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.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
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.
- 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
“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
Self-citation
Cited by
Sorted by citations
Items 1,401–1,500 of 2,854
Marked Mild Cognitive Deficits in Humanized Mouse Model of Alzheimer’s-Type Tau Pathology
Cho, J. D., Kim, Y. A., Rafikian, E. E., Yang, M., & Santa‐María, I. (2021) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2021.634157 · Cited by 15
Digital Histological Study of Neocortical Grey and White Matter Tau Burden Across Tauopathies
Coughlin, D. G., Hiniker, A. O., Peterson, C. S., Kim, Y., Arezoumandan, S., Giannini, L., Pizzo, D. P., Weintraub, D. A., Siderowf, A. D., Litvan, I., et al. (2022) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlac094 · Cited by 15
Self-citationNeuroimmune proteins can differentiate between tauopathies
Cherry, J. D., Baucom, Z. H., Eppich, K. G., Kirsch, D. A., Dixon, E., Tripodis, Y., Bieniek, K. F., Farrell, K. W., Whitney, K. R., Uretsky, M., et al. (2022) · Journal of Neuroinflammation · doi:10.1186/s12974-022-02640-6 · Cited by 15
Self-citationTDP‐43 pathology effect on volume and flortaucipir uptake in Alzheimer's disease
Carlos, A. F., Tosakulwong, N., Weigand, S. D., Senjem, M. L., Schwarz, C. G., Knopman, D. S., Boeve, B. F., Petersen, R. C., Nguyen, A. T., Reichard, R. R., et al. (2022) · Alzheimer s & Dementia · doi:10.1002/alz.12878 · Cited by 16
Self-citationGaramszegi, S. P., Banack, S. A., Duque, L., Metcalf, J. S., Stommel, E. W., Cox, P. A., & Davis, D. A. (2023) · Toxicology Reports · doi:10.1016/j.toxrep.2023.01.002 · Cited by 16
“AD neuropathological changes of each subject were categorized by a board-certified neuropathologist using the National Institute of Aging Alzheimer Disease Association diagnostic criteria (NIA-AA) (Table 2) [37].”
BackgroundMethodAccumulation of pTau231 at the Postsynaptic Density in Early Alzheimer’s Disease
Lilek, J. N., Ajroud, K., Feldman, A. Z., Krishnamachari, S., Ghourchian, S., Gefen, T. D., Spencer, C., Kawles, A., Mao, Q., Tranovich, J. F., et al. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-220848 · Cited by 16
Self-citationBetters, R. K., Luhmann, E. K., Gottschalk, A. C., Xu, Z., Shin, M. R., Ptak, C. P., Fiock, K. L., Radoshevich, L., & Hefti, M. M. (2023) · eNeuro · doi:10.1523/eneuro.0503-22.2023 · Cited by 16
Sakurai, K., Kaneda, D., Morimoto, S., Uchida, Y., Inui, S., Kimura, Y., Kan, H., Kato, T., Ito, K., & Hashizume, Y. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230068 · Cited by 16
Uncovering tau in wasteosomes (corpora amylacea) of Alzheimer’s disease patients
Riba, M., del Valle, J., Romera, C., Alsina, R., Molina‐Porcel, L., Pelegrı́, C., & Vilaplana, J. (2023) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2023.1110425 · Cited by 16
“Notably, regarding the histopathologic assessments of amyloid β deposits (A), staging of NFTs (B), and scoring of neuritic plaques (C) (ABC score; Montine et al., 2012), patients 1, 9, and 10 had an A3B3C3 score, while the score of the patient 8 was A2B1C1, indicating that patient 8 was in a lower Braak stage.”
BackgroundGatto, R. G., Carlos, A. F., Reichard, R. R., Lowe, V. J., Whitwell, J. L., & Josephs, K. A. (2023) · PLoS ONE · doi:10.1371/journal.pone.0284182 · Cited by 17
“All patients had a standardized neuropathologic evaluation following accepted, published methodologies [27,28].”
