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 901–1,000 of 2,854
Kakavand, H., Walker, E., Lum, T., Wilmott, J. S., Selinger, C. I., Smith, E., Saw, R. P. M., Yu, B., Cooper, W. A., Long, G. V., et al. (2016) · Histopathology · doi:10.1111/his.12992 · Cited by 35
SELF-REPORTED MEMORY COMPLAINTS: A COMPARISON OF DEMENTED AND UNIMPAIRED OUTCOMES
Kryscio, R. J., Abner, E. L., Jicha, G. A., Nelson, P. T., Smith, C. D., Eldik, L. J. V., Lou, W., Fardo, D. W., Cooper, G. E., & Schmitt, F. A. (2015) · The Journal of Prevention of Alzheimer s Disease · doi:10.14283/jpad.2015.74 · Cited by 34
Self-citationMeneely, J. P., Chevallier, O. P., Graham, S. F., et al. (2016) · Scientific Reports · doi:10.1038/srep36363 · Cited by 35
Astrocytic changes with aging and Alzheimer's disease‐type pathology in chimpanzees
Munger, E. L., Edler, M. K., Hopkins, W. D., Ely, J. J., ERWIN, J. M., Perl, D. P., Mufson, E. J., Hof, P. R., Sherwood, C. C., & Raghanti, M. A. (2018) · The Journal of Comparative Neurology · doi:10.1002/cne.24610 · Cited by 37
“…astrocyte activation is triggered by the accumulation of amyloid beta protein (Aβ) plaques and hyperphosphorylated tau neurofibrillary tangles (NFT; Armstrong, 2009; Montine et al., 2012; Olabarría, Noristani, Verkhratsky, & Rodríguez, 2010; Rodríguez & Verkhratsky, 2011; Verkhratsky et al., 2010).”
InfluentialBohush, A., Niewiadomska, G., Weis, S., & Filipek, A. (2019) · Journal of Parkinson s Disease · doi:10.3233/jpd-181443 · Cited by 35
Language and spatial dysfunction in Alzheimer disease with white matter thorn-shaped astrocytes
Resende, E. D. P. F., Nolan, A., Petersen, C., Ehrenberg, A. J., Spina, S., Allen, I. E., Rosen, H. J., Kramer, J. H., Miller, B. L., Seeley, W. W., et al. (2020) · Neurology · doi:10.1212/wnl.0000000000008937 · Cited by 37
The application of in vitro ‐derived human neurons in neurodegenerative disease modeling
D’Souza, G. X., Rose, S. E., Knupp, A., Nicholson, D. A., Keene, C. D., & Young, J. E. (2020) · Journal of Neuroscience Research · doi:10.1002/jnr.24615 · Cited by 36
Hendrix, R. D., Ou, Y., Davis, J. E., Odle, A. K., Groves, T. R., Allen, A. R., Childs, G. V., & Barger, S. W. (2021) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2020.10.001 · Cited by 33
“They were acquired from autopsies of individuals diagnosed as AD (without Parkinson’s disease or mixed Lewy body pathology) or age-matched controls (AMC), as per National Institute on Aging-Reagan guidelines (Montine et al., 2012), which incorporate consortium to establish a registry for Alzheimer’s disease evaluation…”
Diabetic phenotype in mouse and humans reduces the number of microglia around β-amyloid plaques
Natunen, T., Martiskainen, H., Marttinen, M., Gabbouj, S., Koivisto, H., Kemppainen, S., Kaipainen, S., Takalo, M., Svobodová, H., Leppänen, L., et al. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00415-2 · Cited by 36
“Typical AD pathology includes accumulation of neuritic plaques composed of βamyloid peptide (Aβ) aggregates, and dystrophic neurites positive for hyperphosphorylated Tau in the form of neurofibrillary tangles (NFTs) [1, 2].”
BackgroundPathological drivers of neurodegeneration in suspected non-Alzheimer’s disease pathophysiology
Wisse, L. E. M., de Florès, R., Xie, L., Das, S. R., McMillan, C. T., Trojanowski, J. Q., Grossman, M., Lee, E. B., Irwin, D. J., Yushkevich, P. A., et al. (2021) · Alzheimer s Research & Therapy · doi:10.1186/s13195-021-00835-2 · Cited by 37
“ABC scores were established using the NIA-AA protocol [27].”
MethodSelf-citationHigher CSF sTNFR1-related proteins associate with better prognosis in very early Alzheimer’s disease
Hu, W. T., Ozturk, T. T., Kollhoff, A. L., Wharton, W., Howell, J. C., Initiative, A. D. N., Weiner, M. W., Aisen, P. S. S., Petersen, R. C., Jack, C. R., et al. (2021) · Nature Communications · doi:10.1038/s41467-021-24220-7 · Cited by 35
Self-citationHistone H3 Lysine 4 and 27 Trimethylation Landscape of Human Alzheimer’s Disease
Persico, G., Casciaro, F., Amatori, S., Rusin, M., Cantatore, F., Perna, A., Alberi, L. A., Fanelli, M., & Giorgio, M. (2022) · Cells · doi:10.3390/cells11040734 · Cited by 35
“During the progression of AD, abnormal tau and Aβ proteins follow distinct sequences of deposition and have been used to define stages/phases (Braak staging for NFT and Thal phases for Aβ) of the disease, measured by postmortem examination of the brain [3].”
