The DOI matches its Crossref record; 66 of the 66 references it cites were found in a registry or an index; 27 of the 65 sources its claims cite were checked for support.
National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach
Open accessAbstract
We present a practical guide for the implementation of recently revised National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease (AD). Major revisions from previous consensus criteria are: (1) recognition that AD neuropathologic changes may occur in the apparent absence of cognitive impairment, (2) an "ABC" score for AD neuropathologic change that incorporates histopathologic assessments of amyloid β deposits (A), staging of neurofibrillary tangles (B), and scoring of neuritic plaques (C), and (3) more detailed approaches for assessing commonly co-morbid conditions such as Lewy body disease, vascular brain injury, hippocampal sclerosis, and TAR DNA binding protein (TDP)-43 immunoreactive inclusions. Recommendations also are made for the minimum sampling of brain, preferred staining methods with acceptable alternatives, reporting of results, and clinico-pathologic correlations.
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11 No full text of the sources · 9 Partly supported · 4 Supported · 3 Supported so far · 1 Own interpretation · accuracy not yet measured
Every source the paper cites for this claim was checked and supports it.
In the paper
“recognition that AD neuropathologic changes may occur in the apparent absence of cognitive impairment”
- Also stated in: § CLINICO-PATHOLOGIC CORRELATION · plain
“Similar neuropathologic changes, albeit usually at lower levels, also occur in individuals who did not show cognitive or behavioral impairments during life [54].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > Abstract
What the sources say
- Supportedcites [54] Sperling RA, Aisen PS, Beckett LA et al (2011) Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement 7:280–292 source
Section 6 reports that AD-related biomarker abnormalities can be detected before overt clinical symptoms and that Aβ accumulation occurs in clinically normal older adults. Section 2 also notes that some people have diagnostic AD neuropathological features at autopsy without having developed dementia during life. No page numbers are available in our copy. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § CLINICO-PATHOLOGIC CORRELATION · plain
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“LBs may be detected in neurons of medulla, pons and midbrain with hematoxylin and eosin (H&E)-stained sections; however, greater sensitivity can be achieved with immunohistochemistry for α-synuclein and this approach is strongly preferred [3,4,13].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE > Method
What the sources say
- Partly supportedcites [3] Alafuzoff I, Parkkinen L, Al-Sarraj S et al (2008) Assessment of alpha-synuclein pathology: a study of the BrainNet Europe Consortium. J Neuropathol Exp Neurol 67:125–143 sourceExperimental — accuracy not yet measured
The Introduction (p. 125) says consensus guidelines recommend α-synuclein immunohistochemistry for synucleinopathies, supporting the preference for that approach. The paper’s staining results and Discussion assess variation among immunohistochemical methods, but do not establish that immunohistochemistry detects Lewy bodies more sensitively than H&E; searches for H&E and hematoxylin–eosin found no such comparison. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [4] Alafuzoff I, Pikkarainen M, Al-Sarraj S et al (2006) Interlaboratory comparison of assessments of Alzheimer disease-related lesions: a study of the BrainNet Europe Consortium. J Neuropathol Exp Neurol 65:740–757 source
- Partly supportedcites [13] Beach TG, White CL, Hamilton RL et al (2008) Evaluation of alpha-synuclein immunohistochemical methods used by invited experts. Acta Neuropathol 116:277–288 sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) calls α-synuclein immunohistochemistry the method of choice for diagnosing Lewy body disorders, supporting its preferred use. The paper compares immunohistochemical methods with one another, however, and does not establish that they detect Lewy bodies more sensitively than H&E staining. (LLM, conf=0.84)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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- Partly supported
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In the paper
“one MVL identified in standard sections of brain (Table 1 regions shaded green) is of unclear relationship to cognitive function, while multiple MVLs in these regions are associated with increased likelihood of cognitive impairment or dementia [24,52,62].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > CEREBROVASCULAR DISEASE and VASCULAR BRAIN INJURY > Reporting
What the sources say
- Partly supportedcites [24] Gorelick PB, Scuteri A, Black SE et al (2011) Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 42:2672–2713 sourceExperimental — accuracy not yet measured
Section 3.2 (page not available in our copy) reports that some studies associate multiple microscopic infarcts with dementia, even after accounting for macroscopic infarcts. It does not establish the claim for MVLs generally or specify that the lesions were identified in standard brain sections. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites [52] Sonnen JA, Larson EB, Crane PK et al (2007) Pathological correlates of dementia in a longitudinal, population-based sample of aging. Ann Neurol 62:406–413 source
- Not checked — no full text of the sourcecites [62] White L (2009) Brain lesions at autopsy in older Japanese-American men as related to cognitive impairment and dementia in the final years of life: a summary report from the Honolulu-Asia aging study. J Alzheimers Dis 18:713–725 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Clinico-pathologic correlations for individuals without cognitive impairment should indicate that it is possible for AD neuropathologic change to predate onset of symptoms by years [54].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > AD NEUROPATHOLOGIC CHANGE > Reporting
What the sources say
- Supportedcites [54] Sperling RA, Aisen PS, Beckett LA et al (2011) Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement 7:280–292 source
Section 2, “Redefining the earliest stages of AD,” says the pathological cascade may begin a decade or more before clinically evident impairment. Section 6 also describes AD-related abnormalities in cognitively normal individuals, supporting the claim that neuropathologic change can predate symptoms by years. (LLM, conf=0.94)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“one MVL identified in standard sections of brain (Table 1 regions shaded green) is of unclear relationship to cognitive function, while multiple MVLs in these regions are associated with increased likelihood of cognitive impairment or dementia [24,52,62].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > CEREBROVASCULAR DISEASE and VASCULAR BRAIN INJURY > Reporting
What the sources say
- Partly supportedcites [24] Gorelick PB, Scuteri A, Black SE et al (2011) Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 42:2672–2713 sourceExperimental — accuracy not yet measured
Section 3.2 (page unavailable) says the number of infarcts needed for cognitive impairment is difficult to determine and reports that multiple microscopic infarcts may be related to dementia. It does not specifically assess the cognitive significance of one MVL identified in standard brain sections. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites [52] Sonnen JA, Larson EB, Crane PK et al (2007) Pathological correlates of dementia in a longitudinal, population-based sample of aging. Ann Neurol 62:406–413 source
- Not checked — no full text of the sourcecites [62] White L (2009) Brain lesions at autopsy in older Japanese-American men as related to cognitive impairment and dementia in the final years of life: a summary report from the Honolulu-Asia aging study. J Alzheimers Dis 18:713–725 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“this may represent pre-clinical LBD [12,22,31].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE > Reporting
What the sources say
- Supportedcites [12] Beach TG, Adler CH, Sue LI et al (2008) Reduced striatal tyrosine hydroxylase in incidental Lewy body disease. Acta Neuropathol 115:445–451 source
The Introduction defines incidental Lewy body disease as Lewy bodies without clinically documented parkinsonism or dementia. The Results and discussion report reduced striatal tyrosine hydroxylase in these individuals and say this suggests ILBD is likely a precursor to Parkinson’s disease and/or dementia with Lewy bodies, supporting the citing sentence’s qualified “may represent” claim. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites [22] Dickson DW, Fujishiro H, DelleDonne A et al (2008) Evidence that incidental Lewy body disease is pre-symptomatic Parkinson’s disease. Acta Neuropathol 115:437–444 source
- Supportedcites [31] Jicha GA, Schmitt FA, Abner E et al (2010) Prodromal clinical manifestations of neuropathologically confirmed Lewy body disease. Neurobiol Aging 31:1805–1813 source
