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 1,201–1,300 of 2,854
Memory Resilience in Alzheimer Disease With Primary Progressive Aphasia
Mesulam, M. M., Coventry, C., Kuang, A., Bigio, E. H., Mao, Q., Flanagan, M. E., Gefen, T. D., Sridhar, J., Geula, C., Zhang, H., et al. (2021) · Neurology · doi:10.1212/wnl.0000000000011397 · Cited by 23
Self-citationPoloni, T. E., Moretti, M., Medici, V., Turturici, E., Belli, G., Cavriani, E., Visonà, S. D., Rossi, M., Fantini, V., Ferrari, R. R., et al. (2022) · Cells · doi:10.3390/cells11193124 · Cited by 24
“Alzheimer’s Disease (AD) severity was assessed on sections immunostained with antibodies against beta-amyloid (4G8, monoclonal antibody, BioLegend San Diego, CA, USA; 1:1000) and phospho-tau (AT8, monoclonal antibody, clone MN1020, Thermo Fisher Scientific Waltham, MA, USA; 1:200) and defined according to Montine’s sc…”
MethodUchida, Y., Onda, K., Hou, Z., Troncoso, J. C., Mori, S., & Oishi, K. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230452 · Cited by 23
“The diagnosis was made based on the National Institute on Aging and Alzheimer’s Association (NIA-AA) guidelines for the neuropathologic assessment of AD [17].”
MethodIoannou, K., Bucci, M., Tzortzakakis, A., Savitcheva, I., Nordberg, A. K., Chiotis, K., & Initiative, A. D. N. (2024) · Molecular Psychiatry · doi:10.1038/s41380-024-02672-9 · Cited by 35
“Evidence from autopsy studies has suggested that isolated tau accumulation in the medial temporal lobe is a common fi nding in CU elderly [50] and is not associated with a neuropathological AD diagnosis even in the presence of A β pathology [76].”
McAleese, K. E., Firbank, M., Hunter, D., Sun, L., Hall, R., Neal, J., Mann, D. M. A., Esiri, M. M., Jellinger, K. A., O'Brien, J. T., et al. (2012) · Neuropathology and Applied Neurobiology · doi:10.1111/j.1365-2990.2012.01310.x · Cited by 24
Niemantsverdriet, E., Goossens, J., Struyfs, H., Martin, J., Goeman, J., Deyn, P. P. D., Vanderstichele, H., & Engelborghs, S. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-150953 · Cited by 23
Lloyd, G. M., Trejo‐Lopez, J. A., Xia, Y., McFarland, K. N., Lincoln, S., Ertekin‐Taner, N., Giasson, B. I., Yachnis, A. T., & Prokop, S. (2020) · Acta Neuropathologica Communications · doi:10.1186/s40478-020-0891-3 · Cited by 24
“Neuropathological hallmarks of AD include extracellular deposits of beta-Amyloid (Aβ), intracellular deposits of neurofibrillary tangles (NFT) and neuron loss [35].”
InfluentialAlzheimer-related genes show accelerated evolution
Nitsche, A., Arnold, C., Ueberham, U., Reiche, K., Fallmann, J., Hackermüller, J., Horn, F., Stadler, P. F., & Arendt, T. (2020) · Molecular Psychiatry · doi:10.1038/s41380-020-0680-1 · Cited by 25
Phosphorylated Aβ peptides in human Down syndrome brain and different Alzheimer’s-like mouse models
Kumar, S., Lemere, C. A., & Walter, J. (2020) · Acta Neuropathologica Communications · doi:10.1186/s40478-020-00959-w · Cited by 24
Ascorbate deficiency decreases dopamine release in gulo–/– and APP/PSEN1 mice
Consoli, D. C., Brady, L. J., Bowman, A. B., Calipari, E. S., & Harrison, F. E. (2020) · Journal of Neurochemistry · doi:10.1111/jnc.15151 · Cited by 23
Multimodal in vivo and postmortem assessments of tau in Lewy body disorders
Coughlin, D. G., Phillips, J. S., Roll, E. E., Peterson, C. S., Lobrovich, R., Rascovsky, K., Ungrady, M. B., Wolk, D. A., Das, S. R., Weintraub, D. A., et al. (2020) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2020.08.003 · Cited by 23
Self-citationMolina‐Martínez, P., Corpas, R., García-Lara, E., Cosín‐Tomás, M., Cristòfol, R. M., Kaliman, P., Solà, C., Molinuevo, J. L., Sánchez‐Valle, R., Antonell, A., et al. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2020.622360 · Cited by 24
Gu, Y., Kociolek, A. J., Fernández, K. K., Cosentino, S., Zhu, C. W., Jin, Z., Leverenz, J. B., & Stern, Y. (2022) · Neurology · doi:10.1212/wnl.0000000000200259 · Cited by 24
“), and staging of AD and Lewy body pathology as outlined in the National Institute on Aging–Alzheimer’s Association pathologic assessment of AD and Lewy body disease.(39) For this study, an AD pathologic diagnosis required both a staging of moderate or frequent neuritic plaques (Consortium to Establish a Registry for…”
MethodEdler, M. K., Munger, E. L., Maycon, H., Hopkins, W. D., Hof, P. R., Sherwood, C. C., & Raghanti, M. A. (2023) · Journal of Neuroscience Research · doi:10.1002/jnr.25167 · Cited by 23
Teipel, S. J., & Grothe, M. J. (2023) · Neurobiology of Disease · doi:10.1016/j.nbd.2023.106070 · Cited by 23
“The neuropathological procedures in ADNI and NACC follow previously established guidelines (Montine et al., 2012) that are captured in the format of the NACC Neuropathology Data Form Version 10 (https://www.alz.washington.edu/NONMEMBER/ BF 10 = 0.071.”