BackgroundSingle-Cell Spatial Proteomic Imaging for Human Neuropathology
Vijayaragavan, K., Cannon, B. J., Tebaykin, D., Bosse, M. M., Baranski, A., Oliveria, J. P., Bukhari, S. A., Mrdjen, D., Corces, M. R., McCaffrey, E., et al. (2022) · Acta Neuropathologica Communications · doi:10.1186/s40478-022-01465-x · Cited by 40
“AD neuropathologic change and severity scores were evaluated by NIA-AA guidelines [5, 85].”
MethodSelf-citationFrigerio, I., Laansma, M. A., Lin, C., Hermans, E. J. M., Bouwman, M. M. A., Bol, J. G. J. M., Graaf, Y. G.-D., Hepp, D. H., Rozemüller, A. J. M., Barkhof, F., et al. (2023) · Translational Neurodegeneration · doi:10.1186/s40035-022-00328-8 · Cited by 35
“covariate in MRI-related analyses since it might influence post-mortem MRI-derived biomarkers [55, 56].”
BackgroundFixemer, S., Ameli, C., Hammer, G. P., Salamanca, L., Huarte, O. U., Schwartz, C., Gérardy, J., Mechawar, N., Skupin, A., Mittelbronn, M. G. A., et al. (2022) · Acta Neuropathologica Communications · doi:10.1186/s40478-022-01342-7 · Cited by 36
“Samples were evaluated regarding Aβ plaques, NFTs and α-synuclein and assessed according to Braak, ABC staging [12, 63] and Mc Keith staging criteria [59] by an affiliated neuropathologist of the Douglas Bell Canada Brain Bank.”
MethodGiannini, L., Ohm, D. T., Rozemüller, A. J. M., Dratch, L., Suh, E. R., Deerlin, V. M. V., Trojanowski, J. Q., Lee, E. B., Swieten, J. C. V., Grossman, M., et al. (2022) · Acta Neuropathologica · doi:10.1007/s00401-022-02487-4 · Cited by 34
“Neuropathological diagnosis was performed by an expert neuropathologist at the Netherlands Brain Bank (AJMR) or at the University of Pennsylvania (EBL, JQT) using established criteria [51, 54].”
MethodSelf-citationManca, M., Standke, H. G., Browne, D. F., Huntley, M. L., Thomas, O. R., Orru, C. D., Hughson, A. G., Kim, Y., Zhang, J., Tatsuoka, C. M., et al. (2023) · Acta Neuropathologica · doi:10.1007/s00401-023-02574-0 · Cited by 34
“Final neuropathology diagnosis for each case was rendered using standard semi-quantitative assessments for each pathology in each brain region [14, 30, 37, 41, 45, 59].”
BackgroundMethodReduced neurogenesis in human hippocampus with Alzheimer's disease
Cao, Y., Liu, P., Bian, H., Jin, S., Liu, J.-Q., Yu, N., Cui, H., Sun, F.-R., Qian, X.-J., Qiu, W.-Y., et al. (2023) · Brain Pathology · doi:10.1111/bpa.13225 · Cited by 27
“…AD brain samples, we used a protocol recommended by the National Institute on Aging – Alzheimer Association for determination of the “ ABC ” score [50], which incorporates histopathologic assessments of amyloid β deposits (A) [51], staging of neurofibrillary tangles (B) [52], and scoring of…”
BackgroundMethodRetinal ganglion cell vulnerability to pathogenic tau in Alzheimer’s disease
Davis, M. R., Robinson, E., Koronyo, Y., Salobrar‐García, E., Rentsendorj, A., Gaire, B. P., Mirzaei, N., Kayed, R., Sadun, A. A., Ljubimov, A. V., et al. (2025) · Acta Neuropathologica Communications · doi:10.1186/s40478-025-01935-y · Cited by 34
Kovács, G. G., van der Zee, J., Hort, J., Kristoferitsch, W., Leitha, T., Höftberger, R., Ströbel, T., Broeckhoven, C. V., & Matěj, R. (2015) · Neuropathology · doi:10.1111/neup.12233 · Cited by 36
An autopsy-confirmed case of progressive supranuclear palsy with predominant postural instability
Kurz, C., Ebersbach, G., Respondek, G., Giese, A., Arzberger, T., & Höglinger, G. U. (2016) · Acta Neuropathologica Communications · doi:10.1186/s40478-016-0391-7 · Cited by 33
“The “ABC” score for AD neuropathologic changes in this case was A3 B2 C2 [18].”