BackgroundMethodYabata, H., Riku, Y., Miyahara, H., Akagi, A., Sone, J., Urushitani, M., Yoshida, M., & Iwasaki, Y. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241512176 · Cited by 16
“Exclusion criteria were as follows: mechanical ventilation for more than a month (n = 2), comorbid neuropathological changes of Alzheimer’s disease that were classified into high grade [39] (n = 1), and comorbid neuropathological changes of limbic/diffuse neocortical stage of Lewy body disease [40] combined with Alzhe…”
BackgroundDeterminants of astrocytic pathology in stem cell models of primary tauopathies
Fiock, K. L., Hook, J. N., & Hefti, M. M. (2023) · Acta Neuropathologica Communications · doi:10.1186/s40478-023-01655-1 · Cited by 20
Pathology‐specific patterns of cerebellar atrophy in neurodegenerative disorders
Chen, Y., Spina, S., Callahan, P. M., Grinberg, L. T., Seeley, W. W., Rosen, H. J., Kramer, J. H., Miller, B. L., & Rankin, K. P. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.13551 · Cited by 14
Saha, P., & Ahmad, F. (2024) · ACS Omega · doi:10.1021/acsomega.3c07178 · Cited by 17
The aldehyde dehydrogenase 2 rs671 variant enhances amyloid β pathology
Wang, X., Wang, J., Chen, Y., Qian, X., Luo, S., Wang, X., Ma, C., & Ge, W. (2024) · Nature Communications · doi:10.1038/s41467-024-46899-0 · Cited by 16
Villareal, J. A. B., Bathe, T., Hery, G. P., Phillips, J. L., Tsering, W., & Prokop, S. (2024) · Journal of Neuroinflammation · doi:10.1186/s12974-024-03196-3 · Cited by 17
“Samples were stored in RNAse-free tubes at -20 C for long-term storage.”
MethodThe Alzheimer's Disease Neuroimaging Initiative Neuropathology Core: An update
Perrin, R. J., Franklin, E. E., Bernhardt, H., Burns, A., Schwetye, K. E., Cairns, N. J., Baxter, M., Weiner, M. W., Morris, J. C., & Initiative, A. D. N. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.14253 · Cited by 20
Self-citationGao, F., Zhan, Y., Wang, Q., Zhang, M., Dai, L., & Shen, Y. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.14521 · Cited by 21
Miners, J. S., Renfrew, R., Swirski, M., & Love, S. (2014) · Acta Neuropathologica Communications · doi:10.1186/s40478-014-0164-0 · Cited by 17
Baschieri, F., Buonaura, G. C., Cecere, A., Barletta, G., Contin, M., Parchi, P., & Cortelli, P. (2017) · Frontiers in Neurology · doi:10.3389/fneur.2017.00225 · Cited by 16
Combined Pathologies in FTLD-TDP Types A and C
Gefen, T. D., Ahmadian, S. S., Mao, Q., Kım, G., Seckin, M. F., Bonakdarpour, B., Ramos, E. M., Coppola, G., Rademakers, R., Rogalski, E. J., et al. (2018) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nly018 · Cited by 16
Self-citationIwasaki, Y., Imamura, K., Iwai, K., et al. (2018) · Neuropathology · doi:10.1111/neup.12503 · Cited by 16
In vivo Brainstem Imaging in Alzheimer’s Disease: Potential for Biomarker Development
Braun, D. J., & Eldik, L. J. V. (2018) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2018.00266 · Cited by 16
Cofilin 2 in Serum as a Novel Biomarker for Alzheimer’s Disease in Han Chinese
Sun, Y., Liang, L., Dong, M., Li, C., Liu, Z., & Gao, H. (2019) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2019.00214 · Cited by 17
Pathological Correlations of Neuropsychiatric Symptoms in Institutionalized People with Dementia
Antonio, E. E., López‐Álvarez, J., Rábano, A., Agüera-Ortíz, L., Sánchez‐Soblechero, A., Amaya, L. J. D., Portela, S., Caramé, C. C., & Olazarán, J. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-200600 · Cited by 16
“AD pathological diagnosis was established only in case of high probability of disease, i.e., frequent neuritic plaques (CERAD 3) and advanced NFT stage (Braak V-VI) [24].”
Application of deep learning to understand resilience to Alzheimer's disease pathology
Lee, C. S., Latimer, C. S., Henriksen, J. C., Blazes, M. S., Larson, E. B., Crane, P. K., Keene, C. D., & Lee, A. (2021) · Brain Pathology · doi:10.1111/bpa.12974 · Cited by 16
“Current National Institute on Aging and Alzheimer's Association (NIAAA) guidelines for the assessment of AD neuropathologic change (ADNC) combine amyloid β (Aβ) plaque distribution (Thal phase), neurofibrillary tangle (NFT) distribution (Braak stage), and neuritic plaque density (Consortium to Establish a Registry for…”
Backgroundde Gordoa, J. S., Zelaya, M. V., Tellechea-Aramburo, P., Acha, B., Roldán, M., López-Molina, C., Coca, V., Galbete, A., Mendióroz, M., & Erro, M. E. (2022) · Frontiers in Neurology · doi:10.3389/fneur.2022.827338 · Cited by 16
Carlos, A. F., & Josephs, K. A. (2022) · Journal of Neurology · doi:10.1007/s00415-022-11073-3 · Cited by 18
Old age amyotrophic lateral sclerosis and limbic TDP‐43 pathology
Murakami, A., Koga, S., Sekiya, H., Oskarsson, B., Boylan, K., Petrucelli, L., Josephs, K. A., & Dickson, D. W. (2022) · Brain Pathology · doi:10.1111/bpa.13100 · Cited by 15
“Given that no patients in the old-ALS had HpScl, it is reasonable to assume that TDP-43 pathology in old-ALS may be associated with ADNC.”