InfluentialDams-O’Connor, K., Awwad, H. O., Hoffman, S. W., Pugh, M. J., Johnson, V. E., Keene, C. D., McGavern, L. M., Mukherjee, P., Opanashuk, L. A., Umoh, N., et al. (2023) · Journal of Neurotrauma · doi:10.1089/neu.2022.0514 · Cited by 23
Aging, Plasminogen Activator Inhibitor 1, Brain Cell Senescence, and Alzheimer's Disease.
Jiang, C., Rana, T., Jin, L., Farr, S. A., Morley, J. E., Qin, H., Liu, G., & Liu, R.-M. (2023) · PubMed Central · doi:10.14336/ad.2022.1220 · Cited by 23
“The subjects had been well characterized by clinical, neuroimaging, neuropsychiatric, and post-mortem neuropathological analyses as: 1) those diagnosed with LOAD with high AD neuropathological changes (Braak stage V or VI, CERAD score 2 or 3, Thal phase 4 or 5) according to the current NIA-AA guidelines [28, 29]; 2) A…”
MethodChai, Y. L., Lee, J. H., Chong, J. R., Ballard, C. G., Francis, P. T., Kennedy, B. K., Arumugam, T. V., Chen, C., Aarsland, D., & Lai, M. K. P. (2023) · Journal of Neuroinflammation · doi:10.1186/s12974-023-02789-8 · Cited by 27
“Neuropathological diagnoses were based on Thal Aβ phases [18], neurofibrillary tangle Braak stages [19] and CERAD criteria for AD [17] which are all combined in the National Institute on Aging—Alzheimer’s Association guidelines [20] and the Newcastle/McKeith criteria for Lewy body disease [16].”
MethodLi, K., Rashid, T., Li, J., Honnorat, N., Nirmala, A. B., Fadaee, E., Wang, D., Charisis, S., Liu, H., Franklin, C. G., et al. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230389 · Cited by 25
“Microscopic sections are prepared from 23 brain regions according to NIA Alzheimer’s Association guidelines [35].”
MethodClinicopathologic Heterogeneity and Glial Activation Patterns in Alzheimer Disease
Kouri, N., Frankenhauser, I., Peng, Z., Labuzan, S. A., Boon, B. D. C., Moloney, C. M., Pottier, C. P., Wickland, D. P., Caetano-Anollés, K., Corriveau‐Lecavalier, N., et al. (2024) · JAMA Neurology · doi:10.1001/jamaneurol.2024.0784 · Cited by 26
Self-citationStefanits, H., Wesseling, C., & Kovács, G. G. (2014) · Neuroscience Letters · doi:10.1016/j.neulet.2014.02.026 · Cited by 23
Cerebrospinal fluid markers detect Alzheimer's disease in nonamnestic dementia
Oboudiyat, C., Gefen, T. D., Varelas, E. A., Weıntraub, S., Rogalski, E. J., Bigio, E. H., & Mesulam, M. M. (2017) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2017.01.006 · Cited by 22
“The AD pathologic scores are based on the National Institute on Aging-Alzheimer’s Association (NIA-AA) criteria for the diagnosis of AD, and all patients diagnosed with AD on autopsy had scores of A3, B3, and C3 [6].”
