The DOI matches its Crossref record; 66 of the 66 references it cites were found in a registry or an index; 27 of the 65 sources its claims cite were checked for support.
National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach
Open accessAbstract
We present a practical guide for the implementation of recently revised National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease (AD). Major revisions from previous consensus criteria are: (1) recognition that AD neuropathologic changes may occur in the apparent absence of cognitive impairment, (2) an "ABC" score for AD neuropathologic change that incorporates histopathologic assessments of amyloid β deposits (A), staging of neurofibrillary tangles (B), and scoring of neuritic plaques (C), and (3) more detailed approaches for assessing commonly co-morbid conditions such as Lewy body disease, vascular brain injury, hippocampal sclerosis, and TAR DNA binding protein (TDP)-43 immunoreactive inclusions. Recommendations also are made for the minimum sampling of brain, preferred staining methods with acceptable alternatives, reporting of results, and clinico-pathologic correlations.
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11 No full text of the sources · 9 Partly supported · 4 Supported · 3 Supported so far · 1 Own interpretation · accuracy not yet measured
Every source the paper cites for this claim was checked and supports it.
In the paper
“recognition that AD neuropathologic changes may occur in the apparent absence of cognitive impairment”
- Also stated in: § CLINICO-PATHOLOGIC CORRELATION · plain
“Similar neuropathologic changes, albeit usually at lower levels, also occur in individuals who did not show cognitive or behavioral impairments during life [54].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > Abstract
What the sources say
- Supportedcites [54] Sperling RA, Aisen PS, Beckett LA et al (2011) Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement 7:280–292 source
Section 6 reports that AD-related biomarker abnormalities can be detected before overt clinical symptoms and that Aβ accumulation occurs in clinically normal older adults. Section 2 also notes that some people have diagnostic AD neuropathological features at autopsy without having developed dementia during life. No page numbers are available in our copy. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § CLINICO-PATHOLOGIC CORRELATION · plain
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“LBs may be detected in neurons of medulla, pons and midbrain with hematoxylin and eosin (H&E)-stained sections; however, greater sensitivity can be achieved with immunohistochemistry for α-synuclein and this approach is strongly preferred [3,4,13].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE > Method
What the sources say
- Partly supportedcites [3] Alafuzoff I, Parkkinen L, Al-Sarraj S et al (2008) Assessment of alpha-synuclein pathology: a study of the BrainNet Europe Consortium. J Neuropathol Exp Neurol 67:125–143 sourceExperimental — accuracy not yet measured
The Introduction (p. 125) says consensus guidelines recommend α-synuclein immunohistochemistry for synucleinopathies, supporting the preference for that approach. The paper’s staining results and Discussion assess variation among immunohistochemical methods, but do not establish that immunohistochemistry detects Lewy bodies more sensitively than H&E; searches for H&E and hematoxylin–eosin found no such comparison. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [4] Alafuzoff I, Pikkarainen M, Al-Sarraj S et al (2006) Interlaboratory comparison of assessments of Alzheimer disease-related lesions: a study of the BrainNet Europe Consortium. J Neuropathol Exp Neurol 65:740–757 source
- Partly supportedcites [13] Beach TG, White CL, Hamilton RL et al (2008) Evaluation of alpha-synuclein immunohistochemical methods used by invited experts. Acta Neuropathol 116:277–288 sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) calls α-synuclein immunohistochemistry the method of choice for diagnosing Lewy body disorders, supporting its preferred use. The paper compares immunohistochemical methods with one another, however, and does not establish that they detect Lewy bodies more sensitively than H&E staining. (LLM, conf=0.84)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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- Partly supported
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In the paper
“one MVL identified in standard sections of brain (Table 1 regions shaded green) is of unclear relationship to cognitive function, while multiple MVLs in these regions are associated with increased likelihood of cognitive impairment or dementia [24,52,62].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > CEREBROVASCULAR DISEASE and VASCULAR BRAIN INJURY > Reporting
What the sources say
- Partly supportedcites [24] Gorelick PB, Scuteri A, Black SE et al (2011) Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 42:2672–2713 sourceExperimental — accuracy not yet measured
Section 3.2 (page not available in our copy) reports that some studies associate multiple microscopic infarcts with dementia, even after accounting for macroscopic infarcts. It does not establish the claim for MVLs generally or specify that the lesions were identified in standard brain sections. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites [52] Sonnen JA, Larson EB, Crane PK et al (2007) Pathological correlates of dementia in a longitudinal, population-based sample of aging. Ann Neurol 62:406–413 source