BackgroundInfluentialSelf-citationTAR DNA-binding protein 43 pathology in Alzheimer's disease with psychosis
Vatsavayi, A. V. V., Kofler, J., DeMichele‐Sweet, M. A. A., Murray, P. S., López, O. L., & Sweet, R. A. (2014) · International Psychogeriatrics · doi:10.1017/s1041610214000246 · Cited by 16
Simulated brain biopsy for diagnosing neurodegeneration using autopsy-confirmed cases
Venneti, S., Robinson, J. L., Roy, S., White, M. T., Baccon, J., Xie, S. X., & Trojanowski, J. Q. (2011) · Acta Neuropathologica · doi:10.1007/s00401-011-0880-5 · Cited by 17
Self-citationIwase, T., Yoshida, M., Hashizume, Y., et al. (2018) · Neuropathology · doi:10.1111/neup.12518 · Cited by 16
“There were low Alzheimer’s disease neuropathologic changes and argyrophilic grains.(5) The density of the senile plaques was graded as Consortium to Establish a Registry”
BackgroundYang, Q., Chen, K., Zhang, H., Zhang, W., Gong, C., Zhang, Q., Liu, P., Sun, T., Xu, Y., Qian, X., et al. (2019) · Neuroscience Bulletin · doi:10.1007/s12264-019-00343-2 · Cited by 17
Koss, D. J., Bondarevaite, O., Adams, S., et al. (2020) · Brain Pathology · doi:10.1111/bpa.12890 · Cited by 16
“The final clinico-pathological diagnoses were established by combining clinical data and neuropathological diagnoses, which were based on assessment of brain tissue according to the National Institute of Aging––Alzheimer’s Association (NIA-AA) criteria (24), including Braak NFT staging (3), Thal phases (32) and Consor…”
MethodBuciuc, M., Whitwell, J. L., Baker, M., Rademakers, R., Dickson, D. W., & Josephs, K. A. (2021) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12727 · Cited by 16
Self-citationCharacterization of cerebellar amyloid-β deposits in Alzheimer disease
Lopez, G., Magaki, S., Williams, C. K., Paganini‐Hill, A., & Vinters, H. V. (2023) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlad107 · Cited by 15
“Cerebellar amyloid-b (A b ) deposits are diagnostic criteria for Thal phase 5 and fulfill criteria for an A3 score in the National Institute on Aging-Alzheimer ’ s Association (NIA-AA) ABC scoring system for evaluating Alzheimer disease (AD) neuro-pathologic change (1 – 4).”
BackgroundSelf-citationFixemer, S., de la Maza, M. M., Hammer, G. P., Jeannelle, F., Schreiner, S., Gérardy, J., Boluda, S., Mirault, D., Mechawar, N., Mittelbronn, M. G. A., et al. (2025) · Acta Neuropathologica · doi:10.1007/s00401-025-02857-8 · Cited by 22
“The neuropathological diagnosis was performed by brain bank intern neuropathologists following Braak [12], ABC staging [60] and McKeith staging criteria [56] based on Aβ plaques, NFTs and α-synuclein.”