MethodSelf-citationRiku, Y., Watanabe, H., Mimuro, M., Iwasaki, Y., Ito, M., Katsuno, M., Sobue, G., & Yoshida, M. (2017) · Journal of Neurology · doi:10.1007/s00415-017-8604-y · Cited by 23
Liu, C. Y., Ohki, Y., Tomita, T., Osawa, S., Reed, B., Jagust, W. J., Berlo, V. V., Jin, L., Chui, H. C., Coppola, G., et al. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-161203 · Cited by 23
Multiple biomarkers improve diagnostic accuracy across Lewy body and Alzheimer's disease spectra
Plastini, M. J., Ruiz, C. A., Young, C. B., Wilson, E. N., Shahid, M., Lamoureux, J., Andreasson, K. I., Kerchner, G. A., Montine, T. J., Henderson, V. W., et al. (2024) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.52034 · Cited by 23
Self-citationAmbient Air Pollution and the Severity of Alzheimer Disease Neuropathology
Kim, B., Blam, K., Elser, H. C., Xie, S. X., Deerlin, V. M. V., Penning, T. M., Weintraub, D. A., Irwin, D. J., Massimo, L. M., McMillan, C. T., et al. (2025) · JAMA Neurology · doi:10.1001/jamaneurol.2025.3316 · Cited by 25
Abner, E. L., Schmitt, F. A., Nelson, P. T., Lou, W., Wan, L., Gauriglia, R., Dodge, H. H., Woltjer, R. L., Yu, L., Bennett, D. A., et al. (2015) · Observational Studies · doi:10.1353/obs.2015.0003 · Cited by 22
“Yet, because of the expense and difficulty of following participants to death and obtaining a brain autopsy, most large dementia risk factor cohort studies Abner et al. are based entirely or primarily on clinical diagnosis (Bienias et al., 2003; Fratiglioni et al., 2007; Montine et al., 2012a).”
BackgroundMethodInfluentialSelf-citationRossi, M., Kai, H., Baiardi, S., Bartoletti‐Stella, A., Carlà, B., Zenesini, C., Capellari, S., Kitamoto, T., & Parchi, P. (2019) · Acta Neuropathologica Communications · doi:10.1186/s40478-019-0706-6 · Cited by 24
López, O. L., Chang, Y., Ives, D. G., Snitz, B. E., Fitzpatrick, A. L., Carlson, M. C., Rapp, S. R., Williamson, J. D., Tracy, R. P., DeKosky, S. T., et al. (2019) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2019.04.008 · Cited by 22
MRI and flortaucipir relationships in Alzheimer's phenotypes are heterogeneous
Josephs, K. A., Tosakulwong, N., Graff‐Radford, J., Weigand, S. D., Buciuc, M., Machulda, M. M., Jones, D. T., Schwarz, C. G., Senjem, M. L., Ertekin‐Taner, N., et al. (2020) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.51038 · Cited by 22
“Alzheimer’s disease is a pathological entity characterized by the presence of beta-amyloid and tau immunoreactive plaques and neurofibrillary tangles.(1,2) It is well recognized that Alzheimer’s disease can have different presenting dementia phenotypes dominated by episodic memory loss, aphasia, executive dysfunction,…”
BackgroundSegmentation of Tau Stained Alzheimers Brain Tissue Using Convolutional Neural Networks
Wurts, A. J., Oakley, D. H., Hyman, B. T., & Samsi, S. (2020) · Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC) · doi:10.1109/embc44109.2020.9175832 · Cited by 22
“Current neuropatho-logic diagnostic criteria for AD take into account the distribution of NFTs, but not the density of tau pathology, which can vary substantially between cases with the same overall distribution of tau [11].”
BackgroundSelf-citationKaranth, S. D., Schmitt, F. A., Nelson, P. T., Katsumata, Y., Kryscio, R. J., Fardo, D. W., Harp, J. P., & Abner, E. L. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210293 · Cited by 22
Self-citationGlobal cognitive trajectory patterns in Alzheimer’s disease
Cohen, C. I., Reisberg, B., & Yaffee, R. (2022) · International Psychogeriatrics · doi:10.1017/s1041610222000047 · Cited by 22
“…for the presence of intermediate or high scores on the National Institute on Aging – Alz-heimer ’ s Association AD Neuropathologic Change criteria ( “ ABC score ” ); (Montine et al ., 2012); this difference between AD groups did not attain statistical signi fi cance ( χ 2 = 2.60, df = 1, p = .11).”
BackgroundInfluentialBossaerts, L., Hens, E., Cacace, R., Asselbergh, B., & Broeckhoven, C. V. (2022) · Acta Neuropathologica Communications · doi:10.1186/s40478-022-01346-3 · Cited by 21
“[68] d Scoring for meningeal and parenchymal CAA: 0, no CAA; 1, scant beta amyloid deposition; 2, some circumferential beta amyloid; 3, widespread circumferential beta amyloid, according to Love et al.”
BackgroundTheofilas, P., Piergies, A. M. H., Oh, I. M., Lee, Y. B., Li, S. H., Pereira, F. L., Petersen, C., Ehrenberg, A. J., Eser, R. A., Ambrose, A. J., et al. (2022) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12819 · Cited by 22
“All brains underwent standardised neuropathological assessment for neurodegenerative diseases that follow universally accepted guidelines [22,23].”