- Not checked — no full text of the sourcecites [62] White L (2009) Brain lesions at autopsy in older Japanese-American men as related to cognitive impairment and dementia in the final years of life: a summary report from the Honolulu-Asia aging study. J Alzheimers Dis 18:713–725 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Clinico-pathologic correlations for individuals without cognitive impairment should indicate that it is possible for AD neuropathologic change to predate onset of symptoms by years [54].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > AD NEUROPATHOLOGIC CHANGE > Reporting
What the sources say
- Supportedcites [54] Sperling RA, Aisen PS, Beckett LA et al (2011) Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement 7:280–292 source
Section 2, “Redefining the earliest stages of AD,” says the pathological cascade may begin a decade or more before clinically evident impairment. Section 6 also describes AD-related abnormalities in cognitively normal individuals, supporting the claim that neuropathologic change can predate symptoms by years. (LLM, conf=0.94)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“one MVL identified in standard sections of brain (Table 1 regions shaded green) is of unclear relationship to cognitive function, while multiple MVLs in these regions are associated with increased likelihood of cognitive impairment or dementia [24,52,62].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > CEREBROVASCULAR DISEASE and VASCULAR BRAIN INJURY > Reporting
What the sources say
- Partly supportedcites [24] Gorelick PB, Scuteri A, Black SE et al (2011) Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 42:2672–2713 sourceExperimental — accuracy not yet measured
Section 3.2 (page unavailable) says the number of infarcts needed for cognitive impairment is difficult to determine and reports that multiple microscopic infarcts may be related to dementia. It does not specifically assess the cognitive significance of one MVL identified in standard brain sections. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites [52] Sonnen JA, Larson EB, Crane PK et al (2007) Pathological correlates of dementia in a longitudinal, population-based sample of aging. Ann Neurol 62:406–413 source
- Not checked — no full text of the sourcecites [62] White L (2009) Brain lesions at autopsy in older Japanese-American men as related to cognitive impairment and dementia in the final years of life: a summary report from the Honolulu-Asia aging study. J Alzheimers Dis 18:713–725 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“this may represent pre-clinical LBD [12,22,31].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE > Reporting
What the sources say
- Supportedcites [12] Beach TG, Adler CH, Sue LI et al (2008) Reduced striatal tyrosine hydroxylase in incidental Lewy body disease. Acta Neuropathol 115:445–451 source
The Introduction defines incidental Lewy body disease as Lewy bodies without clinically documented parkinsonism or dementia. The Results and discussion report reduced striatal tyrosine hydroxylase in these individuals and say this suggests ILBD is likely a precursor to Parkinson’s disease and/or dementia with Lewy bodies, supporting the citing sentence’s qualified “may represent” claim. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites [22] Dickson DW, Fujishiro H, DelleDonne A et al (2008) Evidence that incidental Lewy body disease is pre-symptomatic Parkinson’s disease. Acta Neuropathol 115:437–444 source
- Supportedcites [31] Jicha GA, Schmitt FA, Abner E et al (2010) Prodromal clinical manifestations of neuropathologically confirmed Lewy body disease. Neurobiol Aging 31:1805–1813 source
The Introduction (page unavailable) says Lewy body pathology has been found in autopsied people described as normal and suggests that DLB pathology may predate clinical diagnosis. The Discussion (page unavailable) also says the study’s subjects were cognitively and neurologically normal at enrollment. Together, these support the qualified suggestion that LBD without apparent cognitive or motor deficits may be pre-clinical. (LLM, conf=0.91)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“LBs are frequent in the setting of moderate-to-severe levels of AD neuropathologic change [27,59], including some early-onset familial AD cases [32,33].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE
What the sources say
- Supportedcites [32] Leverenz JB, Fishel MA, Peskind ER et al (2006) Lewy body pathology in familial Alzheimer disease: evidence for disease- and mutation-specific pathologic phenotype. Arch Neurol 63:370–376 source
The Results report Lewy body pathology in the amygdala of 24 of 25 familial AD cases with PSEN1 mutations. The section on PSEN1-associated AD reports a mean age at onset of about 43 years in the groups it compares, supporting the early-onset qualifier. The indexed copy provides section labels but no page numbers. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites [33] Lippa CF, Duda JE, Grossman M et al (2007) DLB and PDD boundary issues: diagnosis, treatment, molecular pathology, and biomarkers. Neurology 68:812–819 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Accumulation of Aβ plaques and NFTs follows distinct regional progressions across brain regions as AD advances.”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > AD NEUROPATHOLOGIC CHANGE
What the sources say