The Introduction (page unavailable) says Lewy body pathology has been found in autopsied people described as normal and suggests that DLB pathology may predate clinical diagnosis. The Discussion (page unavailable) also says the study’s subjects were cognitively and neurologically normal at enrollment. Together, these support the qualified suggestion that LBD without apparent cognitive or motor deficits may be pre-clinical. (LLM, conf=0.91)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“LBs are frequent in the setting of moderate-to-severe levels of AD neuropathologic change [27,59], including some early-onset familial AD cases [32,33].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE
What the sources say
- Supportedcites [32] Leverenz JB, Fishel MA, Peskind ER et al (2006) Lewy body pathology in familial Alzheimer disease: evidence for disease- and mutation-specific pathologic phenotype. Arch Neurol 63:370–376 source
The Results report Lewy body pathology in the amygdala of 24 of 25 familial AD cases with PSEN1 mutations. The section on PSEN1-associated AD reports a mean age at onset of about 43 years in the groups it compares, supporting the early-onset qualifier. The indexed copy provides section labels but no page numbers. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites [33] Lippa CF, Duda JE, Grossman M et al (2007) DLB and PDD boundary issues: diagnosis, treatment, molecular pathology, and biomarkers. Neurology 68:812–819 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Accumulation of Aβ plaques and NFTs follows distinct regional progressions across brain regions as AD advances.”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > AD NEUROPATHOLOGIC CHANGE
What the sources say
- Partly supportedcites [14] Braak H, Alafuzoff I, Arzberger T et al (2006) Staging of Alzheimer disease-associated neurofibrillary pathology using paraffin sections and immunocytochemistry. Acta Neuropathol 112:389–404 sourceExperimental — accuracy not yet measured
The staging-system section describes a predictable regional progression of neurofibrillary pathology, from transentorhinal and entorhinal regions to limbic and then neocortical areas. It does not describe a separate regional progression of Aβ plaques or compare that progression with NFTs. Its references to neuritic plaques occur in the context of tau-immunoreactive pathology, not an Aβ-plaque staging scheme. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [15] Braak H, Braak E (1991) Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol 82:239–259 source
- Not checked — no full text of the sourcecites [57] Thal DR, Rub U, Orantes M, Braak H (2002) Phases of A beta-deposition in the human brain and its relevance for the development of AD. Neurology 58:1791–1800 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“CVD and vascular brain injury (VBI) [50] commonly are encountered in the brains with AD neuropathologic change [25].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > CEREBROVASCULAR DISEASE and VASCULAR BRAIN INJURY
What the sources say
- Partly supportedcites [25] Grinberg LT, Thal DR (2010) Vascular pathology in the aged human brain. Acta Neuropathol 119:277–290 sourceExperimental — accuracy not yet measured
The ‘Cerebral amyloid angiopathy’ section (page unavailable) reports that around 80–100% of AD patients have CAA, supporting the claim that cerebrovascular disease commonly accompanies AD pathology. It identifies infarction and hemorrhage as possible complications of CAA, but does not establish that vascular brain injury itself is commonly found in AD brains. (LLM, conf=0.82)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“LBs are frequent in the setting of moderate-to-severe levels of AD neuropathologic change [27,59], including some early-onset familial AD cases [32,33].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE
What the sources say
- Not checked — no full text of the sourcecites [27] Hamilton RL (2000) Lewy bodies in Alzheimer’s disease: a neuropathological review of 145 cases using alpha-synuclein immunohistochemistry. Brain Pathol 10:378–384 source
- Supportedcites [59] Uchikado H, Lin WL, DeLucia MW, Dickson DW (2006) Alzheimer disease with amygdala Lewy bodies: a distinct form of alpha-synucleinopathy. J Neuropathol Exp Neurol 65:685–697 source
The Materials and Methods section (page unavailable) says all 347 cases met pathologic criteria for AD and had Braak NFT stage IV or greater, indicating advanced AD in almost all cases. The “Frequency of α-Synuclein Pathology in Alzheimer Disease” section (page unavailable) reports Lewy-body pathology in 62 AD/ALB and 149 AD/LBD cases, supporting that Lewy bodies are frequent in this setting. (LLM, conf=0.90)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 2
- Probably not a substantial claim. 1
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Relatively isolated HS may occur in very old individuals, and in this context it is associated with TDP-43-immunoreactive inclusions and with cognitive impairment [45,47].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > HIPPOCAMPAL SCLEROSIS and TAR DNA BINDING PROTEIN (TDP)-43 INCLUSIONS > Reporting
What the sources say
- Partly supportedcites [45] Nelson PT, Abner EL, Schmitt FA et al (2010) Modeling the association between 43 different clinical and pathological variables and the severity of cognitive impairment in a large autopsy cohort of elderly persons. Brain Pathol 20:66–79 sourceExperimental — accuracy not yet measured
The Discussion reports that hippocampal sclerosis (HS) was associated with lower MMSE scores and states that HS is associated with TDP-43 proteinopathy. The Results describe TDP-43-positive inclusions. Neither passage establishes these associations specifically for relatively isolated HS in very old individuals. (LLM, conf=0.86)
- Supportedcites [47] Nelson PT, Schmitt FA, Lin Y et al (2011) Hippocampal sclerosis in advanced age: clinical and pathological features. Brain 134:1506–1518 source
The Introduction describes hippocampal sclerosis in older individuals as unrelated to Alzheimer’s pathology and associated with significant cognitive dysfunction. The Discussion reports aberrant TDP-43 staining in approximately 90% of patients with hippocampal sclerosis, and Table 7 describes HS-Ageing as most prevalent in the oldest-old and associated with dementia. The association is not universal, but the citing sentence does not claim that it is. (LLM, conf=0.92)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
In the paper
“Although not part of this classification scheme, it is important to realize that LBD also occurs frequently in the olfactory bulb in older adults and should be sampled when possible [20].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE > Method
What the sources say
- Not checked — no full text of the sourcecites [20] Del Tredici K, Rub U, De Vos RA et al (2002) Where does Parkinson disease pathology begin in the brain? J Neuropathol Exp Neurol 61:413–426 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“A subset of senile plaques called neuritic plaques appear closely associated with neuronal injury and are characterized by the occurrence of dystrophic neurites that frequently have phospho-tau immunoreactivity [19,36,37,55].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > AD NEUROPATHOLOGIC CHANGE
What the sources say
- Not checked — no full text of the sourcecites [19] DeKosky ST, Scheff SW (1990) Synapse loss in frontal cortex biopsies in Alzheimer’s disease: correlation with cognitive severity. Ann Neurol 27:457–464 source
- Not checked — no full text of the sourcecites [36] Masliah E, Mallory M, Deerinck T et al (1993) Re-evaluation of the structural organization of neuritic plaques in Alzheimer’s disease. J Neuropathol Exp Neurol 52:619–632 source
- Not checked — no full text of the sourcecites [37] Masliah E, Terry RD, Mallory M et al (1990) Diffuse plaques do not accentuate synapse loss in Alzheimer’s disease. Am J Pathol 137:1293–1297
- Not checked — no full text of the sourcecites [55] Terry RD, Masliah E, Salmon DP et al (1991) Physical basis of cognitive alterations in Alzheimer’s disease: synapse loss is the major correlate of cognitive impairment. Ann Neurol 30:572–580 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
Many other neurodegenerative disorders can cause dementia and may be co-morbid with AD neuropathologic change, especially in the elderly.
“There are many other neurodegenerative disorders that can cause dementia in addition to those discussed here, and any may be co-morbid with AD neuropathologic change, especially in the elderly.”
The paper relies on this without support.
Multiple diseases in the cerebrum can conspire to worsen cognitive symptoms.
“Multiple diseases in cerebrum can conspire to worsen cognitive symptoms; however, it often is difficult to judge the extent to which each disease observed at autopsy may have contributed to a given patient’s cognitive state.”
The paper relies on this without support.
Abnormal neuropil and neuronal cytoplasmic α-synuclein immunoreactivity are usually present with Lewy bodies but will not be apparent by H&E; in some instances, these changes occur in the absence of Lewy bodies.
