plaques 25–27 .”
Alasmar, Z., Tremblay, C., Moqadam, R., Serrano, G. E., Beach, T. G., Atri, A., Su, Y., Initiative, T. A. D. N., Zeighami, Y., & Dadar, M. (2025) · medRxiv · doi:10.1101/2025.05.30.25328630 · Cited by 2
“Neuropathology assessments included the rating scales used to classify core AD neuropathological hallmarks as the AD neuropathologic change according to the National Institute on Aging and Alzheimer’s Association (NIA-AA) guidelines [29,30].”
Self-citationPathogenic tau inhibits synaptic plasticity by blocking eIF4B-mediated local protein synthesisPreprint
Kauwe, G., Lokitiyakul, D., Wong, I. L., Schneider, K., Sridhar, V., Sellegounder, D., Ngwala, Y. Y., Yao, L., Chen, J. H., Pareja-Navarro, K. A., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.09.11.675671 · Cited by 2
Distinct tau filament folds in familial frontotemporal dementia due to the MAPT S305I mutationPreprint
Pan, H. S., Merz, G. E., Nana, A. L., Le, M. Q., Jo, H., Quddus, A., Yung, A., Kormos, R. C., Melo, A. A., Ramos, E. M., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.02.12.705620 · Cited by 1
Metadata
- Authors
- Montine, T. J., Phelps, C. H., Beach, T. G., Bigio, E. H., Cairns, N. J., Dickson, D. W., Duyckaerts, C., Frosch, M. P., Masliah, E., Mirra, S. S., Nelson, P. T., Schneider, J. A., Thal, D. R., Trojanowski, J. Q., Vinters, H. V., & Hyman, B. T.
- Affiliations
- University of Washington (US)
- National Institutes of Health (US)
- Banner Sun Health Research Institute (US)
- Northwestern University (US)
- Washington University in St. Louis (US)
- Mayo Clinic (US)
- Pitié-Salpêtrière Hospital (FR)
- Harvard University (US)
- University of California San Diego (US)
- SUNY Downstate Health Sciences University (US)
- University of Kentucky (US)
- Rush University Medical Center (US)
- Universität Ulm (DE)
- University of Pennsylvania (US)
- University of California, Los Angeles (US)
- Corresponding author
- Montine, Thomas J.
- ORCID
- Venue
- Acta Neuropathologica
- Published
- 2011-11-20
- Volume
- 123
- Issue
- 1
- Pages
- 1-11
- ISSN
- 0001-6322 (ISSN-L)
- 1432-0533
- PMC
- PMC3268003
- OpenAlex
- W2128228199
- Cited by
- 2,894
- References
- 66
- Citations by year
- 2026: 254 · 2025: 290 · 2024: 329 · 2023: 251 · 2022: 284 · 2021: 257 · 2020: 244 · 2019: 183 · 2018: 164 · 2017: 148 · 2016: 144 · 2015: 136 · 2014: 92 · 2013: 69 · 2012: 46
- FWCI
- 39.19
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Acta Neuropathologica (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5u01ag024904-10)
- National Institute on Aging (U01-AG-024904, R01AG017917, AG18840, AG-15819, R01AG015866, P30AG028383, R01AG042210, R01AG018440, U01AG016976, P50AG005131, P50AG016570, P01AG003949, P30AG010124, R01AG015819, P30AG010161, AG24904, P50AG005681, P30AG019610, P01AG003991, P50AG005136, P50AG005134, P30AG013854, U19AG010483, RF1AG015819, P01AG012435, U19AG024904, P30AG062421)
- National Institute of Neurological Disorders and Stroke (P50NS062684)
- 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 deposition, neurofibrillary tangles, neuritic plaques, ABC score, Lewy body disease, vascular brain injury, hippocampal sclerosis, TDP-43 inclusions, staining techniques, clinicopathological correlation, preclinical Alzheimer's disease
- MeSH terms
- Alzheimer Disease, Brain, Cerebrovascular Disorders, DNA-Binding Proteins, Hippocampus, Humans, Sclerosis, United States, Cerebrovascular Trauma, Lewy Body Disease, National Institute on Aging (U.S.)
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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.
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