BackgroundGelpí, E., Baiardi, S., Nos, C., Dellavalle, S., Aldecoa, I., Ruiz‐García, R., Ispierto, L., Escudero, D., Casado, V., Barranco, E., et al. (2022) · Acta Neuropathologica Communications · doi:10.1186/s40478-022-01415-7 · Cited by 25
“2012 [17] (A for amyloid-phase 0–3; B for Braak neurofibrillary stage 0–3; C for CERAD neuritic plaque score 0–3)”
BackgroundThe Spectrum of Alzheimer-Type Pathology in Cognitively Normal Individuals
Walker, J. M., Dehkordi, S. K., Schaffert, J., Goette, W. F., White, C. L., Richardson, T. E., & Zare, H. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220898 · Cited by 26
circRNA from APP Gene Changes in Alzheimer’s Disease Human Brain
Urdánoz‐Casado, A., de Gordoa, J. S., Robles, M., Roldán, M., Macías, M., Acha, B., Blanco‐Luquin, I., & Mendióroz, M. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24054308 · Cited by 23
Luo, D., Li, J., Liu, H., Wang, J., Xia, Y., Qiu, W., Wang, N., Wang, X., Wang, X., Ma, C., et al. (2023) · Advanced Science · doi:10.1002/advs.202300876 · Cited by 20
Mixed methodology in human brain research: integrating MRI and histology
Alkemade, A., Großmann, R., Bazin, P., & Forstmann, B. U. (2023) · Brain Structure and Function · doi:10.1007/s00429-023-02675-2 · Cited by 27
Jain, L., Khrestian, M., Formica, S. V., Tuason, E. D., Pillai, J. A., Rao, S. M., Oguh, O., Lippa, C. F., López, O. L., Berman, S. B., et al. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.13398 · Cited by 23
Faust, P. L., McCreary, M., Musacchio, J. B., et al. (2024) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.52068 · Cited by 22
“…marked hypoxic – ischemic damage, concurrent Alzheimer’s-type changes that would meet criteria for high likelihood of AD (NIAA-AA guidelines 34 ), or evidence of other neurodegenerative disease pathology such as progressive supranuclear palsy, corticobasal degeneration, Lewy body disease,…”
BackgroundWoodworth, D. C., Nguyen, K. M., Sordo, L., Scambray, K. A., Head, E., Kawas, C. H., Corrada, M. M., Nelson, P. T., & Sajjadi, S. A. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02728-8 · Cited by 27
“In addition to the TDP-43 pathologies listed above, we used information from other pathologies available in NACC data, assessed using standard guidelines [34, 57].”
MethodSelf-citationMelief, E. J., Cudaback, E., Jorstad, N. L., Sherfield, E., Postupna, N. O., Wilson, A. M., Darvas, M., Montine, K. S., Keene, C. D., & Montine, T. J. (2015) · Journal of Neuroscience Research · doi:10.1002/jnr.23592 · Cited by 22
“There is extensive pathological overlap between PDD and DLB, and both commonly coexist with AD pathologic changes (Montine et al., 2012).”
Self-citationGrau‐Rivera, O., Gelpí, E., Rey, M. J., et al. (2013) · Journal of Neurology · doi:10.1007/s00415-013-7101-1 · Cited by 22
Nelson, P. T., Wang, W., Wilfred, B. R., Wei, A. L., Dimayuga, J., Huang, Q., Ighodaro, E. T., Artiushin, S., & Fardo, D. W. (2015) · Journal of Neurochemistry · doi:10.1111/jnc.13202 · Cited by 22
Self-citationSandin, L., Bergkvist, L., Nath, S., Kielkopf, C. S., Janefjord, C., Helmfors, L., Zetterberg, H., Blennow, K., Li, H., Nilsberth, C., et al. (2016) · FEBS Journal · doi:10.1111/febs.13830 · Cited by 21
Regional analysis and genetic association of nigrostriatal degeneration in Lewy body disease
Kasanuki, K., Heckman, M. G., Diehl, N. N., Murray, M. E., Koga, S., Soto, A. I., Ross, O. A., & Dickson, D. W. (2017) · Movement Disorders · doi:10.1002/mds.27184 · Cited by 22
“Of the 492 LBD cases included in this study, 212 cases (43%) had intermediate-to-high AD neuropathologic change.(22) As might be expected, the frequency of comorbid AD pathology was greatest in the dementiapredominant subgroup (75%) and lower in parkinsonism1dementia (22%) and parkinsonism-predominant (9%) subgroups.”