“Abnormal neuropil and neuronal cytoplasmic α-synuclein immunoreactivity are usually present with LBs but will not be apparent by H&E; in some instances, these changes occur in the absence of LBs.”
The paper relies on this without support.
Diffuse white matter injury is a form of VBI but it is more difficult to judge objectively and is not specific to VBI.
“Diffuse white matter injury is a form of VBI but it is more difficult to judge objectively and is not specific to VBI.”
The paper relies on this without support.
Hippocampal sclerosis can be observed in the context of AD neuropathologic change, FTLD, and VBI, likely reflecting a heterogeneous etiology.
“HS can be observed in the context of AD neuropathologic change, frontotemporal lobar degeneration (FTLD), and VBI, likely reflecting a heterogeneous etiology.”
The paper relies on this without support.
Hippocampal sclerosis can be focal, so its absence in the recommended screening section does not rule out the possibility of HS elsewhere in the hippocampal formation.
“HS can be focal, thus its absence in the recommended screening section does not rule out the possibility of HS elsewhere in the hippocampal formation.”
The paper relies on this without support.
Hippocampal sclerosis can occur in several different diseases and has varying clinical implications in different settings.
“Clinico-pathological correlations need to recognize that HS can occur in several different diseases and has varying clinical implications in different settings.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The new NIA criteria use the same combination of NPs and Braak stage as the minimum lesion density necessary for attributing the cause of dementia to AD (39, 40).”
From Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer Disease Centers, 2005–2010 (2012) · cites this paper as [40]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The definitive diagnosis of AD requires microscopic examination of multiple brain regions employing staining methods that can detect Alzheimer type neuropathologic change [24], with diagnosis based upon the morphology and density of lesions and their topographic distribution.”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [24]
The cited source says what the claim attributes to it.
In the citing paper
“This finding is highlighted by the fact that nearly one third of patients with pathological findings of high likelihood Alzheimer’s disease [24] were thought to other disorders, and 3% were considered clinically normal at the time of their last clinical exam (Table 2).”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [24]
The cited source says what the claim attributes to it.
In the citing paper
“However, both Aβ and paired helical filament (PHF) tau deposits are required to fulfill neuropathologic criteria for AD [105,106]”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [105]
The cited source says what the claim attributes to it.
In the citing paper
“Autopsy analyses classified the level of ADNC from “none” to “high” using an established scoring system when available.”
From Automatic classification of AD pathology in FTD phenotypes using natural speech (2024) · cites this paper as [30]
The cited source says what the claim attributes to it.
In the citing paper
“Participants in the Confirmed-AD group (n ¼ 1854) were diagnosed with primary or contributing ADdementia at their last UDS visit before death and met our criteria for ADNC: moderate to frequent neuritic plaques and Braak stages III through VI, which loosely aligns with NIA-AA criteria for intermediate or high ADNC (13).”
From Concordance of Clinical Alzheimer Diagnosis and Neuropathological Features at Autopsy (2020) · cites this paper as [13]
The cited source says what the claim attributes to it.
In the citing paper
“The shortcomings of the NIA-Reagan criteria have been recognized and a revised set of criteria are currently in press (39, 40).”
From Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer Disease Centers, 2005–2010 (2012) · cites this paper as [40]
The cited source says what the claim attributes to it.
In the citing paper
“In the revision of the 1997 criteria, combinations of plaque and tangle pathologies considered sufficient to cause dementia and qualify for the neuropathological diagnosis of AD are explicitly stated (40, 41).”
From Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer Disease Centers, 2005–2010 (2012) · cites this paper as [40]
The cited source says what the claim attributes to it.
In the citing paper
“Neuropathologic diagnosis of AD was in accordance with current NIA-AA guidelines (Hyman et al., 2012; Montine et al., 2012).”
From Cholesterol and matrisome pathways dysregulated in astrocytes and microglia (2022) · cites this paper as Montine et al., 2012
In the citing paper
“Neuropathological assessment was performed by 2 authors (T.G.B. and T.J.M.) blinded to clinical and imaging results and using NIA–AA diagnostic scoring guidelines.5,40”
From Positron Emission Tomography Imaging With [ 18 F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [40]
In the citing paper
“Additional changes that may also occur in the brains of AD patients include amyloid angiopathy, age-related brain atrophy, synaptic pathology, white matter rarefaction, granulovacuolar degeneration, neuron loss, TDP-43 proteinopathy, and neuroinflammation (20-26), which may contribute to cognitive impairment; however, these are not considered pathognomonic features of AD (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“In contrast, dense and extensive neocortical NFTs are very consistently associated with dementia and thus, according to new diagnostic criteria, these are required to constitute high burden of AD neuropathologic change (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“The current revision of the National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of AD stipulate that subjects with moderately dense neuritic AβPs may be regarded as having an intermediate level of AD neuropathologic change and that other potential contributors to cognitive impairment and dementia should be sought (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“There is no universally applied rubric for CVD pathologic diagnosis, although the recent National Institute on Aging–Alzheimer’s Association criteria attempted to systematize neuropathologic assessment of this complex form of brain injury (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“Alzheimer's disease cases met criteria for a high likelihood of AD (Montine et al., 2012).”
From Alzheimer's amyloid‐β and tau protein accumulation is associated with decreased expression of the LDL receptor‐associated protein in human brain tissue (2020) · cites this paper as Montine et al., 2012
Citations
Cites
McKhann, G. M., Knopman, D. S., Chertkow, H., Hyman, B. T., Jack, C. R., Kawas, C. H., Klunk, W. E., Koroshetz, W. J., Manly, J. J., Mayeux, R., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.005 · Cited by 18,657 · cited 1×
“‘‘Alzheimer’s disease’’ refers to a constellation of cognitive and behavioral changes that are typical for patients who have substantial amounts of its hallmark lesions [6, 39].”
Self-citationNeuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123 · cited 8×
“‘‘Intermediate’’ or ‘‘High’’ AD neuropathologic change (italicized) is considered sufficient explanation for dementia a NFT stage should be determined by the method of Braak [14, 15] b Ab/amyloid plaque score should be determined by the method of Thal et al.”
InfluentialStaging of brain pathology related to sporadic Parkinson’s disease
Braak, H., Tredici, K. D., Rüb, U., de Vos, R. A. I., Jansen Steur, E. N. H., & Braak, E. (2003) · Neurobiology of Aging · doi:10.1016/s0197-4580(02)00065-9 · Cited by 10,777 · cited 2×
“Given our focus on cognitive impairment and dementia rather than movement disorders [16], we recommend a modification of Fig.”
Albert, M. S., DeKosky, S. T., Dickson, D., Dubois, B., Feldman, H. H., Fox, N. C., Gamst, A., Holtzman, D. M., Jagust, W. J., Petersen, R. C., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.008 · Cited by 10,152 · cited 1×
“‘‘Alzheimer’s disease’’ refers to a constellation of cognitive and behavioral changes that are typical for patients who have substantial amounts of its hallmark lesions [6, 39].”
Self-citationSperling, R. A., Aisen, P. S., Beckett, L. A., Bennett, D. A., Craft, S., Fagan, A. M., Iwatsubo, T., Jack, C. R., Kaye, J., Montine, T. J., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.003 · Cited by 7,155 · cited 2×
“Similar neuropathologic changes, albeit usually at lower levels, also occur in individuals who did not show cognitive or behavioral impairments during life [54].”