Morderer, D., Wren, M. C., Liu, F., Kouri, N., Maistrenko, A., Khalil, B., Pobitzer, N., Salemi, M., Phinney, B. S., Bu, G., et al. (2025) · Molecular Neurodegeneration · doi:10.1186/s13024-025-00817-0 · Cited by 21
Self-citationCommon neuropathologic change drivers of hippocampal sclerosis of ageing
Woodworth, D. C., Lou, J., Yong, W. H., Head, E., Corrada, M. M., Nelson, P. T., & Sajjadi, S. A. (2025) · Brain · doi:10.1093/brain/awaf158 · Cited by 16
“29,30 Variables that followed staging schemes included ADNC (none/low/intermediate/high), A score (obtained by binning the Thal phase of amyloid into four categories of 0, 1–2, 3 and 4–5, B score (obtained by binning Braak neurofibrillary tangle stages into four categories of 0, I–II, III–IV and…”
Self-citationGawor, K., Verrept, S., Arekatla, G., Wouters, D., Ronisz, A., Hecht, M., Laureyssen, C., Donck, H. V., Lahaije, B., Ospitalieri, S., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70483 · Cited by 18
Self-citationCognitive and neuropsychological trajectories in patients with mixed neurodegenerative pathologies
Almeida, F., Marx, G. A., Rohde, S. K., Gonzales, M. M., Maldonado‐Díaz, C., Hiya, S., Clare, K. M., Samanamud, J. L., Slocum, C., Kauffman, J., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70575 · Cited by 15
“9,10,34,35,46,47 Cases included as various combinationsofADNC,LATE,LBD,andCVDwereselectedexclusively from cases with sufficient available data to stage all four of these neuropathologic variables.”
Chen, C., Maner-Smith, K. M., Khadka, M., Ahn, J. Y., Gulbin, X. L., Ivanova, A., Dammer, E. B., Seyfried, N. T., Bennett, D. A., Hajjar, I. M., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-64328-8 · Cited by 19
“Pathological diagnosis was ascertained based on a standardized classi fi cation system utilizing semi-quantitative histo-pathological assessments of A β plaques and tau neuro fi brillary tangles 87 .”
The Role of Amyloid- and Tau PET in the New Era of Alzheimer Disease Therapies
Chiotis, K., Wang, Y., Joie, R. L., & Rabinovici, G. D. (2025) · Journal of Nuclear Medicine · doi:10.2967/jnumed.124.268339 · Cited by 18
“Early neuropathologic studies mapped the regional spread of A b and NFTs across brain areas, establishing staging schemes ( 2 , 3 ) that remain central to AD neuropatho-logic diagnosis ( 4 ).”
Braak neurofibrillary tangle staging prediction from in vivo MRI metrics
Dallaire‐Théroux, C., Beheshti, I., Potvin, O., Dieumegarde, L., Saïkali, S., Duchesne, S., & Initiative, A. D. N. (2019) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1016/j.dadm.2019.07.001 · Cited by 16
“, mid-frontal, superior/middle temporal, inferior parietal, occipital, entorhinal and hippocampus; as described in the study by Montine et al [2]) were stained with tau or phosphorylated-tau antibodies or silverbased histochemistry and assessed for Braak NFT staging as described earlier.”
MethodResultInfluentialEarly Dendritic Dystrophy in Human Brains With Primary Age-Related Tauopathy
Shi, Y., Tu, T., Jiang, J., Zhang, Q., Ai, J.-Q., Pan, A., Manavis, J., Tu, E., & Yan, X. (2020) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2020.596894 · Cited by 14
“Specifically, AD-type lesions (if present) were scored following an examination of the sections from various brain regions according to the National Institutes of Health guideline (Jellinger and Bancher, 1998; Braak et al., 2006; Montine et al., 2012).”
MethodCharcot–Bouchard aneurysms revisited: clinicopathologic correlations
Magaki, S., Chen, Z., Haeri, M., Williams, C. K., Khanlou, N., Yong, W. H., & Vinters, H. V. (2021) · Modern Pathology · doi:10.1038/s41379-021-00847-1 · Cited by 17
Self-citationAlpha adaptins show isoform‐specific association with neurofibrillary tangles in Alzheimer's disease
Srinivasan, S., Gál, J., Bachstetter, A. D., & Nelson, P. T. (2021) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12776 · Cited by 15
“The neuropathological hallmarks of LOAD are extracellular amyloid-β (Aβ) plaques, and neurofibrillary tangles (NFTs) composed of intracellular tau protein aggregates.(1) Although much has been learnt about Aβ plaques and NFTs, we lack a complete understanding of the cellular pathways that contribute to and react to th…”
BackgroundSelf-citationKothapalli, S. V. V. N., Benzinger, T. L. S., Aschenbrenner, A. J., Perrin, R. J., Hildebolt, C. F., Goyal, M. S., Fagan, A. M., Raichle, M. E., Morris, J. C., & Yablonskiy, D. A. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210503 · Cited by 15
Tremblay, C., Serrano, G. E., Intorcia, A. J., Mariner, M., Sue, L. I., Arce, R. A., Atri, A., Adler, C. H., Belden, C. M., Shill, H. A., et al. (2022) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlac042 · Cited by 15
Self-citationSilva‐Rodríguez, J., Labrador‐Espinosa, M. Á., Moscoso, A., Schöll, M., Mir, P., Grothe, M. J., & Initiative, A. D. N. (2022) · Journal of Nuclear Medicine · doi:10.2967/jnumed.122.264213 · Cited by 15
Identification of a Putative α-synuclein Radioligand Using an in silico Similarity Search
Janssen, B., Tian, G., Lengyel‐Zhand, Z., Hsieh, C., Lougee, M. G., Riad, A., Xu, K., Hou, C., Weng, C.-C., Lopresti, B. J., et al. (2023) · Molecular Imaging and Biology · doi:10.1007/s11307-023-01814-9 · Cited by 14
“…were dissected from 1-cm-thick coronal slices taken at autopsy and frozen at -80°C or fixed in formalin for extensive histological and immunohistochemistry examinations using established AD and PD neuropathological criteria to ensure the absence of potentially confounding co-pathologies [34, 35].”