Sortilin Fragments Deposit at Senile Plaques in Human Cerebrum
Hu, X., Hu, Z., Li, Z., Ruan, C., Qiu, W., Pan, A., Li, C.-Q., Cai, Y., Shen, L., Chu, Y., et al. (2017) · Frontiers in Neuroanatomy · doi:10.3389/fnana.2017.00045 · Cited by 32
“Brain samples were assessed for AD type-neuropathology using sections from temporal, parietal, frontal and occipital lobes, with the extent of pathology (if present) scored according to Braak’s staging and the NIH guideline (Jellinger and Bancher, 1988; Braak et al., 2006; Montine et al., 2012).”
MethodMicroglia changes associated to Alzheimer's disease pathology in aged chimpanzees
Edler, M. K., Sherwood, C. C., Meindl, R. S., Munger, E. L., Hopkins, W. D., Ely, J. J., ERWIN, J. M., Perl, D. P., Mufson, E. J., Hof, P. R., et al. (2018) · The Journal of Comparative Neurology · doi:10.1002/cne.24484 · Cited by 37
“Brain areas and layers were selected based on NFT staging and Aβ deposition phases as reported in humans with AD and in aged chimpanzees (Braak & Braak, 1991; Edler et al., 2017; Gearing, Rebeck, Hyman, Tigges, & Mirra, 1994; Gearing, Tigges, Mori, & Mirra, 1996; Montine et al., 2012; Rosen et al., 2008).”
MethodValidation of machine learning models to detect amyloid pathologies across institutions
Vizcarra, J. C., Gearing, M., Keiser, M. J., Glass, J. D., Dugger, B. N., & Gutman, D. A. (2020) · Acta Neuropathologica Communications · doi:10.1186/s40478-020-00927-4 · Cited by 40
Tau pathology associates with in vivo cortical thinning in Lewy body disorders
Spotorno, N., Coughlin, D. G., Olm, C. A., Wolk, D. A., Vaishnavi, S., Shaw, L. M. J., Dahodwala, N. A., Morley, J. F., Duda, J. E., Deik, A., et al. (2020) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.51183 · Cited by 34
Self-citationOtoki, Y., Kato, S., Nakagawa, K., Harvey, D. J., Jin, L., Dugger, B. N., & Taha, A. Y. (2021) · NeuroMolecular Medicine · doi:10.1007/s12017-020-08636-w · Cited by 34
Gessi, S., Poloni, T. E., Negro, G., Varani, K., Pasquini, S., Vincenzi, F., Borea, P. A., & Merighi, S. (2021) · Cells · doi:10.3390/cells10092344 · Cited by 36
Eckermann, M., Schmitzer, B., van der Meer, F., Franz, J., Hansen, O., Stadelmann, C., & Salditt, T. (2021) · Proceedings of the National Academy of Sciences of the United States of America · doi:10.1073/pnas.2113835118 · Cited by 35
“…a larger pool, here consisting of postmortem paraffin-embedded tissue blocks of several individuals, both of an AD and of a control group (CTRL), categorized by neuropathological assessment based on the National Institute of Aging – Alzheimer’s Association (NIA-AA)–recommended ABC staging (20, 21).”
MethodStreit, W. J., Rotter, J., Winter, K., Müller, W. C., Khoshbouei, H., & Bechmann, I. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-215334 · Cited by 37
Winder, Z., Sudduth, T. L., Anderson, S., Patel, E., Neltner, J. H., Martin, B. J., Snyder, K., Abner, E. L., Jicha, G. A., Nelson, P. T., et al. (2022) · Alzheimer s & Dementia · doi:10.1002/alz.12639 · Cited by 33
Self-citationAmeen‐Ali, K. E., Bretzin, A. C., Lee, E. B., Folkerth, R. D., Hazrati, L., Iacono, D., Keene, C. D., Kofler, J., Kovács, G. G., Nolan, A., et al. (2022) · Acta Neuropathologica Communications · doi:10.1186/s40478-022-01353-4 · Cited by 34
Self-citationA History of Senile Plaques: From Alzheimer to Amyloid Imaging
Beach, T. G. (2022) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlac030 · Cited by 37
Self-citationLouis, E. D., Hernandez, D. I., Hernandez, N. C., Flowers, X. E., Kuo, S., Vonsattel, J. P., & Faust, P. L. (2022) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlac068 · Cited by 35
Banerjee, P., Sahoo, A., Anand, S., Bir, A., & Chakrabarti, S. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-150514 · Cited by 37
“and parahippocampal gyrus [3, 4].”
Telomerase Activity is Downregulated Early During Human Brain Development
Ishaq, A., Hanson, P. S., Morris, C. M., & Saretzki, G. C. (2016) · Genes · doi:10.3390/genes7060027 · Cited by 34
“All brains were assessed neuropathologically according to published criteria [31–34] and were free of any disease-related pathologies.”