Self-citationDiagnosis and management of dementia with Lewy bodies: Third report of the DLB consortium
McKeith, I. G., Dickson, D. W., Lowe, J., Emre, M., O'Brien, J. T., Feldman, H., Cummings, J., Duda, J. E., Lippa, C., Perry, E. K., et al. (2005) · Neurology · doi:10.1212/01.wnl.0000187889.17253.b1 · Cited by 5,069
Self-citationMirra, S. S., Heyman, A., McKeel, D., Sumi, S. M., Crain, B. J., Brownlee, L. M., Vogel, F. S., Hughes, J. P., Belle, G. V., Berg, L., et al. (1991) · Neurology · doi:10.1212/wnl.41.4.479 · Cited by 4,961 · cited 11×
“Region Stain for A /amyloid plaques [57] Stain for NFTs [14,15] Stain for NPs [41] Stain for LBs H&E”
InfluentialSelf-citationDeJesus-Hernandez, M., Mackenzie, I. R., Boeve, B. F., Boxer, A. L., Baker, M., Rutherford, N. J., Nicholson, A. M., Finch, N. A., Flynn, H., Adamson, J., et al. (2011) · Neuron · doi:10.1016/j.neuron.2011.09.011 · Cited by 4,936 · cited 1×
“With the exception of individuals with mutations in TARDBP, GRN, VCP or c9ORF72 [10, 18], it is not clear whether TDP-43 proteinopathy in these other neurodegenerative diseases is”
Self-citationTerry, R. D., Masliah, E., Salmon, D. P., Butters, N., DeTeresa, R., Hill, R., Hansen, L. A., & Katzman, R. (1991) · Annals of Neurology · doi:10.1002/ana.410300410 · Cited by 4,397 · cited 1×
“frequently have phospho-tau immunoreactivity [19, 36, 37, 55].”
Self-citationGorelick, P. B., Scuteri, A., Black, S. E., DeCarli, C., Greenberg, S. M., Iadecola, C., Launer, L. J., Laurent, S., Lopez, O. L., Nyenhuis, D., et al. (2011) · Stroke · doi:10.1161/str.0b013e3182299496 · Cited by 3,811
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Sorted by citations
Items 1,801–1,900 of 2,854
Hänninen, J. J., Nakajima, M., Vanninen, A., Hytönen, S., Rummukainen, J. K., Koivisto, A. M., Jääskeläinen, J. E., Soininen, H. S., Sutela, A., Vanninen, R. L., et al. (2021) · Free Neuropathology · doi:10.17879/freeneuropathology-2022-3331 · Cited by 9
“For ADNC evaluation, NIA-AA criteria were used [23].”
MethodWang, X., Wang, D., Li, X., Wang, W., Gao, P., Lou, B., Pfeuffer, J., Zhang, X., Zhu, J., Li, C., et al. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.974651 · Cited by 8
Three-Dimensional Imaging of Fibrinogen and Neurovascular Alterations in Alzheimer’s Disease
Merlini, M., Sözmen, E. G., Subramanian, K. S., Nana, A. L., Seeley, W. W., & Akassoglou, K. (2022) · Methods in molecular biology · doi:10.1007/978-1-0716-2655-9_5 · Cited by 8
Huie, E. Z., Escudero, A., Saito, N. H., Harvey, D. J., Nguyen, M.-L., Lucot, K. L., LaGrande, J., Mungas, D., DeCarli, C. S., Lamar, M., et al. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-220558 · Cited by 8
Self-citationThe role of sex differences in depression in pathologically defined Alzheimer’s disease
Tremblay, C., Choudhury, P., Belden, C. M., Goldfarb, D., Lorenzini, I., Beach, T. G., & Serrano, G. E. (2023) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2023.1156764 · Cited by 9
“Neuropathological AD diagnoses were defined as having “intermediate” or “high” criteria according to the National Institute on Aging/Reagan Institute criteria combined with a history of clinical dementia (Nia and Group, R. I. W, 1997; Hyman et al., 2012; Montine et al., 2012).”
MethodSelf-citationIverson, G. L., Jamshidi, P., Fisher‐Hubbard, A., Deep‐Soboslay, A., Hyde, T. M., Kleinman, J. E., deJong, J. L., Shepherd, C. E., Hazrati, L., & Castellani, R. J. (2023) · Frontiers in Neurology · doi:10.3389/fneur.2023.1143882 · Cited by 9
Uncovering the distinct macro-scale anatomy of dysexecutive and behavioural degenerative diseases
Corriveau‐Lecavalier, N., Barnard, L. R., Botha, H., Graff‐Radford, J., Ramanan, V. K., Lee, J., Dicks, E., Rademakers, R., Boeve, B. F., Machulda, M. M., et al. (2023) · Brain · doi:10.1093/brain/awad356 · Cited by 10
Self-citationCarlos, A. F., Sekiya, H., Koga, S., Gatto, R. G., Casey, M. C., Pham, N. T. T., Sintini, I., Machulda, M. M., Jack, C. R., Lowe, V. J., et al. (2023) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlad105 · Cited by 8
Self-citationInui, S., Kaneda, D., Sakurai, K., Uchida, Y., Abe, O., & Hashizume, Y. (2024) · Magnetic Resonance in Medical Sciences · doi:10.2463/mrms.mp.2023-0093 · Cited by 8
Huntingtin CAG repeats in neuropathologically confirmed tauopathies: Novel insights
Pérez‐Oliveira, S., Castilla‐Silgado, J., Painous, C., Aldecoa, I., Menéndez‐González, M., Estrada, M. B., Corte-Torres, M. D., Tomás‐Zapico, C., Compta, Y., Muñoz, E., et al. (2024) · Brain Pathology · doi:10.1111/bpa.13250 · Cited by 7
Kim, A., Yoshida, K., Kovács, G. G., & Forrest, S. L. (2024) · Modern Pathology · doi:10.1016/j.modpat.2024.100533 · Cited by 8
Alzheimer’s Disease Neuropathological Change in Aged Non-Primate Mammals
Ferrer, I. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25158118 · Cited by 13
“…Aging-Alzheimer’s Association (NIA-AA) defined AD as a neurodegenerative disease starting with brain A β deposition, followed by NFT pathology [64,65], and clinically categorized it as preclinical AD, mild cognitive impairment (MCI) due to AD, and mild, moderate, and severe Alzheimer’s dementia…”
BackgroundStereological approaches to dementia research using human brain tissue
Erskine, D., & Khundakar, A. A. (2016) · Journal of Chemical Neuroanatomy · doi:10.1016/j.jchemneu.2016.01.004 · Cited by 8
Patient and Caregiver Assessment of the Benefits From the Clinical Use of Amyloid PET Imaging
Mustafa, R., Brosch, J. R., Rabinovici, G. D., Dickerson, B. C., Carrillo, M. C., Glazier, B. S., Gao, S., Tierney, M., Fargo, K. N., Austrom, M. G., et al. (2017) · Alzheimer Disease & Associated Disorders · doi:10.1097/wad.0000000000000220 · Cited by 8
Mixed neuropathology in frontotemporal lobar degeneration
Pennington, C. M., Marini, L., Coulthard, E. J., & Love, S. (2020) · Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration · doi:10.1080/21678421.2020.1733019 · Cited by 8
A Clinicopathologic Study of Movement Disorders in Frontotemporal Lobar Degeneration
Pablo‐Fernández, E. D., González‐Herrero, B., Santacruz, D. M. C., Rossor, M. N., Schott, J. M., Lashley, T., Holton, J. L., Fox, N. C., Révész, T., Warren, J. D., et al. (2020) · Movement Disorders · doi:10.1002/mds.28356 · Cited by 10
Grinberg, L. T. (2022) · LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) · Cited by 6
Leveraging molecular biomarkers to make the common diagnosis in the uncommon patient
Day, G. S., Gordon, B. A., Bucelli, R. C., Perrin, R. J., Lopez-Chiriboga, A. S., & Ances, B. M. (2021) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2021.577474 · Cited by 8
van Engelen, M. E., Rozemüller, A. J. M., Erkoyun, H. U., Groot, C., Fieldhouse, J. L. P., Koene, T., Ossenkoppele, R., Gossink, F. T., Krudop, W. A., Vijverberg, E. G. B., et al. (2021) · Neurocase · doi:10.1080/13554794.2021.1905855 · Cited by 8
“Autopsy further pointed out that the temporal horns were slightly dilated and the amygdala was relatively small, with microscopic amyloid plaques and tangles, with an A3 B2 C2 score fitting an intermediate score for Alzheimer’s disease (AD) neuropathological change (Montine et al., 2012).”