MethodJellinger, K. A. (2023) · Journal of Neural Transmission · doi:10.1007/s00702-023-02660-3 · Cited by 17
Illustrated Neuropathologic Diagnosis of Alzheimer’s Disease
Doher, N., Davoudi, V., Magaki, S., Townley, R. A., Haeri, M., & Vinters, H. V. (2023) · Neurology International · doi:10.3390/neurolint15030054 · Cited by 16
“Intermediate or High better justify the AD diagnosis for clinical dementia [38].”
BackgroundMethodInfluentialSelf-citationIchimata, S., Martínez-Valbuena, I., Lee, S., Li, J., Karakani, A. M., & Kovács, G. G. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241411596 · Cited by 15
“Based on the results, the level of AD neuropathological change was categorized into four groups (not, low, intermediate, and high) using the National Institute on Aging-Alzheimer’s Association (NIA-AA) guidelines [69].”
MethodPonce-López, T., Tostado, J. A. G. Á., Dias, F., & Maltez, K. H. M. (2023) · Biomolecules · doi:10.3390/biom13091289 · Cited by 16
“It is susceptible to neurofibrillary tangles and Aβ deposition [53], which may induce neurotoxicity and can result in increased microglial activity linked to hippocampal atrophy and neuroinflammation in AD [54].”
BackgroundBei, J., Miranda-Morales, E. G., Gan, Q., Qiu, Y., Husseinzadeh, S., Liew, J. Y., Chang, Q., Krishnan, B., Gaitas, A., Yuan, S., et al. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230347 · Cited by 18
Tsering, W., Hery, G. P., Phillips, J. L., Lolo, K., Bathe, T., Villareal, J. A. B., Ruan, I. Y., & Prokop, S. (2023) · Acta Neuropathologica Communications · doi:10.1186/s40478-023-01688-6 · Cited by 15
“Both phosphorylated tau (p-tau) antibody staining and Gallyas silver staining are currently used to visualize NP [50, 72].”
MethodParadela, R. S., Justo, A. F. O., Paes, V. R., Leite, R. E. P., Pasqualucci, C. A., Grinberg, L. T., Naslavsky, M. S., Zatz, M., Nitríni, R., Filho, W. J., et al. (2023) · Acta Neuropathologica Communications · doi:10.1186/s40478-023-01681-z · Cited by 16
“In addition, although our Biobank has implemented the ABC scoring system for the neuropathologic assessment of AD [45], most cases included in this study did not have this information.”
MethodTaghdiri, F., Khodadadi, M., Sadia, N., Mushtaque, A., Scott, O. F. T., Hirsch‐Reinshagen, V., Tator, C. H., Wennberg, R. A., Kovács, G. G., & Tartaglia, M. C. (2024) · European Journal of Neurology · doi:10.1111/ene.16259 · Cited by 16
“The neuropathological diagnoses were based on the consensus neuropathological criteria provided by consensus studies for CTE [15, 16 ], AD [ 24], LBD [25], corticobasal degeneration (CBD) [26], PSP [27 ], argyrophilic grain disease (AGD) [28], ageing-related tau astrogliopathy [29 ], primary…”
MethodCorrelation of Presynaptic and Postsynaptic Proteins with Pathology in Alzheimer’s Disease
Serrano, G. E., Walker, J. E., Nelson, C. M., Glass, M. J., Arce, R. A., Intorcia, A. J., Cline, M. P., Nabaty, N. L., Acuña, A. M., Steed, A. H., et al. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25063130 · Cited by 15
“AD pathology was assessed according to the National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease (NIA-AA) [39].”