MethodWalker, D. G., Lue, L.-F., Tang, T. M., Adler, C. H., Caviness, J. N., Sabbagh, M. N., Serrano, G. E., Sue, L. I., & Beach, T. G. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.03.007 · Cited by 33
Self-citationCykowski, M. D., Powell, S. Z., Schulz, P. E., Takei, H., Rivera, A. L., Jackson, R. E., Roman, G., Jicha, G. A., & Nelson, P. T. (2017) · Archives of Pathology & Laboratory Medicine · doi:10.5858/arpa.2016-0469-sa · Cited by 33
“Pathologically, HS-aging is defined by neuron loss and gliosis in the hippocampal sector CA1 and subiculum that is out of proportion to the burden of AD neuropathologies.(7,13,17,18) This results in ‘‘sclerosis,’’ or hardening of the atrophic hippocampus, as well as severe astrogliosis and neuronal loss.”
InfluentialSelf-citationWalker, J. M., Goette, W. F., Farrell, K. W., Iida, M. A., Karlovich, E., The PART Working Group, White, C. L., Crary, J. F., & Richardson, T. E. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.12966 · Cited by 35
Pre-Analytical Variables Influencing Stability of Blood-Based Biomarkers of Neuropathology
Panikkar, D., Vivek, S., Crimmins, E. M., Faul, J. D., Langa, K. M., & Thyagarajan, B. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230384 · Cited by 39
“…addressed by availability of automated instrumentation and certified reference material that has been used by the commercial assay manufacturers [19, 20], the effect of pre-analytical variation on biomarker variation such as draw time, time between blood draw and blood processing,…”
Bermejo‐Pareja, F., & del Ser, T. (2024) · Journal of Clinical Medicine · doi:10.3390/jcm13020536 · Cited by 39
Walker, L., Simpson, H., Thomas, A. J., & Attems, J. (2024) · Acta Neuropathologica Communications · doi:10.1186/s40478-023-01714-7 · Cited by 35
“94 cases fulfilled neuropathological criteria for high AD neuropatho-logic change according to NIA ‐ AA criteria [45] inclusive of Braak stage [8], Thal phase [55] and CERAD score [44], and clinically diagnosed with AD [43].”
MethodJosephs, K. A., Tosakulwong, N., Weigand, S. D., Graff‐Radford, J., Schwarz, C. G., Senjem, M. L., Machulda, M. M., Kantarci, K., Knopman, D. S., Nguyen, A. T., et al. (2024) · Science Translational Medicine · doi:10.1126/scitranslmed.ado8076 · Cited by 40
Self-citationA comparative study of the dentate gyrus in hippocampal sclerosis in epilepsy and dementia
Bandopadhyay, R., Liu, J. Y. W., Sisodiya, S. M., & Thom, M. (2013) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12087 · Cited by 33
Graham, S. F., Nasaruddin, M. L., Carey, M. P., McGuinness, B., Hölscher, C., Kehoe, P. G., Love, S., Passmore, A. P., Elliott, C. T., Meharg, A. A., et al. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-141869 · Cited by 33
Šmid, L. M., Kepe, V., Vinters, H. V., Bresjanac, M., Toyokuni, T., Satyamurthy, N., Wong, K. P., Huang, S., Silverman, D. H. S., Miller, K. J., et al. (2013) · Journal of Alzheimer s Disease · doi:10.3233/jad-122434 · Cited by 33
Self-citationAlafuzoff, I. I., Pikkarainen, M., Neumann, M., Arzberger, T., Al‐Sarraj, S., Bódi, I., Bogdanović, N., Bugiani, O., Ferrer, I., Gelpí, E., et al. (2014) · Journal of Neural Transmission · doi:10.1007/s00702-014-1304-1 · Cited by 33
Self-citationNeuropathology of supercentenarians - four autopsy case studies
Takao, M., Hirose, N., Arai, Y., Mihara, B., & Mimura, M. (2016) · Acta Neuropathologica Communications · doi:10.1186/s40478-016-0368-6 · Cited by 33
“Eventually, National Institute on Aging (NIA)-Reagan criteria (1997) and NIA-Alzheimer’s Association (NIA-AA) guidelines (2012) were applied for determining the level of AD pathological change [12, 13].”
Mi, Z., Abrahamson, E. E., Ryu, A. Y., Fish, K. N., Sweet, R. A., Mufson, E. J., & Ikonomović, M. D. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.01.022 · Cited by 36
“Introduction Alzheimer’s disease (AD) is a chronic neurodegenerative disorder with a clinical presentation of dementia and distinct neuropathology hallmarks including amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFTs) (Montine et al., 2012).”