BackgroundLong‐standing multiple system atrophy‐Parkinsonism with limbic and FTLD‐type α‐synuclein pathology
Coughlin, D. G., Dryden, I., Goodwill, V., et al. (2021) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12783 · Cited by 8
“Overall, AD neuropathologic change was low (A3 B1 C1) [8].”
BackgroundTeipel, S. J., Grothe, M. J., & Initiative, A. D. N. (2022) · European Journal of Neurology · doi:10.1111/ene.15270 · Cited by 8
“The neuro-pathological procedures follow previously established guidelines [12] that are captured in the format of the Neuropathology Data Form Version 10 of the National Alzheimer Coordinating Center”
Reduced mtDNA Copy Number in the Prefrontal Cortex of C9ORF72 Patients
Álvarez‐Mora, M. I., Podlesniy, P., Riazuelo, T., Molina‐Porcel, L., Gelpí, E., & Rodríguez‐Revenga, L. (2022) · Molecular Neurobiology · doi:10.1007/s12035-021-02673-7 · Cited by 8
Cancer and Vascular Comorbidity Effects on Dementia Risk and Neuropathology in the Oldest-Old
Lachner, C., Day, G. S., Camsari, G. B., Kouri, N., Ertekin‐Taner, N., Boeve, B. F., Labuzan, S. A., Lucas, J. A., Thompson, E. A., Siddiqui, H., et al. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220440 · Cited by 8
Self-citationPires, G., Ueberheide, B. M., Wısnıewskı, T., & Drummond, E. (2022) · Methods in molecular biology · doi:10.1007/978-1-0716-2655-9_14 · Cited by 8
Carlos, A. F., Machulda, M. M., Rutledge, M. H., Nguyen, A. T., Reichard, R. R., Baker, M., Rademakers, R., Dickson, D. W., Petersen, R. C., & Josephs, K. A. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-221094 · Cited by 11
Self-citationVizcarra, J. C., Teich, A. F., Dugger, B. N., & Gutman, D. A. (2023) · Free Neuropathology · doi:10.17879/freeneuropathology-2023-4696 · Cited by 8
Bier, J., Verschraegen, J., Vandenberghe, R. R., Guillaume, B., Picard, G., Otte, G., Mormont, E., Gilles, C., Segers, K., Sieben, A., et al. (2015) · Acta Neurologica Belgica · doi:10.1007/s13760-014-0423-7 · Cited by 8
“The new pathological criteria for AD (Q17 and Q18) were not included in this more clinically oriented study [13].”
Global Brain Involvement in Posterior Cortical Atrophy: Multimodal MR Imaging Investigation
Glick-Shames, H., Keadan, T., Backner, Y., Bick, A. S., & Levin, N. (2020) · Brain Topography · doi:10.1007/s10548-020-00788-z · Cited by 8
Can Creutzfeldt-Jakob disease unravel the mysteries of Alzheimer?
Kovács, G. G. (2016) · Prion · doi:10.1080/19336896.2016.1228507 · Cited by 8
Nuclear alpha-synuclein is present in the human brain and is modified in dementia with Lewy bodiesPreprint
Koss, D. J., Erskine, D., Porter, A., Palmoski, P., Leite, M., Attems, J., & Outeiro, T. F. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.10.20.465125 · Cited by 8
Saito, K., Goulding, D. S., Nolt, G. L., Dimas, S. H., Moore, L. C., Stevens, I. O., Anderson, S., Snipes, J. A., Macauley, S. L., Nelson, P. T., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.05.16.654329 · Cited by 9
Self-citationKim, E.-J., Vatsavayai, S., & Seeley, W. W. (2016) · The Behavioral Neurology of Dementia · doi:10.1017/9781139924771.008 · Cited by 7
Hemispheric Asymmetry and Atypical Lobar Progression of Alzheimer-Type Tauopathy
Tremblay, C., Serrano, G. E., Intorcia, A. J., Curry, J. R., Sue, L. I., Nelson, C. M., Walker, J. E., Glass, M. J., Arce, R. A., Fleisher, A., et al. (2022) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlac008 · Cited by 8
Self-citationVontell, R., Gober, R., Dallmeier, J., Brzostowicki, D. J., Barreda, A., Blennow, K., Zetterberg, H., Kvartsberg, H., Gultekin, S. H., Vaccari, J. P. D. R., et al. (2024) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1002/trc2.12444 · Cited by 7
Jicha, G. A., Tucker, T. C., Arnold, S. M., & Nelson, P. T. (2024) · Alzheimer s Research & Therapy · doi:10.1186/s13195-024-01532-6 · Cited by 7
“…neuropathologies, for example: Aβ and tau in amyloid plaques and neurofibrillary tangles of Alzheimer’s disease neuropathologic changes (ADNC) [34]; α-Synuclein in Lewy body diseases (LBDs) [35, 36]; and, TDP-43 proteinopathy in frontotemporal lobar degeneration (FTLD-TDP) [37] and in…”
BackgroundSelf-citationAlzheimer’s Disease-Related Cerebrospinal Fluid Biomarkers in Progressive Supranuclear Palsy
Ishiguro, T., & Kasuga, K. (2024) · Brain Sciences · doi:10.3390/brainsci14090859 · Cited by 7
“Alzheimer’s Disease (AD) is pathologically characterized by the extracellular deposition of β -amyloid (A β ), as well as the intracellular accumulation of hyperphosphorylated tau [31].”
BackgroundCohen, J. S., Phillips, J. T., Das, S. R., Olm, C. A., Radhakrishnan, H., Rhodes, E., Cousins, K. A. Q., Xie, S. X., Nasrallah, I. M., Yushkevich, P. A., et al. (2024) · NeuroImage Clinical · doi:10.1016/j.nicl.2024.103714 · Cited by 8
“Based on modern neuropathological criteria using NIA-AA criteria (Montine et al., 2012) we categorized cases as LBD/AD + with evidence of an “ ABC score ” (Montine et al., 2012) consistent with “ intermediate ” or “ high ” AD neuropathological change; or LBD/AD-if the ABC score was “ not ” or “ low…”
Toledo, J. B., Salmon, D. P., Armstrong, M. J., & Galasko, D. (2024) · Alzheimer s Research & Therapy · doi:10.1186/s13195-024-01628-z · Cited by 7
Distinct subcellular localization of tau and alpha-synuclein in lewy body disease
Fischer, D. L., Menard, M. A., Abdelaziz, O. Z., Kanaan, N. M., Cobbs, V. G., Kennedy, R., Serrano, G. E., Beach, T. G., & Volpicelli‐Daley, L. A. (2025) · Acta Neuropathologica Communications · doi:10.1186/s40478-024-01913-w · Cited by 7
Self-citationLoss of endothelial CD2AP causes sex-dependent cerebrovascular dysfunction
Vandal, M., Institóris, Á., Réveret, L., Korin, B., Gunn, C., Hirai, S., Jiang, Y., Lee, S., Lee, J. Y., Bourassa, P., et al. (2025) · Neuron · doi:10.1016/j.neuron.2025.01.006 · Cited by 7
Liou, J., Li, J., Berardinelli, J., Jin, H., Santini, T., Noh, J., Farhat, N., Wu, M., Aizenstein, H. J., Mettenburg, J., et al. (2025) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlaf010 · Cited by 7
“46,47 Immunohistochemical staining for β -amyloid was performed to generate Thal phases.”