Self-citationDetecting the effect of genetic diversity on brain composition in an Alzheimer’s disease mouse model
Gurdon, B., Yates, S. C., Csucs, G., Groeneboom, N. E., Hadad, N., Telpoukhovskaia, M., Ouellette, A., Ouellette, T., O’Connell, K. M. S., Singh, S., et al. (2024) · Communications Biology · doi:10.1038/s42003-024-06242-1 · Cited by 15
“AD inducesdetrimental changesinbrain composition 16 ; therefore, changes in gene expression in bulk tissue may be masked or confounded by changes in cell-type composition across varying disease stages 17 .”
Martá-Ariza, M., Leitner, D. F., Kanshin, E., Suazo, J., Giusti Pedrosa, A., Thierry, M., Lee, E. B., Devinsky, O., Drummond, E., Fortea, J., et al. (2025) · Acta Neuropathologica · doi:10.1007/s00401-025-02844-z · Cited by 15
Liou, J., Lou, J. J., Aguilar, L. F., Nakagiri, J., Yong, W. H., Hom, C. L., Doran, E. W., Totoiu, M. O., Lott, I. T., Mapstone, M. E., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.14479 · Cited by 16
Ehrenberg, A. J., Sant, C., Pereira, F. L., Li, S. H., Buxton, J., Langlois, S., Trinidad, M. I., Oh, I. M., Leite, R. E. P., Rodriguez, R. D., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70087 · Cited by 16
Berger–Sieczkowski, E., Milenković, I., Venkataramani, V., Giera, R., Ströbel, T., Höftberger, R., Liberski, P. P., Auff, E., Wirths, O., Bayer, T. A., et al. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-141524 · Cited by 16
Challenges in the Neuropathological Diagnosis of Dementias
Jellinger, K. A. (2012) · International Journal of Neuropathology · doi:10.7726/ijn.2013.1002 · Cited by 15
“Histopathological examination of the brain establishes that AD-related lesions are present in sufficient densities to distinguish AD from age-related lesions and allows detection of other dementing disorders (Duyckaerts et al., 2009; Hyman et al., 2012; Montine et al., 2012).”
BackgroundMethodInfluentialLam, B., Khan, A., Keith, J. L., Rogaeva, E. A., Bilbao, J. M., George‐Hyslop, P. S., Ghani, M., Freedman, M., Stuss, D. T., Chow, T. W., et al. (2016) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2016.08.014 · Cited by 15
“These findings were consistent with a diagnosis of Alzheimer’s disease (A3B3C3) [22].”
BackgroundResultHe, B., Zheng, M., Liu, Q., Shi, Z., Long, S., Lu, X.-L., Pei, Z., Yuan, T., Su, H., & Yao, X. (2017) · Molecular Neurobiology · doi:10.1007/s12035-017-0446-1 · Cited by 16
Tan, R. H., Yang, Y., & Halliday, G. M. (2017) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12455 · Cited by 14
Alafuzoff, I. I. (2018) · Handbook of clinical neurology · doi:10.1016/b978-0-444-63639-3.00010-4 · Cited by 15
Aβ and the dementia syndrome: Simple versus complex perspectives
Hunter, S., Smailagic, N., & Brayne, C. (2018) · European Journal of Clinical Investigation · doi:10.1111/eci.13025 · Cited by 15
Neuroimaging of Diseases Causing Dementia
Masdeu, J. C. (2019) · Neurologic Clinics · doi:10.1016/j.ncl.2019.08.003 · Cited by 16
Klotz, S., Fischer, P. A., Hinterberger, M., Ricken, G., Hönigschnabl, S., Gelpí, E., & Kovács, G. G. (2020) · Neuropathology · doi:10.1111/neup.12708 · Cited by 15
“Overall, Alzheimer’s disease neuropathological change corresponded to an intermediate severity score (A2B2C2) according to current NIA/AA criteria.(32) Phosphorylated TDP-43 immunoreactivity was extensive and consisted of a high density of fine neuropil threads, compact and more frequently diffuse granular or dash-lik…”
BackgroundKelly, S. C., Nelson, P. T., & Counts, S. (2021) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlab017 · Cited by 15
Self-citationPhilbert, S. A., Xu, J., Unwin, R. D., Dowsey, A. W., & Cooper, G. J. S. (2021) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2021.02.107 · Cited by 15
Grekhnev, D. A., Kaznacheyeva, E. V., & Vigont, V. A. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23020624 · Cited by 16
“The neuropathological hallmarks of AD are amyloid aggregates, hyperphosphorylation of the tau protein, and neurofibrillary tangles [92,96].”