BackgroundMethodLópez‐Sánchez, N., Fontán‐Lozano, Á., Pallé, A., González-Álvarez, V., Rábano, A., Trejo, J. L., & Frade, J. M. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.04.008 · Cited by 33
“Severity of Alzheimer pathology was scored according to the National Institute on AgingdAlzheimer’s Association Guidelines, following the “ABC” protocol (Montine et al., 2012).”
DeBay, D. R., Reid, G. A., Macdonald, I. R., Mawko, G., Burrell, S., Martin, E. V., Bowen, C. V., & Darvesh, S. (2017) · Brain Research · doi:10.1016/j.brainres.2017.07.009 · Cited by 33
Takeda, T. (2017) · Neuropathology · doi:10.1111/neup.12428 · Cited by 34
“Cognitive decline may also be linked to the additive presence of tau pathology, which is most commonly diagnosed as Alzheimer pathology.(10,11) It is rather unusual if tau accumulation that meets the diagnostic criteria for Alzheimer disease (AD) is identified in patients with ALS/FTLD-TDP.”
Abu‐Rumeileh, S., Capellari, S., & Parchi, P. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-171181 · Cited by 35
Nelson, P. T., Gal, Z. T., Wang, W., Niedowicz, D. M., Artiushin, S., Wycoff, S., Wei, A. L., Jicha, G. A., & Fardo, D. W. (2019) · Neurobiology of Disease · doi:10.1016/j.nbd.2019.01.013 · Cited by 33
“Briefly, over 20 brain areas were sampled in each case using methods compatible with National Institute on Aging-Alzheimer’s Association consensus recommendation (Montine et al., 2012).”
Self-citationAPOE Effect on Amyloid-β PET Spatial Distribution, Deposition Rate, and Cut-Points
Toledo, J. B., Habes, M., Sotiras, A., Bjerke, M., Yong Fan, A., Weiner, M. W., Shaw, L. M. J., Davatzikos, C. A., Trojanowski, J. Q., & Initiative, A. D. N. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-181282 · Cited by 36
“Because the APOE ε4 allele is such a strong risk factor for sporadic AD, the odds of having preclinical AD pathology in CN subjects and of having underlying AD pathology in cognitively impaired subjects is increased and therefore PET SUVRs may be higher [2, 26, 27].”
Self-citationIkezu, S., Dixie, K. L. I., Koro, L., Watanabe, T., Kaibuchi, K., & Ikezu, T. (2020) · Acta Neuropathologica Communications · doi:10.1186/s40478-020-0890-4 · Cited by 34
Damodarasamy, M., Vernon, R. B., Pathan, J. L., Keene, C. D., Day, A. J., Banks, W. A., & Reed, M. J. (2020) · Fluids and Barriers of the CNS · doi:10.1186/s12987-020-00219-y · Cited by 33
Jankovská, N., Olejár, T., & Matěj, R. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms22010007 · Cited by 35
Al-Baradie, R. S., Pu, S., Liu, D., Zeinolabediny, Y., Ferris, G. R., Sanfeli, C., Corpas, R., García-Lara, E., Alsagaby, S. A., Alshehri, B., et al. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.644213 · Cited by 35
Ranasinghe, K. G., Petersen, C., Kudo, K., Mizuiri, D., Rankin, K. P., Rabinovici, G. D., Gorno‐Tempini, M., Seeley, W. W., Spina, S., Miller, B. L., et al. (2021) · Alzheimer s & Dementia · doi:10.1002/alz.12349 · Cited by 34
Mitigating Effect of Estrogen in Alzheimer’s Disease-Mimicking Cerebral Organoid
Kim, J. Y., Mo, H., Kim, J., Kim, J. W., Nam, Y., Rim, Y. A., & Ju, J. H. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.816174 · Cited by 33
Deep learning from multiple experts improves identification of amyloid neuropathologies
Wong, D. R., Tang, Z., Mew, N. C., Das, S., Athey, J., McAleese, K. E., Kofler, J., Flanagan, M. E., Borys, E., White, C. L., et al. (2022) · Acta Neuropathologica Communications · doi:10.1186/s40478-022-01365-0 · Cited by 37
“We found that models trained from a consensus of experts were able to (1) reproduce consensus annotations, (2) prospectively filter and enrich for neuropathologies in new whole slide images (WSIs), (3) and exceed the performance of models trained from individual experts at the same tasks.”