Smallwood, M. J., Alghayth, M. A., Knight, A. R., Tveen‐Jensen, K., Pitt, A. R., Spickett, C. M., Llewellyn, D. J., Pula, G., Wearn, A. R., Vanhatalo, A., et al. (2025) · Redox Biology · doi:10.1016/j.redox.2025.103612 · Cited by 7
“AD brains had detailed neuropathological assessment according to the National Institute on Aging-Alzheimer ’ s Association guidelines [47], and AD pathology was a sufficient explanation for the dementia in these cases.”
Afrakoti, L. G. M. P., Moghadam, S. D., & Hadinezhad, P. (2025) · Journal of Alzheimer s Disease Reports · doi:10.1177/25424823251329188 · Cited by 12
“25,26 A β oligomers, particularly A β 42 , are highly neurotoxic and interact with receptors such as NMDA and AMPA.”
InfluentialAlzheimer’s Disease and Other Dementias
Brugulat‐Serrat, A., Shaaban, C. E., Emrani, S., & Sundermann, E. E. (2025) · Springer eBooks · doi:10.1007/978-3-031-87228-0_5 · Cited by 7
Frigerio, I., Morella, M. L., Winkelaar, A. B., Vorgia, D. T., Brevé, J. J. P., Boiten, W. A., van der Gaag, B., Calandri, I. L., Jonker, A. J., Berendse, H. W., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-61052-1 · Cited by 12
Retinal manifestations and their diagnostic significance in Alzheimer's disease
Abhyankar, S. D., Little, K., Stitt, A. W., & Bhatwadekar, A. D. (2025) · Journal of Alzheimer s Disease Reports · doi:10.1177/25424823251361937 · Cited by 8
Argyrophilic grain disease: epidemiology and association with cognitive decline and parkinsonism
Arakawa, A., Matsubara, T., Shioya, A., Hara, M., Hiroyoshi, Y., Kurihara, M., Morimoto, S., Kato, T., Higashihara, M., Sengoku, R., et al. (2025) · Brain Communications · doi:10.1093/braincomms/fcaf352 · Cited by 7
“However, the prevalence of Alzheimer’s disease cases (those categorized as ‘high’ in NIA-AA criteria 59 ) is not significantly higher (7.9% versus 7.4%).”
InfluentialKivisäkk, P., Fatima, H. A., Wu, C., Padmanabhan, N., Romero, D., Gorham, T., Weik, M., Dodge, H. H., Scherzer, C. R., Das, S., et al. (2026) · Neurology · doi:10.1212/wnl.0000000000214351 · Cited by 11
Self-citationA quantitative DOPA decarboxylase biomarker for diagnosis in Lewy body disorders
Bolsewig, K., Bellomo, G., Hok‐A‐Hin, Y. S., Idrissi, I. A., Vermunt, L., Lleó, A., Alcolea, D. A., Sieben, A., Engelborghs, S., Simonsen, A. H., et al. (2026) · Nature Medicine · doi:10.1038/s41591-026-04212-0 · Cited by 11
Povala, G., Bellaver, B., Lussier, F. Z., Amaral, L., Bauer‐Negrini, G., Ferreira, P. C. L., Rocha, A., Ruppert, E. P., Medeiros, M. S., Tissot, C., et al. (2026) · The Lancet · doi:10.1016/s0140-6736(26)00417-4 · Cited by 10
“This view aligns with previous frameworks for preclinical Alzheimer’s disease, 24,25 cognitive impairment due to Alzheimer’s disease, 6,26 neuropathological diagnostic criteria, 27 and expert opinions.”
Frontotemporal lobar degeneration: Study of a clinicopathological cohort
Gil, M. J., Palomo, M. S. M., Cuadrado, M. L., Fernández, C., Góméz, E., Matesanz, C., Calero, M., & Rábano, A. (2018) · Journal of Clinical Neuroscience · doi:10.1016/j.jocn.2018.10.024 · Cited by 9
Jellinger, K. A. (2022) · Parkinsonism & Related Disorders · doi:10.1016/j.parkreldis.2022.105273 · Cited by 7
Horvat, L. L., Španić, E., Leko, M. B., Zubčić, K., Horvat, L., Mustapić, M., Hof, P. R., & Šimić, G. (2023) · Biomedicines · doi:10.3390/biomedicines11041004 · Cited by 7
“With the recent definition of Alzheimer’s disease (AD) as a biological spectrum, using the National Institute on Aging/Alzheimer’s Association (NIA-AA) research framework [19,20], it is now possible to classify different pathophysiologically defined subtypes of AD [21].”
MethodKim, A., Martínez-Valbuena, I., Li, J., Lang, A. E., & Kovács, G. G. (2023) · Biomolecules · doi:10.3390/biom13060936 · Cited by 8
“* Subjects were given an ABC score based on the neuropathologic assessment of Alzheimer’s disease in ref [43].”
MethodUnderstanding solvent effects on solvatomorphisms of donepezil-maleic acid
Liu, M., Xing, W., Zou, Y., et al. (2023) · Journal of Molecular Structure · doi:10.1016/j.molstruc.2023.136898 · Cited by 7
Pasquini, L., Pereira, F. L., Seddighi, S., Zeng, Y., Wei, Y., Illán‐Gala, I., Vatsavayai, S. C., Friedberg, A., Lee, A. J., Brown, J. A., et al. (2024) · Brain · doi:10.1093/brain/awae205 · Cited by 8
Alldred, M. J., Pidikiti, H., Ibrahim, K. W., Lee, S. H., Heguy, A., Hoffman, G. E., Roussos, P., Wısnıewskı, T., Węgiel, J., Stutzmann, G. E., et al. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02768-0 · Cited by 8
“Neuropathology score criteria followed the National Institute on Aging-Alzheimer’s Association ‘ABC’ system (Supplementary Materials and Methods) [90].”
Astrocyte–Neuron Interactions in Alzheimer’s Disease
Muñoz‐Castro, C., & Serrano‐Pozo, A. (2024) · Advances in neurobiology · doi:10.1007/978-3-031-64839-7_14 · Cited by 7
Alzheimer's disease clinical variants show distinct neuroinflammatory profiles with neuropathology
Boon, B. D. C., Frigerio, I., de Gooijer, D., Morrema, T. H. J., Bol, J. G. J. M., Galis, Y., Heymans, M. W., Bank, N. B., Murray, M. E., Amsterdam, N. A. B. C., et al. (2024) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.13009 · Cited by 7
“Neuropathological diagnosis was established according to international guidelines of Brain Net Europe II consortium and NIA-AA criteria for AD neuropathological change [23].”
InfluentialYang, C. G., Sun, Z.-P., Jiang, J., Cai, X.-L., Wang, Y., Wang, H., Che, C., Tu, E., Pan, A., Zhang, Y., et al. (2024) · Scientific Reports · doi:10.1038/s41598-024-77026-0 · Cited by 7
“The definition of AD is evolving from a clinicopathological to a biological entity with the advance in the identification of fluid and brain imaging biomarkers 14,34,97–99 .”
BackgroundSaez-Calveras, N., Vaquer‐Alicea, J., White, C. L., Tak, Y., Cosentino, S., Faust, P. L., Louis, E. D., & Diamond, M. I. (2025) · Acta Neuropathologica · doi:10.1007/s00401-024-02843-6 · Cited by 9
“The level of AD neuropathologic change (ADNC) was rated according to National Institute on Aging and Alzheimer’s Association (NIA-AA) guidelines using an “ABC” score as none, low, intermediate, or high [37].”