BackgroundEttema, L., Lochocki, B., Hoozemans, J. J. M., de Boer, J. F., & Ariese, F. (2022) · Journal of Optics · doi:10.1088/2040-8986/ac5b51 · Cited by 15
“• Furthermore, in contrast to the blue excitation used in the mentioned study, a different study conducted by Thal et al [11] used UV light instead of blue light for excitation, leading to blue light being emitted by the plaque.”
MethodMazumder, S., Kiernan, M. C., Halliday, G. M., Timmins, H. C., & Mahoney, C. (2022) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12845 · Cited by 14
A novel histological staging of hippocampal sclerosis that is evident in gray matter loss in vivo
Ortega‐Cruz, D., Uceda‐Heras, A., Iglesias, J. E., Zea‐Sevilla, M. A., Strange, B. A., & Rábano, A. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.12942 · Cited by 16
Hippocampal sclerosis of aging at post‐mortem is evident on MRI more than a decade prior
Ortega‐Cruz, D., Iglesias, J. E., Rábano, A., & Strange, B. A. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.13352 · Cited by 16
“Probability (0-3) of Alzheimer’s Disease Neuropathological Change (ADNC) was assessed based on National Institute on Aging (NIA) guidelines [29], including Thal Aβ stage, Braak stage, .”
Leino, M., Popova, S. N., & Alafuzoff, I. I. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-170192 · Cited by 15
On the origin of tau seeding activity in Alzheimer’s disease
Heinsen, H., & Grinberg, L. T. (2018) · Acta Neuropathologica · doi:10.1007/s00401-018-1890-3 · Cited by 15
The presubiculum is preserved from neurodegenerative changes in Alzheimer’s disease
Murray, C. E., Gami‐Patel, P., Gkanatsiou, E., Brinkmalm, G., Portelius, E., Wirths, O., Heywood, W., Blennow, K., Ghiso, J. A., Holton, J. L., et al. (2018) · Acta Neuropathologica Communications · doi:10.1186/s40478-018-0563-8 · Cited by 15
“The criteria for the neuropathological diagnosis of FBD and FDD have been previously described [30, 31] while for that of AD standard diagnostic criteria were used [9, 52, 74].”
MethodTripathy, A., Shade, A., Erskine, B., Bailey, K., Grande, A. J., deLong, J. J., Perry, G. L., & Castellani, R. J. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-181039 · Cited by 16
“Although specific sampling and immunohistochemistry protocols are subject to change, the assessments generally followed the 2016 NINDS/NIBIB recommendations for CTE diagnosis [21] and modified NIA-AA 2012 consensus guidelines for assessment of AD neuropathologic change [22].”
Transcriptome-wide piRNA profiling in human brains for aging genetic factors.
Mao, Q., Fan, L., Wang, X., Lin, X., Cao, Y., Zheng, C., Zhang, Y., Zhang, H., García-Milian, R., Kang, L., et al. (2019) · PubMed · Cited by 15
Yang, K. Y., Chen, G., Sheng, C., Xie, Y., Li, Y., Hu, X., Sun, Y., & Han, Y. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-200082 · Cited by 16
“) plaques and neu-rofibrillary tangles [2, 3].”
Atomic-level differences between brain parenchymal- and cerebrovascular-seeded Aβ fibrils
Scherpelz, K. P., Wang, S., Pytel, P., Madhurapantula, R. S., Srivastava, A. K., Sachleben, J. R., Orgel, J., Ishii, Y., & Meredith, S. C. (2021) · Scientific Reports · doi:10.1038/s41598-020-80042-5 · Cited by 12
Neuropathological Correlates of White Matter Hyperintensities in Cerebral Amyloid Angiopathy
Makkinejad, N., Zotin, M. C. Z., van den Brink, H., Auger, C. A., Eigen, K. A. V., Iglesias, J. E., Greenberg, S. M., Perosa, V., & van Veluw, S. J. (2024) · Journal of the American Heart Association · doi:10.1161/jaha.124.035744 · Cited by 14
Bermudez, C. L., Syrjanen, J. A., Stricker, N. H., Algeciras‐Schimnich, A., Kouri, N., Kremers, W. K., Petersen, R. C., Jack, C. R., Knopman, D. S., Dickson, D. W., et al. (2025) · The Journal of Prevention of Alzheimer s Disease · doi:10.1016/j.tjpad.2025.100224 · Cited by 15
“According to the National Institute on Aging Alzheimer’s Association (NIA-AA) criteria [ 20 , 34 ], we ascertained ADNC by describing (A) Thal amyloid phase for the distribution of A 𝛽 plaques [ 35 ], (B) Braak tangle stage [ 36 ], and (C) CERAD neuritic plaque score [ 33 ].”