MethodSex Differences for Clinical Correlates of Alzheimer's Pathology in People with Lewy Body Pathology
Bayram, E., Coughlin, D. G., & Litvan, I. (2022) · Movement Disorders · doi:10.1002/mds.29044 · Cited by 36
“Neuropathological variables consisted of LB pathology staging(5) and AD pathology staging, including Thal phase (amyloid-β plaque score), Braak tau stage (neurofibrillary tangle stage), and Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) score (neuritic plaque score).(28) Level of substantia nigra n…”
MethodLi, Y., Jin, Y., Pan, J., He, X., Zhong, S., Zhang, R., Choi, L., Su, W., & Chen, J. (2022) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.2c02140 · Cited by 33
Long‐Duration Progressive Supranuclear Palsy: Clinical Course and Pathological Underpinnings
Ječmenica‐Lukić, M., Respondek, G., Kurz, C., Compta, Y., Gelpí, E., Ferguson, L. W., Rajput, A. H., Troakes, C., the MDS‐endorsed PSP study group, Swieten, J. C. V., et al. (2022) · Annals of Neurology · doi:10.1002/ana.26455 · Cited by 32
Ji, Y., Liu, M., Huo, Y. R., Liu, S., Shi, Z., Liu, S., Wısnıewskı, T., & Wang, J. (2013) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000350872 · Cited by 33
Phenotypic characteristics of Alzheimer patients carrying an ABCA7 mutation
den Bossche, T. V., Sleegers, K., Cuyvers, E., Engelborghs, S., Sieben, A., Roeck, A. D., Cauwenberghe, C. V., Vermeulen, S., den Broeck, M. V., Laureys, A., et al. (2016) · Neurology · doi:10.1212/wnl.0000000000002628 · Cited by 33
“(2012).(12) CSF biomarker profile (Ab1-42, total tau, p-tau181P) characteristics.”
BackgroundWhite matter changes in the perforant path area in patients with amyotrophic lateral sclerosis
Mollink, J., Hiemstra, M., Miller, K. L., Huszar, I. N., Jenkinson, M., Raaphorst, J., Wiesmann, M., Ansorge, O., Pallebage‐Gamarallage, M., & van Cappellen van Walsum, A. M. (2019) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12555 · Cited by 28
The neuropathology of intimate partner violence
Dams-O’Connor, K., Seifert, A. C., Crary, J. F., Delman, B. N., Bigio, M. R. D., Kovács, G. G., Lee, E. B., Nolan, A., Pruyser, A., Selmanovic, E., et al. (2023) · Acta Neuropathologica · doi:10.1007/s00401-023-02646-1 · Cited by 39
“In all cases, histologic sampling followed standardized protocols for evaluation of neurodegenerative disease, including CTE, with histochemical and immunohistochemical staining as previously reported [7, 40].”
MethodIkeda, C., Yokota, O., Nagao, S., Ishizu, H., Oshima, E., Hasegawa, M., Okahisa, Y., Terada, S., & Yamada, N. (2015) · Brain Pathology · doi:10.1111/bpa.12319 · Cited by 32
“None of the subjects had a high level of Alzheimer’s disease (AD) neuropathologic changes with Braak NFT stages V–VI (5, 34), CBD (11), Pick’s disease, white matter tauopathy with globular glial inclusions (24), primary TDP-43 proteinopathies, or the NFTs of senile dementia (50).”
BackgroundTajeddinn, W., Fereshtehnejad, S., Ahmed, M. S., Yoshitake, T., Kehr, J., Shahnaz, T., Milovanovic, M., Behbahani, H., Höglund, K., Winblad, B. G., et al. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160022 · Cited by 31
Ramos‐Campoy, O., Polo, R. Á., Grau‐Rivera, O., Antonell, A., Clarimón, J., Rojas‐García, R., Charif, S., Santiago-Valera, V., Hernandez, I., Aguilar, M., et al. (2018) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nly047 · Cited by 32
Clinico-Neuropathological Findings in the Oldest Old from the Georgia Centenarian Study
Tanprasertsuk, J., Johnson, E. J., Johnson, M. A., Poon, L. W., Nelson, P. T., Davey, A., Martin, P., Barbey, A. K., Barger, K., Wang, X.-D., et al. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-181110 · Cited by 30
“In the GCS, 38% of demented centenarians (GDS 4–7) were diagnosed with either absence or low likelihood of AD according to the NIARI criteria [39, 53].”
Self-citationShepherd, C. E., Affleck, A. J., Bahar, A. Y., Carew‐Jones, F., & Halliday, G. M. (2019) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2019.10.025 · Cited by 32
Katsumata, Y., Fardo, D. W., Bachstetter, A. D., Artiushin, S., Wang, W., Wei, A. L., Brzezinski, L. J., Nelson, B. G., Huang, Q., Abner, E. L., et al. (2019) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlz116 · Cited by 32
“The gold standard endophenotypes for indicating the presence and severity of LOAD are the neuropathologic hallmarks: Amyloid-b (Ab) plaques and neurofibrillary tangles (NFTs) composed of Tau proteins (4).”
BackgroundSelf-citationClinical and pathologic features of cognitive-predominant corticobasal degeneration
Sakae, N., Santos, O. A., Pedraza, O., Litvan, I., Murray, M. E., Duara, R., Uitti, R. J., Wszołek, Z. K., Graff‐Radford, N. R., Josephs, K. A., et al. (2020) · Neurology · doi:10.1212/wnl.0000000000009734 · Cited by 37
Self-citationLiu, K. Y., Reeves, S., McAleese, K. E., Attems, J., Francis, P. T., Thomas, A. J., & Howard, R. J. (2020) · Brain · doi:10.1093/brain/awaa315 · Cited by 33
“for all cases and included the National Institute on AgingAlzheimer’s Association (NIA-AA) criteria (Montine et al., 2012).”