Shaw, J. S., Huang, P. C., Rosenberg, P. B., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70039 · Cited by 7
Bilateral ganglioglioma of the trigeminal nerve in an 83‐year‐old man
Hargus, G., Bink, A., Nagel, I., et al. (2013) · Neuropathology · doi:10.1111/neup.12054 · Cited by 7
Does ALS‐FUS without FUS mutation represent ALS‐FET? Report of three cases
Borrego‐Écija, S., Cortés‐Vicente, E., Cervera‐Carles, L., et al. (2018) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12527 · Cited by 7
Li, Y., He, X. M., Jin, Y., Wang, J., Liang, F., Pei, R., Li, P., Wang, Y., & Su, W. (2020) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2020.00207 · Cited by 9
“Alzheimer’s disease (AD) is the most common age-related progressive neurodegenerative disorder and is characterized by cognitive deficits (Montine et al., 2012).”
BackgroundSakurai, K., Kaneda, D., Inui, S., Uchida, Y., Morimoto, S., Nihashi, T., Kato, T., Ito, K., & Hashizume, Y. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210043 · Cited by 7
“…by applying the following inclusion criteria: 1) neuropathological diagnoses according to the published criteria of AD, AGD, and SD-NFT [3, 16, 17], 2) dementia status according to the major neurocognitive disorders of the DSM-V criteria, and 3) acquisition of MRI examinations including…”
Priemer, D. S., & Folkerth, R. D. (2021) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlab059 · Cited by 7
A Mutant Variant of E2F4 Triggers Multifactorial Therapeutic Effects in 5xFAD Mice
López‐Sánchez, N., Ramón‐Landreau, M., Trujillo, C., Garrido‐García, A., & Frade, J. M. (2022) · Molecular Neurobiology · doi:10.1007/s12035-022-02764-z · Cited by 7
“The severity of the Alzheimer pathology was scored according to the “National Institute on Aging-Alzheimer’s association guidelines for the neuropathologic assessment of Alzheimer’s disease,” following the “ABC” protocol [29].”
MethodPalmieri, I., Poloni, T. E., Medici, V., Zucca, S., Davin, A., Pansarasa, O., Ceroni, M., Tronconi, L., Guaita, A., Gagliardi, S., et al. (2022) · Biomedicines · doi:10.3390/biomedicines10071687 · Cited by 7
Assessment of Current Practices Across Alzheimer's Disease Research Centers Biorepositories
Lucot, K. L., Suarez, W., Mifflin, K., et al. (2022) · Biopreservation and Biobanking · doi:10.1089/bio.2022.0022 · Cited by 7
“28,29,37 Even with current guidelines, although it is stated for specific stains, specific antibodies/protocols are not given, thus there is room for interpretation given the nature of each neuropathology core’s specific research questions.”
Mei, F., Hu, J., Wu, Z., Zhang, G., Liu, A., Li, X., Zhu, M., Gan, Y., Liang, L., Zhao, X., et al. (2022) · Cell Reports · doi:10.1016/j.celrep.2022.111101 · Cited by 7
Ichimata, S., Kim, A., Nishida, N., & Kovács, G. G. (2022) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12869 · Cited by 7
“(ADNC) was divided into four categories (Not, Low, Intermediate and High) following the National Institute on Aging-Alzheimer’s Association guidelines [26].”
MethodCerebral Microbleeds in Advanced Dementia: Clinical and Pathological Correlates
Boyano, I., Ramos, A., López‐Álvarez, J., Mendoza-Rebolledo, C., Osa-Ruiz, E., Rodríguez, I., Pérez, A., Alfayate, E., González, B., Fernández, L. R., et al. (2018) · American Journal of Alzheimer s Disease & Other Dementias® · doi:10.1177/1533317518770783 · Cited by 7
Cholinergic Neurons in Nucleus Subputaminalis in Primary Progressive Aphasia
Hamodat, H., Fisk, J. D., & Darvesh, S. (2019) · Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques · doi:10.1017/cjn.2019.6 · Cited by 7
Speech and Language Presentations of FTLD-TDP Type B Neuropathology
Lee, D. J., Bigio, E. H., Rogalski, E. J., & Mesulam, M. M. (2020) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlz132 · Cited by 7
Self-citationLibard, S., Walter, J., & Alafuzoff, I. I. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-201469 · Cited by 8
“The reference cases in the TMA were split into three groups, according to the level of ADNC pathology, as recommended by the National Institute on Aging and Alzheimer’s Association’s guidelines, into low, intermediate, and high grade of ADNC [14, 15].”
MethodKlotz, S., Ricken, G., Preusser, M., Dieckmann, K. U., Widhalm, G., Rössler, K., Fischer, P. A., Kalev, O., Wöehrer, A., Kovács, G. G., et al. (2022) · Brain Pathology · doi:10.1111/bpa.13058 · Cited by 6
“[17] ßA4: none (−); isolated (i) 1– 5 plaques; mild (+) 6– 15 plaques; moderate (++) 15– 30 plaques; severe (+++) >30 plaques.”
Fanciulli, A., Leys, F., Lehner, F., Sidoroff, V., Ruf, V., Raccagni, C., Mahlknecht, P., Kuipers, D. J. S., van IJcken, W. F. J., Stockner, H., et al. (2022) · Brain Communications · doi:10.1093/braincomms/fcac175 · Cited by 7
“4M; Braak and Braak stage IV; Thal phase 3; CERAD B; NIA classi fi cation A2, B2, C2) 45 – 48 , as well as advanced argyrophilic grain disease changes with pretangles and numerous argyrophilic grains (Fig.”
Propranolol Reduces p-tau Accumulation and Improves Behavior Outcomes in a Polytrauma Murine Model
Singer, K. E., McGlone, E., Collins, S. M., Wallen, T. E., Morris, M. C., Schuster, R. M., England, L. G., Robson, M. J., & Goodman, M. D. (2022) · Journal of Surgical Research · doi:10.1016/j.jss.2022.09.017 · Cited by 8
Cerebrovascular pathology: the dark side of neurodegeneration
Carare, R. O., & Kalaria, R. N. (2016) · Acta Neuropathologica · doi:10.1007/s00401-016-1573-x · Cited by 7
“Medial temporal lobe and hippocampal atrophy accompanied by variable hippocampal sclerosis are widely accepted as consistent pathological features in Alzheimer’s disease [7] but they are also apparent in vascular dementia.”
BackgroundIntorcia, A. J., Filon, J. R., Hoffman, B., Serrano, G. E., Sue, L. I., & Beach, T. G. (2019) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/570093 · Cited by 7
Self-citationZamani, J., Sadr, A., & Javadi, A. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.08.18.256321 · Cited by 7
Falla, D. S., Villegas‐Lanau, C. A., White, C. L., Serrano, G. E., Acosta‐Uribe, J., Mejía‐Cupajita, B., Villalba‐Moreno, N. D., Lu, P., Glatzel, M., Kofler, J., et al. (2023) · medRxiv · doi:10.1101/2023.08.14.23294081 · Cited by 7
“Pathology categories investigated included the major AD-specific lesions: senile or amyloid plaques (NACC variable NPTHAL; all plaque types classified by Thal amyloid phase [17], neurofibrillary tangles (NACC variable NPBRAAK; classified by Braak stage [18,19]), neuritic plaques (NACC variable NPNEUR; classified accor…”
BackgroundMethodInfluentialSelf-citationLewis, A. J., van den Heuvel, L., Fabrizio, M. D., Bandelier, K., Proniakova, D., Burger, D., Shafiei, N., Ekundayo, K., Offringa, S., Huisman, E., et al. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.07.25.605088 · Cited by 7
Saunders, C., Rocha-Rangel, P., Desai, R., Quadri, Z., Lui, H., Hunt, J. B., Liang, H., Rogers, C. B., Nash, K. R., Tsoi, P. S., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.02.28.639952 · Cited by 7
Self-citationOatman, S. R., Reddy, J. S., Atashgaran, A., Wang, X., Min, Y., Quicksall, Z., Vanelderen, F., Carrasquillo, M. M., Liu, C.-C., Yamazaki, Y., et al. (2026) · Nature Communications · doi:10.1038/s41467-026-68864-9 · Cited by 6
Self-citationOhm, D. T., Rhodes, E., Bahena, A., Capp, N., Lowe, M., Sabatini, P., Trotman, W., Olm, C. A., Phillips, J., Prabhakaran, K., et al. (2023) · Frontiers in Neurology · doi:10.3389/fneur.2023.1245886 · Cited by 6
Alves, V. C., Figueiro‐Silva, J., Trullás, R., Ferrer, I., & Carro, E. (2024) · Genes · doi:10.3390/genes15030385 · Cited by 6
“The neuropathological diagnosis of sporadic AD was based on neurofibrillary tangle pathology and A β plaques [14].”