Self-citationTong, Q., & Chen, L. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210114 · Cited by 14
“Independently of clinical diagnoses, all cases were subjected to a standardized neuropathological assessment using international neuropathological criteria including neuritic Braak stages [11], Thal amyloid phases [12], CERAD scores [13], NIA-AA scores [14], and McKeith criteria [8].”
Kon, T., Mori, F., Tanji, K., et al. (2022) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlac015 · Cited by 14
Scambray, K. A., Nguyen, H. L., & Sajjadi, S. A. (2023) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlad020 · Cited by 14
Heylen, A., Vermeiren, Y., Kema, I. P., van Faassen, M. H. J. R., van der Ley, C., Dam, D. V., & Deyn, P. P. D. (2023) · Pharmaceuticals · doi:10.3390/ph16040615 · Cited by 16
Characteristics of amnestic patients with hypometabolism patterns suggestive of Lewy body pathology
Silva‐Rodríguez, J., Labrador‐Espinosa, M. Á., Moscoso, A., Schöll, M., Mir, P., Grothe, M. J., & Initiative, A. D. N. (2023) · Brain · doi:10.1093/brain/awad194 · Cited by 14
“7 Patients were considered to have autopsy-confirmed Alzheimer’s disease when presenting intermediate or high ADNC, 23 and the presence of Lewy body neuropathological changes (LBNC) was denoted when Lewy bodies were present in limbic or neocortical regions or the amygdala.”
Localized proteomic differences in the choroid plexus of Alzheimer's disease and epilepsy patients
Leitner, D., Kanshin, E., Faustin, A., Thierry, M., Friedman, D. J., Devore, S., Ueberheide, B. M., Devinsky, O., & Wısnıewskı, T. (2023) · Frontiers in Neurology · doi:10.3389/fneur.2023.1221775 · Cited by 17
“For AD cases (n= 8), the inclusion criteria were those cases with severe AD pathology as indicated by the neuropathology score A3B3C3 (69) and part of the NYU ADRC, which allowed for age matching to the other groups.”
MethodNeuropathologic Changes of Alzheimer’s Disease and Related Dementias: Relevance to Future Prevention
White, L. R., Corrada, M. M., Kawas, C. H., Cholerton, B., Edland, S. E., Flanagan, M. E., & Montine, T. J. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230331 · Cited by 13
Self-citationDeep learning for risk-based stratification of cognitively impaired individuals
Romano, M. F., Zhou, X., Balachandra, A. R., Jadick, M. F., Qiu, S., Nijhawan, D. A., Joshi, P. S., Mohammad, S., Lee, P. H., Smith, M. J., et al. (2023) · iScience · doi:10.1016/j.isci.2023.107522 · Cited by 13
Katanga, J., Hamilton, C. A., Walker, L., Attems, J., & Thomas, A. J. (2023) · Brain Pathology · doi:10.1111/bpa.13188 · Cited by 14
“These separate classifiers were then combined in accordance with the NIA-AA criteria as ‘ none ’ , ‘ low ’ , ‘ intermediate ’ or ‘ high ’ level of AD neuropathological change [29].”
MethodLongitudinal hippocampal atrophy in hippocampal sclerosis of aging
Li, J. X., Nguyen, H. L., Qian, T., Woodworth, D. C., & Sajjadi, S. A. (2023) · Aging Brain · doi:10.1016/j.nbas.2023.100092 · Cited by 14
“3 likelihood ADNC based on NIA-AA criteria, and LATE-NC was defined as positive if TDP-43 was present in the hippocampus, entorhinal/inferior temporal cortex, or the neocortex [1,12,13].”
Su, H., Masters, C. L., Bush, A. I., Barnham, K. J., Reid, G. E., & Vella, L. J. (2023) · PROTEOMICS · doi:10.1002/pmic.202300063 · Cited by 13
“Pathophysiological assessments include the detection of biomarkers, mainly A β 40, A β 42, total tau and phosphorylated tau (p-tau) species in CSF and blood, and imaging (PET and MRI) [136–142].”
Background
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.)
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.
A language model drew the claims from the paper on 2026-10-18, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-18 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
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 ›
Are you an author, or do you see a problem with this page? Request a review