Frye, B. M., Craft, S., Latimer, C. S., Keene, C. D., Montine, T. J., Register, T. C., Orr, M. E., Kavanagh, K., Macauley, S. L., & Shively, C. A. (2021) · American Journal of Primatology · doi:10.1002/ajp.23260 · Cited by 34
“To support direct translation to clinical studies, the brain collection protocol was adapted from the National Institute on Aging and Alzheimer’s Association (NIA-AA) guidelines for the collection of human brains for AD repositories (Montine et al., 2012).”
MethodSelf-citationTherapeutic Potential of Human Stem Cell Implantation in Alzheimer’s Disease
Chan, H. J., Yanshree, Roy, J., Tipoe, G. L., Fung, M., & Lim, L. W. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms221810151 · Cited by 33
“Various neuropsychological, clinical, neuroimaging, and laboratory techniques are currently used to diagnose AD [24].”
Pathological manifestation of human endogenous retrovirus K in frontotemporal dementia
Phan, K., He, Y. Z., Fu, Y., Dzamko, N. L., Bhatia, S., Gold, J., Rowe, D. B., Ke, Y. D., Ittner, L. M., Hodges, J. R., et al. (2021) · Communications Medicine · doi:10.1038/s43856-021-00060-w · Cited by 33
Neuropathologic Features of Antemortem Atrophy-Based Subtypes of Alzheimer Disease
Mohanty, R., Ferreira, D., Frerich, S., Muehlboeck, J., Grothe, M. J., Westman, E., & Initiative, A. D. N. (2022) · Neurology · doi:10.1212/wnl.0000000000200573 · Cited by 32
The therapeutic potential of triptolide and celastrol in neurological diseases
Cui, Y., Jiang, X., & Feng, J. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.1024955 · Cited by 33
“The main pathological features of AD include the formation of extracellular pathological plaques (formed by the accumulation of amyloid-beta (Aβ) peptides) and the presence of intracellular neurofibril entanglements (formed by aggregations of hyperphosphorylated Tau proteins) (Montine et al., 2012).”
BackgroundNeuropathologic analysis of Tyr69His TTR variant meningovascular amyloidosis with dementia
Ziskin, J. L., Greicius, M. D., Zhu, W., Okumu, A. N., Adams, C. M., & Plowey, E. D. (2015) · Acta Neuropathologica Communications · doi:10.1186/s40478-015-0216-0 · Cited by 33
“AT8 immunostains revealed Braak stage II [29], or transentorhinal B1 stage [24], of neurofibrillary degeneration based on the presence of neurofibrillary tangles in the Pre α neurons of the entorhinal cortex and only a few neurofibrillary tangles in the CA1 sector of the hippocampus.”
BackgroundMethodGenomics and CSF analyses implicate thyroid hormone in hippocampal sclerosis of aging
Initiative, A. D. N., Nelson, P. T., Katsumata, Y., Nho, K. T., Artiushin, S., Jicha, G. A., Wang, W., Abner, E. L., Saykin, A. J., Kukull, W. A., et al. (2016) · Acta Neuropathologica · doi:10.1007/s00401-016-1641-2 · Cited by 31
“Hippocampal sclerosis (HS), characterized by cell loss and astrocytosis in the hippocampus [53, 65], is a common finding at autopsy of old persons [14, 47, 65, 100].”
Self-citationLachén‐Montes, M., Zelaya, M. V., Segura, V., Fernández‐Irigoyen, J., & Santamaría, E. (2017) · Oncotarget · doi:10.18632/oncotarget.18193 · Cited by 30
Mixed TDP-43 proteinopathy and tauopathy in frontotemporal lobar degeneration: nine case series
Kim, E., Brown, J. A., Deng, J., Hwang, J., Spina, S., Miller, Z., DeMay, M. G., Valcour, V., Karydas, A., Ramos, E. M., et al. (2018) · Journal of Neurology · doi:10.1007/s00415-018-9086-2 · Cited by 32
Abu‐Rumeileh, S., Giannini, G., Polischi, B., Albini‐Riccioli, L., Milletti, D., Oppi, F., Maserati, M. S., Capellari, S., Mantovani, P., Palandri, G., et al. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-181012 · Cited by 33
Reply: the early pathological process in sporadic Alzheimer’s disease
Braak, H., & Tredici, K. D. (2013) · Acta Neuropathologica · doi:10.1007/s00401-013-1170-1 · Cited by 36
“Together with sensitive silver stains, AT8 is the antibody of choice for abnormal tau in current consensus statements [2, 21, 45].”