BackgroundSelf-citationTDP-43 Neuropathologic Associations in the Nun Study and the Honolulu-Asia Aging Study
Flanagan, M. E., Cholerton, B., Latimer, C. S., Hemmy, L. S., Edland, S. D., Montine, K. S., White, L. R., & Montine, T. J. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180162 · Cited by 22
Self-citationNOTCH3 is non-enzymatically fragmented in inherited cerebral small-vessel disease
Young, K. Z., Lee, S. J., Zhang, X., Cartee, N. M. P., Torres, M., Keep, S. G., Gabbireddy, S. R., Fontana, J. L., Qi, L., & Wang, M. M. (2020) · Journal of Biological Chemistry · doi:10.1074/jbc.ra119.007724 · Cited by 22
Epigenetic regulation in the pathophysiology of Lewy body dementia
Chouliaras, L., Kumar, G. S., Thomas, A. J., Lunnon, K., Chinnery, P. F., & O'Brien, J. T. (2020) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2020.101822 · Cited by 24
Phenotypic Similarities Between Late-Onset Autosomal Dominant and Sporadic Alzheimer Disease
Day, G. S., Musiek, E. S., Roe, C. M., Norton, J. B., Goate, A., Cruchaga, C., Cairns, N. J., & Morris, J. C. (2016) · JAMA Neurology · doi:10.1001/jamaneurol.2016.1236 · Cited by 21
Self-citationLü, N., Jin, Z., Liu, N., Zhu, C., Wei, H., & Xu, Q. (2025) · Journal of Neuroinflammation · doi:10.1186/s12974-025-03546-9 · Cited by 23
“All brain samples were evaluated by the NHBBDF following the ABC score for the level of AD neuropathologic change [19].”
Amyloid and tau: neither chicken nor egg but two partners in crime!
Attems, J., & Jellinger, K. A. (2013) · Acta Neuropathologica · doi:10.1007/s00401-013-1167-9 · Cited by 21
“Only the simultaneous presence of both Aβ and moderate to severe amounts of tau pathology in a specific topographical pattern represents by internationally accepted criteria the neuropathological correlate of AD [8, 16, 19] but—as noted by Mann and Hardy—“the question as to which of these proteinaceous structures is p…”
BackgroundMid‐life and late‐life vascular risk factor burden and neuropathology in old age
Conner, S. C., Pase, M. P., Carneiro, H. A., Raman, M. R., McKee, A. C., Alvarez, V. E., Walker, J. M., Satizábal, C. L., Himali, J. J., Stein, T. D., et al. (2019) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.50936 · Cited by 21
“A global CAA severity score was determined using NIA-AA guidelines.(16) Briefly, the absence of CAA was scored as 0, mild CAA (1) was defined as scattered Ab-positive vessels; moderate CAA (2) was defined as intense Ab-positivity; severe CAA (3) was defined as widespread intense Ab-positivity in vessels in multiple br…”
MethodThe effect of ApoE ε 4 on clinical and structural MRI markers in prodromal Alzheimer’s disease
Initiative, A. D. N., Zhang, C., Kong, M., Wei, H., Zhang, H., Ma, G., & Ba, M. (2020) · Quantitative Imaging in Medicine and Surgery · doi:10.21037/qims.2020.01.14 · Cited by 21
Amyloid pathology and synaptic loss in pathological aging
Gkanatsiou, E., Nilsson, J., Toomey, C. E., Vrillon, A., Kvartsberg, H., Portelius, E., Zetterberg, H., Blennow, K., Brinkmalm, A., Lashley, T., et al. (2021) · Journal of Neurochemistry · doi:10.1111/jnc.15487 · Cited by 23
Godrich, D., Martin, E. R., Schellenberg, G. D., Pericak‐Vance, M. A., Cuccaro, M. L., Scott, W. K., Kukull, W. A., Montine, T. J., & Beecham, G. W. (2022) · Alzheimer s & Dementia · doi:10.1002/alz.12516 · Cited by 23
“Future directions: With these results, we are interested in (1) investigating the rate of progression and cognitive decline as a function of neuropathologic lesion combinations, (2) integrating genetic information to identify genetic variants associated with neuropathologic lesions, and (3) exploring determinants of A…”
BackgroundSelf-citationAI-enabled in silico immunohistochemical characterization for Alzheimer's disease
He, B. D., Bukhari, S. A., Fox, E. J., Abid, A., Shen, J., Kawas, C. H., Corrada, M. M., Montine, T. J., & Zou, J. (2022) · Cell Reports Methods · doi:10.1016/j.crmeth.2022.100191 · Cited by 20
Self-citationWidespread CNS pathology in amyotrophic lateral sclerosis homozygous for the D90A SOD1 mutation
Forsberg, K., Graffmo, K. S., Stenvall, E., Tabikh, N., Marklund, S. L., Brännström, T., & Andersen, P. M. (2022) · Acta Neuropathologica · doi:10.1007/s00401-022-02519-z · Cited by 22
“ABC staging [36] was performed using antibodies against hyperphosphorylated PFH-Tau and amyloid beta (Table 2).”