MethodRosen, G. A., Kirsch, D. A., Nicks, R., et al. (2024) · Frontiers in Neuroscience · doi:10.3389/fnins.2024.1474617 · Cited by 6
Genome-wide association study of neuropathological features in Lewy body disease
Valentino, R. R., Koga, S., Soto‐Beasley, A. I., Ono, D., Wieczorek, M. A., Johnson, P. W., White, L. J., Watkins, M. M., Murray, M. E., Kasanuki, K., et al. (2025) · Brain · doi:10.1093/brain/awaf105 · Cited by 7
Self-citationPerez, S. E., Nadeem, M., He, B., Miguel, J. C., Moreno, D. G., Moreno‐Rodríguez, M., Malek‐Ahmadi, M. H., Hales, C. M., & Mufson, E. J. (2025) · Brain Pathology · doi:10.1111/bpa.70004 · Cited by 7
“62 Cases were also evaluated for transactive response DNA-binding protein 43 kDa (TDP-43) inclusions 63 and assigned an ABC criteria.”
Rauchmann, B., Ersözlü, E., Luedecke, D., Franzmeier, N., & Perneczky, R. (2025) · Scientific Reports · doi:10.1038/s41598-025-98338-9 · Cited by 8
Coomans, E. M., van Tol, B. G. J., Groot, C., Smith, R. A., Palmqvist, S., Stomrud, E., Pontecorvo, M. J., Shcherbinin, S., Kennedy, I. A., Kotari, V., et al. (2025) · European Journal of Nuclear Medicine and Molecular Imaging · doi:10.1007/s00259-025-07384-y · Cited by 6
“We assessed both single Braak NFT stages (ranging from Braak stage I to VI) as well combined Braak NFT stages (Braak stage I-II; Braak stage III-IV and Braak stage V-VI) [28 ].”
Jamison, D., Kadamangudi, S., Tumurbaatar, B., Zhang, W.-R., Palmer, L. K., Kunkel, S., Kayed, R., Limón, A., & Taglialatela, G. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251352382 · Cited by 5
Quantification of Alzheimer disease neuropathology using tissue microarrays
Nguyen-Hao, H.-T., Liu, J., Novelli, M., Maskey, D., Schwartz, R. S., Harari, O., & Sutherland, G. T. (2025) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlaf064 · Cited by 6
Mastenbroek, S. E., Collij, L. E., Vogel, J. W., Caldera, S., Serrano, G. E., Adler, C. H., Vargiu, C. M., Palmqvist, S., Barkhof, F., Parchi, P., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-62458-7 · Cited by 6
Self-citationBerson, E., Perna, A., Bukhari, S. A., Kim, Y., Xue, L., Seong, D., Mataraso, S. J., Ghanem, M., Chang, A. L., Montine, K. S., et al. (2025) · Brain · doi:10.1093/brain/awaf285 · Cited by 7
“To capture the strongest difference between ADD and AD resilience, we applied stringent neuropathological and clinical criteria to define AD resilience as previously described, 2,31 therefore discarding cases with intermediate neuropathologic changes or mild cognitive impairment.”
Self-citationComparison of multiple quantitative strategies for neuropathologic image analyses
Kanner, H., Tilton, C. M., Alvarez, V. E., Stein, T. D., McKee, A. C., & Cherry, J. D. (2025) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlaf098 · Cited by 6
Purkinje Cell Loss in Essential Tremor: Collective Data From 215 Brains Over a 21‐Year Period
Kerridge, C. A., Hernandez, R. S., Hernandez, N. C., Faust, P. L., & Louis, E. D. (2025) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.70204 · Cited by 6
“All ET, 2 SCA, and 93 control brains had a complete neuropathological assessment at the NYBB, including determination of the extent of Alzheimer's disease neuropathological change (ADNC) and Lewy pathology (LP), as detailed in Supporting Information [36–42].”
Specific atrophy patterns distinguish tau and TDP-43 pathology: a longitudinal MRI ante-mortem study
Salman, Y., Goloubeva, J., Huyghe, L., Quenon, L., Tomé, S. O., Hanseeuw, B. J., & Initiative, A. D. N. (2025) · Acta Neuropathologica Communications · doi:10.1186/s40478-025-02200-y · Cited by 6
“ADNC was established according to the criteria of Montine et al. [34].”
Metadata
- Authors
- Montine, T. J., Phelps, C. H., Beach, T. G., Bigio, E. H., Cairns, N. J., Dickson, D. W., Duyckaerts, C., Frosch, M. P., Masliah, E., Mirra, S. S., Nelson, P. T., Schneider, J. A., Thal, D. R., Trojanowski, J. Q., Vinters, H. V., & Hyman, B. T.
- Affiliations
- University of Washington (US)
- National Institutes of Health (US)
- Banner Sun Health Research Institute (US)
- Northwestern University (US)
- Washington University in St. Louis (US)
- Mayo Clinic (US)
- Pitié-Salpêtrière Hospital (FR)
- Harvard University (US)
- University of California San Diego (US)
- SUNY Downstate Health Sciences University (US)
- University of Kentucky (US)
- Rush University Medical Center (US)
- Universität Ulm (DE)
- University of Pennsylvania (US)
- University of California, Los Angeles (US)
- Corresponding author
- Montine, Thomas J.
- ORCID
- Venue
- Acta Neuropathologica
- Published
- 2011-11-20
- Volume
- 123
- Issue
- 1
- Pages
- 1-11
- ISSN
- 0001-6322 (ISSN-L)
- 1432-0533
- PMC
- PMC3268003
- OpenAlex
- W2128228199
- Cited by
- 2,894
- References
- 66
- Citations by year
- 2026: 254 · 2025: 290 · 2024: 329 · 2023: 251 · 2022: 284 · 2021: 257 · 2020: 244 · 2019: 183 · 2018: 164 · 2017: 148 · 2016: 144 · 2015: 136 · 2014: 92 · 2013: 69 · 2012: 46
- FWCI
- 39.19
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Acta Neuropathologica (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5u01ag024904-10)
- National Institute on Aging (U01-AG-024904, R01AG017917, AG18840, AG-15819, R01AG015866, P30AG028383, R01AG042210, R01AG018440, U01AG016976, P50AG005131, P50AG016570, P01AG003949, P30AG010124, R01AG015819, P30AG010161, AG24904, P50AG005681, P30AG019610, P01AG003991, P50AG005136, P50AG005134, P30AG013854, U19AG010483, RF1AG015819, P01AG012435, U19AG024904, P30AG062421)
- National Institute of Neurological Disorders and Stroke (P50NS062684)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, amyloid-beta deposition, neurofibrillary tangles, neuritic plaques, ABC score, Lewy body disease, vascular brain injury, hippocampal sclerosis, TDP-43 inclusions, staining techniques, clinicopathological correlation, preclinical Alzheimer's disease
- MeSH terms
- Alzheimer Disease, Brain, Cerebrovascular Disorders, DNA-Binding Proteins, Hippocampus, Humans, Sclerosis, United States, Cerebrovascular Trauma, Lewy Body Disease, National Institute on Aging (U.S.)
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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