Caffeine for Prevention of Alzheimer’s Disease: Is the A2A Adenosine Receptor Its Target?
Merighi, S., Travagli, A., Nigro, M., Pasquini, S., Cappello, M., Contri, C., Varani, K., Vincenzi, F., Borea, P. A., & Gessi, S. (2023) · Biomolecules · doi:10.3390/biom13060967 · Cited by 37
Ambeskovic, M., Hopkins, G., Hoover, T. D., Joseph, J. T., Montina, T., & Metz, G. A. S. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241914769 · Cited by 33
Fazeli, E., Child, D. D., Bucks, S. A., Stovarsky, M., Edwards, G., Rose, S. E., Yu, C.-E., Latimer, C., Kitago, Y., Bird, T., et al. (2024) · Acta Neuropathologica · doi:10.1007/s00401-023-02670-1 · Cited by 29
“While LBD limited to the amygdala is frequently observed in association with advanced ADNC [30, 52], ADAD due to PSEN1 , PSEN2, and APP have been associated with brainstem, and limbic and diffuse LBD [45, 48] similar to what we find in this family.”
BackgroundMethodResultInfluentialHase, Y., Jobson, D., Cheong, J., Gotama, K. T., Maffei, L., Hase, M., Hamdan, A., Ding, R., Polivkoski, T., Horsburgh, K. J., et al. (2024) · Acta Neuropathologica Communications · doi:10.1186/s40478-024-01737-8 · Cited by 32
“Braak staging scores and Alzheimer’s Disease Neuropathologic changes [36] were different in mixed and AD cases compared to all other groups (‡ P 0.05).”
BackgroundMethodResultInfluentialTau fibrils evade autophagy by excessive p62 coating and TAX1BP1 exclusion
Ferrari, L., Bauer, B., Qiu, Y., Schuschnig, M., Klotz, S., Anrather, D., Juretschke, T., Beli, P., Gelpí, E., & Martens, S. (2024) · Science Advances · doi:10.1126/sciadv.adm8449 · Cited by 35
Ferroptosis and pathogenesis of neuritic plaques in Alzheimer disease
Streit, W. J., Phan, L. T., & Bechmann, I. (2024) · Pharmacological Reviews · doi:10.1124/pharmrev.123.000823 · Cited by 36
Schneeberger, S., Kim, S. J., Geesdorf, M., Friebel, E., Eede, P., Jendrach, M., Boltengagen, A., Braeuning, C., Ruhwedel, T., Hülsmeier, A. J., et al. (2025) · Nature Aging · doi:10.1038/s43587-025-00816-2 · Cited by 33
“Patients with AD were stratified by the ‘ABC’ score for AD neuro-pathology as defined by Montine et al. 98 .”
Applicability of digital analysis and imaging technology in neuropathology assessment
Dunn, W. D., Gearing, M., Park, Y., Zhang, L., Hanfelt, J., Glass, J. D., & Gutman, D. A. (2015) · Neuropathology · doi:10.1111/neup.12273 · Cited by 31
“In recent years, these three scoring systems have been combined to produce an “ABC” (Amyloid, Braak, CERAD) composite score describing the total level of AD neuropathological changes.(6,7) Histopathological scoring systems are semi-quantitative”
Alterations and interactions of subcortical modulatory systems in Alzheimer's disease
Leko, M. B., Hof, P. R., & Šimić, G. (2021) · Progress in brain research · doi:10.1016/bs.pbr.2020.07.016 · Cited by 31
Merighi, S., Battistello, E., Casetta, I., Gragnaniello, D., Poloni, T. E., Medici, V., Cirrincione, A., Varani, K., Vincenzi, F., Borea, P. A., et al. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-201437 · Cited by 33
Emerging insights into the role of albumin with plasma exchange in Alzheimer’s disease management
Costa, M., & Páez, A. (2021) · Transfusion and Apheresis Science · doi:10.1016/j.transci.2021.103164 · Cited by 32
Multiomics Profiling of Alzheimer’s Disease Serum for the Identification of Autoantibody Biomarkers
Segundo‐Acosta, P. S., Montero‐Calle, A., Falk, A. J., Alonso‐Navarro, M., Pin, E., Andersson, E., Hellström, C., Sánchez-Martínez, M., Rábano, A., Solís‐Fernández, G., et al. (2021) · Journal of Proteome Research · doi:10.1021/acs.jproteome.1c00630 · Cited by 30
Tsujikawa, K., Hamanaka, K., Riku, Y., Hattori, Y., Hara, N., Iguchi, Y., Ishigaki, S., Hashizume, A., Miyatake, S., Mitsuhashi, S., et al. (2022) · Science Advances · doi:10.1126/sciadv.abm5029 · Cited by 33
“Neuropathological diagnosis of PSP (44), CBD (45), AD (46), PD (47), and DLB (48) was made in accordance with the published guidelines.”
Result
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