MethodAlzheimer’s disease is an inherent, natural part of human brain aging: an integrated perspective
Ferrer, I. (2022) · Free Neuropathology · doi:10.17879/freeneuropathology-2022-3806 · Cited by 25
Španić, E., Leko, M. B., Horvat, L. L., Brgić, K., Vogrinc, Ž., Boban, M., Klepac, N., Borovečki, F., & Šimić, G. (2023) · Neurology International · doi:10.3390/neurolint15030053 · Cited by 21
“AD diagnosis was based on NIA-AA (National Institute on AgingAlzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease) [38,39], NINCDS-ADRDA (National Institute of Neurological and Communicative Disorders and Stroke and Alzheimer’s Disease and Related Disorders Association), and DSM…”
MethodWang, Z., Tan, L., Gao, P., Ma, Y., Fu, Y., Sun, Y., Yu, J., & Initiative, A. D. N. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.13413 · Cited by 22
LATE-NC risk alleles (in TMEM106B, GRN, and ABCC9 genes) among persons with African ancestry
Katsumata, Y., Fardo, D. W., Shade, L. M. P., Bowen, J. D., Crane, P. K., Jarvik, G. P., Keene, C. D., Larson, E. B., McCormick, W. C., McCurry, S. M., et al. (2023) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlad059 · Cited by 21
Self-citationAgeing-Related Neurodegeneration and Cognitive Decline
Alafuzoff, I. I., & Libard, S. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25074065 · Cited by 27
“It has been recommended for many years that all alterations observed in the postmortem brain are assessed and reported, whereas the interpretation, i.e., the estimation of significance and assessment of causalities, varies from center to center [8].”
BackgroundInfluentialPathologic and cognitive correlates of plasma biomarkers in neurodegenerative disease
Cousins, K. A. Q., Phillips, J. S., Das, S. R., O’Brien, K. S., Tropea, T. F., Chen‐Plotkin, A. S., Shaw, L. M. J., Nasrallah, I. M., Mechanic-Hamilton, D. J., McMillan, C. T., et al. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.13777 · Cited by 21
“ADNC was scored according to ABC criteria, 34 and Braak stage deter-minedtauspread.”
MethodImmunosenescence: A new direction in anti-aging research
Li, H., Lin, S., Wang, Y., Shi, Y., Fang, X., Wang, J., Cui, H., Bian, Y., & Qi, X. (2024) · International Immunopharmacology · doi:10.1016/j.intimp.2024.112900 · Cited by 21
Denning, A. E., Ittyerah, R., Levorse, L. M., Sadeghpour, N., Athalye, C., Chung, E. P., Ravikumar, S., Dong, M., Duong, M. T., Li, Y., et al. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02789-9 · Cited by 20
“Neuropathologists also applied the 2012 NIA-AA criteria for global neuropathological Thal, Braak, and Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) staging, as well as neuropathological diagnoses [65].”
MethodPostupna, N. O., Keene, C. D., Crane, P. K., Gonzalez‐Cuyar, L. F., Sonnen, J. A., Hewitt, J. L., Rice, S., Howard, K., Montine, K. S., Larson, E. B., et al. (2015) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0000000000000153 · Cited by 21
“Figure 1 presents scatter plots of AA42 levels (n = 976) stratified by Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) score for neuritic plaques (18) and scatter plots of PHF-T levels (n = 973) stratified by Braak stage (19) (grouped into 1 of 3 categories, as recently recommended)(20, 21) for all…”
BackgroundMethodInfluentialSelf-citationPlowey, E. D., & Ziskin, J. L. (2016) · Acta Neuropathologica Communications · doi:10.1186/s40478-016-0388-2 · Cited by 20
“system [12], which is based in part on the Braak staging system of neurofibrillary degeneration [2–4],”
Alghamdi, A. A., Vallortigara, J., Howlett, D. R., Broadstock, M., Hortobágyi, T., Ballard, C. G., Thomas, A. J., O'Brien, J. T., Aarsland, D., Attems, J., et al. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-160946 · Cited by 22
“Institute on Aging - Alzheimer’s Association (NIA-AA) guidelines [1, 25-28].”
BackgroundDublin, S., Walker, R. L., Gray, S. L., Hubbard, R. A., Anderson, M. L., Yu, O., Montine, T. J., Crane, P. K., Sonnen, J. A., & Larson, E. B. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-160374 · Cited by 20
“…Registry for Alzheimer’s Disease [CERAD] staging criteria, [22, 23] neurofibrillary tangles assessed by Braak staging, [24, 25] and amyloid angiopathy [26]), cerebrovascular disease (cerebral microin-farcts, macroscopic infarcts, and atherosclerosis), Lewy bodies, and hippocampal sclerosis [20, 27].”
Self-citationGeut, H., Vergouw, L. J. M., Galis, Y., Ingrassia, A. M. T., de Jong, F. J., Quadri, M., Bonifati, V., Lemstra, A. W., Rozemüller, A. J. M., & van de Berg, W. D. J. (2019) · Parkinsonism & Related Disorders · doi:10.1016/j.parkreldis.2019.02.011 · Cited by 22
Christensen, K. R., Beach, T. G., Serrano, G. E., & Kanaan, N. M. (2019) · Acta Neuropathologica Communications · doi:10.1186/s40478-019-0675-9 · Cited by 23
Self-citationRelationship Between18F-Flortaucipir Uptake and Histologic Lesion Types in 4-Repeat Tauopathies
Josephs, K. A., Tosakulwong, N., Weigand, S. D., Buciuc, M., Lowe, V. J., Dickson, D. W., & Whitwell, J. L. (2021) · Journal of Nuclear Medicine · doi:10.2967/jnumed.121.262685 · Cited by 24
“All patients had a standardized neuropathologic evaluation in accordance with accepted published methodologies ( 9 ), including immunohistochemistry to detect 4R tau immunoreactive lesions using an antibody to phospho-tau (CP13; 1:1,000; IgG1 to phospho-serine 202, gift from the late Peter Davies,…”
MethodSelf-citationXu, B., Xiong, F., Tian, R., Zhan, S., Gao, Y., Qiu, W., Wang, R., Ge, W., & Ma, C. (2015) · Experimental Gerontology · doi:10.1016/j.exger.2015.11.016 · Cited by 21
Exploring the link between dystrophic microglia and the spread of Alzheimer's neuropathology
Shahidehpour, R. K., Nelson, P. T., Katsumata, Y., & Bachstetter, A. D. (2024) · Brain · doi:10.1093/brain/awae258 · Cited by 21
Self-citationPatient eligibility for amyloid-targeting immunotherapies in Alzheimer's disease
Rosen, J., & Jessen, F. (2025) · The Journal of Prevention of Alzheimer s Disease · doi:10.1016/j.tjpad.2025.100102 · Cited by 21
Chemical imaging delineates Aβ plaque polymorphism across the Alzheimer’s disease spectrum
Koutarapu, S., Ge, J., Dulewicz, M., Srikrishna, M., Szadziewska, A., Wood, J. I., Blennow, K., Zetterberg, H., Michno, W., Ryan, N. S., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-59085-7 · Cited by 29
Neuropsychiatric symptoms and progression to pathologically confirmed Alzheimer’s disease
Sharif, S. F., Guan, D. X., Bodnar, T. S., Joseph, J. T., Zetterberg, H., Smith, E. E., & Ismail, Z. (2025) · Brain · doi:10.1093/brain/awaf156 · Cited by 24
“41 For LBD pathology, participants were dichotomized based on the presence/absence of alpha-synuclein immunoreactivity anywhere in the brain.”
Amyloid-Beta Pathology and Cognitive Performance in Centenarians
Rohde, S. K., Luimes, M. C., Lorenz, L. M. C., Fierro‐Hernández, P., Rozemüller, A. J. M., Hulsman, M., Zhang, M., Graat, M., van der Hoorn, M. E., Daatselaar, D., et al. (2025) · JAMA Neurology · doi:10.1001/jamaneurol.2025.1734 · Cited by 26
Lysosomal proteomics reveals mechanisms of neuronal APOE4-associated lysosomal dysfunction
Krogsaeter, E., McKetney, J., Valiente‐Banuet, L., Marquez, A., Willis, A., Cakir, Z., Stevenson, E. J., Jang, G. Μ., Rao, A. T., Li, E., et al. (2025) · Autophagy · doi:10.1080/15548627.2025.2576613 · Cited by 22
Two distinct pathological substrates associated with MMSE-pentagons item deficit in DLB and AD
Beretta, L., Caminiti, S. P., Santangelo, R., Magnani, G., Pellegrini, F. F., Caffarra, P., & Perani, D. (2019) · Neuropsychologia · doi:10.1016/j.neuropsychologia.2019.107174 · Cited by 21
Lindbergh, C. A., Hillblom Aging Network, Casaletto, K. B., Staffaroni, A. M., Joie, R. L., Iaccarino, L., Edwards, L., Tsoy, E., Elahi, F. M., Walters, S. M., et al. (2020) · Neuropsychology · doi:10.1037/neu0000696 · Cited by 21
“A definitive diagnosis is made on postmortem examination by evaluating for βamyloid (Aβ) plaques and neurofibrillary tau deposits in brain tissue (Montine et al., 2012).”
BackgroundGrober, E. H., Qi, Q., Kuo, L., Hassenstab, J. J., Perrin, R. J., & Lipton, R. B. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-200946 · Cited by 18
“A positive outcome was defined by Braak stage ≥III coupled with either Thal phase ≥3 or CERAD ≥2 [30, 31].”
MethodInfluentialBachstetter, A. D., Garrett, F. G., Jicha, G. A., & Nelson, P. T. (2021) · Acta Neuropathologica Communications · doi:10.1186/s40478-021-01152-3 · Cited by 20
Self-citationSajjadi, S. A., Bukhari, S. A., Scambray, K. A., Yan, R., Kawas, C. H., Montine, T. J., & Corrada, M. M. (2022) · Neurology · doi:10.1212/wnl.0000000000201345 · Cited by 20
“MVLs were scored positive if there were 2 or more MVLs in the screening sections.(8) Finally, arteriolosclerosis and CAA were scored positive in those with moderate to severe pathologic change of each according to the published criteria.”
MethodSelf-citationLuo, D., Liu, H., Liu, H., Wu, W., Zhu, H., Ge, W., & Ma, C. (2022) · Aging and Disease · doi:10.14336/ad.2022.0607 · Cited by 19
“The ‘ABC’ dementia score defined by the National Institute on Aging–Alzheimer’s Association guidelines was used for the neuropathological assessment of each sample [14].”
Study of neuropathological changes and dementia in 100 centenarians in The 90+ Study
Neuville, R. S., Biswas, R., Ho, C., Bukhari, S. A., Sajjadi, S. A., Paganini‐Hill, A., Montine, T. J., Corrada, M. M., & Kawas, C. H. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.12981 · Cited by 21
Self-citationGibbons, L. E., Power, M. C., Walker, R. L., Kumar, R. G., Murphy, A., Latimer, C. S., Nolan, A., Melief, E. J., Beller, A., Bogdani, M., et al. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-221224 · Cited by 21
ER stress induced immunopathology involving complement in CADASIL: implications for therapeutics
Panahi, M., Hase, Y., Gallart‐Palau, X., Mitra, S., Watanabe, A., Low, R. W. C., Yamamoto, Y., Falla, D. S., Hainsworth, A. H., Ihara, M., et al. (2023) · Acta Neuropathologica Communications · doi:10.1186/s40478-023-01558-1 · Cited by 20
“The overall ABC scoring for AD type of pathology was determined to be absent or low in CADASIL and SVD cases [34].”
Hiya, S., Maldonado‐Díaz, C., Walker, J. M., & Richardson, T. E. (2023) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlad098 · Cited by 24
Frequency of Comorbid Pathologies and Their Clinical Impact in Multiple System Atrophy
Sekiya, H., Koga, S., Murakami, A., Deture, M. A., Ross, O. A., Uitti, R. J., Cheshire, W. P., Wszołek, Z. K., & Dickson, D. W. (2023) · Movement Disorders · doi:10.1002/mds.29670 · Cited by 21
Self-citationNeuronal SNCA transcription during Lewy body formation
Kon, T., Forrest, S. L., Lee, S., Martínez-Valbuena, I., Li, J., Nassir, N., Uddin, M. J., Lang, A. E., & Kovács, G. G. (2023) · Acta Neuropathologica Communications · doi:10.1186/s40478-023-01687-7 · Cited by 20
“All cases had a routine neuropathological assessment based on the current consensus criteria including Braak LBD stage [8], Lewy pathology consensus criteria [4], and Alzheimer’s disease neuropathological change (ADNC) [51].”
MethodTherapeutic Effects of Aβ-Specific Regulatory T Cells in Alzheimer’s Disease: A Study in 5xFAD Mice
Park, S.-Y., Yang, J., Yang, H., Cho, I., Kim, J. Y., & Bae, H. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25020783 · Cited by 21
“Studies have demonstrated that the extracellular deposition of A β peptide leads to the formation of senile plaques, while intracellular neurofibrillary tangles, composed of hyperphosphorylated tau protein, also develop [20,23].”
BackgroundSon, G., Neylan, T. C., & Grinberg, L. T. (2024) · Molecular Neurodegeneration · doi:10.1186/s13024-023-00695-4 · Cited by 21
“The first part of this question requires the collection of brain tissue from cases at progressive disease stages, which can be achieved in some tauopathies such as AD [108], PSP [109], and CTE [110].”
BackgroundSerrano, G. E., Sabbagh, M. N., Sue, L. I., Hidalgo, J. A., Schneider, J. A., Bedell, B. J., Deerlin, V. M. V., Suh, E. R., Akiyama, H., Joshi, A. D., et al. (2014) · Journal of Alzheimer s Disease · doi:10.3233/jad-140162 · Cited by 21
Self-citationPatterns of Tau and α-Synuclein Pathology in the Visual System
Rahimi, J., Milenković, I., & Kovács, G. G. (2015) · Journal of Parkinson s Disease · doi:10.3233/jpd-140485 · Cited by 22
Kakavand, H., Crainic, O., Lum, T., O'Toole, S. A., Kefford, R. F., Thompson, J. F., Wilmott, J. S., Long, G. V., & Scolyer, R. A. (2014) · Pathology · doi:10.1097/pat.0000000000000077 · Cited by 20
Donabedian, P. L., Evanoff, M., Monge, F. A., Whitten, D. G., & Chi, E. Y. (2017) · ACS Omega · doi:10.1021/acsomega.7b00231 · Cited by 20
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