- Partly supportedcites [14] Braak H, Alafuzoff I, Arzberger T et al (2006) Staging of Alzheimer disease-associated neurofibrillary pathology using paraffin sections and immunocytochemistry. Acta Neuropathol 112:389–404 sourceExperimental — accuracy not yet measured
The staging-system section describes a predictable regional progression of neurofibrillary pathology, from transentorhinal and entorhinal regions to limbic and then neocortical areas. It does not describe a separate regional progression of Aβ plaques or compare that progression with NFTs. Its references to neuritic plaques occur in the context of tau-immunoreactive pathology, not an Aβ-plaque staging scheme. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [15] Braak H, Braak E (1991) Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol 82:239–259 source
- Not checked — no full text of the sourcecites [57] Thal DR, Rub U, Orantes M, Braak H (2002) Phases of A beta-deposition in the human brain and its relevance for the development of AD. Neurology 58:1791–1800 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“CVD and vascular brain injury (VBI) [50] commonly are encountered in the brains with AD neuropathologic change [25].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > CEREBROVASCULAR DISEASE and VASCULAR BRAIN INJURY
What the sources say
- Partly supportedcites [25] Grinberg LT, Thal DR (2010) Vascular pathology in the aged human brain. Acta Neuropathol 119:277–290 sourceExperimental — accuracy not yet measured
The ‘Cerebral amyloid angiopathy’ section (page unavailable) reports that around 80–100% of AD patients have CAA, supporting the claim that cerebrovascular disease commonly accompanies AD pathology. It identifies infarction and hemorrhage as possible complications of CAA, but does not establish that vascular brain injury itself is commonly found in AD brains. (LLM, conf=0.82)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“LBs are frequent in the setting of moderate-to-severe levels of AD neuropathologic change [27,59], including some early-onset familial AD cases [32,33].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE
What the sources say
- Not checked — no full text of the sourcecites [27] Hamilton RL (2000) Lewy bodies in Alzheimer’s disease: a neuropathological review of 145 cases using alpha-synuclein immunohistochemistry. Brain Pathol 10:378–384 source
- Supportedcites [59] Uchikado H, Lin WL, DeLucia MW, Dickson DW (2006) Alzheimer disease with amygdala Lewy bodies: a distinct form of alpha-synucleinopathy. J Neuropathol Exp Neurol 65:685–697 source
The Materials and Methods section (page unavailable) says all 347 cases met pathologic criteria for AD and had Braak NFT stage IV or greater, indicating advanced AD in almost all cases. The “Frequency of α-Synuclein Pathology in Alzheimer Disease” section (page unavailable) reports Lewy-body pathology in 62 AD/ALB and 149 AD/LBD cases, supporting that Lewy bodies are frequent in this setting. (LLM, conf=0.90)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 2
- Probably not a substantial claim. 1
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Relatively isolated HS may occur in very old individuals, and in this context it is associated with TDP-43-immunoreactive inclusions and with cognitive impairment [45,47].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > HIPPOCAMPAL SCLEROSIS and TAR DNA BINDING PROTEIN (TDP)-43 INCLUSIONS > Reporting
What the sources say
- Partly supportedcites [45] Nelson PT, Abner EL, Schmitt FA et al (2010) Modeling the association between 43 different clinical and pathological variables and the severity of cognitive impairment in a large autopsy cohort of elderly persons. Brain Pathol 20:66–79 sourceExperimental — accuracy not yet measured
The Discussion reports that hippocampal sclerosis (HS) was associated with lower MMSE scores and states that HS is associated with TDP-43 proteinopathy. The Results describe TDP-43-positive inclusions. Neither passage establishes these associations specifically for relatively isolated HS in very old individuals. (LLM, conf=0.86)
- Supportedcites [47] Nelson PT, Schmitt FA, Lin Y et al (2011) Hippocampal sclerosis in advanced age: clinical and pathological features. Brain 134:1506–1518 source
The Introduction describes hippocampal sclerosis in older individuals as unrelated to Alzheimer’s pathology and associated with significant cognitive dysfunction. The Discussion reports aberrant TDP-43 staining in approximately 90% of patients with hippocampal sclerosis, and Table 7 describes HS-Ageing as most prevalent in the oldest-old and associated with dementia. The association is not universal, but the citing sentence does not claim that it is. (LLM, conf=0.92)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
In the paper
“Although not part of this classification scheme, it is important to realize that LBD also occurs frequently in the olfactory bulb in older adults and should be sampled when possible [20].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE > Method
What the sources say
- Not checked — no full text of the sourcecites [20] Del Tredici K, Rub U, De Vos RA et al (2002) Where does Parkinson disease pathology begin in the brain? J Neuropathol Exp Neurol 61:413–426 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“A subset of senile plaques called neuritic plaques appear closely associated with neuronal injury and are characterized by the occurrence of dystrophic neurites that frequently have phospho-tau immunoreactivity [19,36,37,55].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > AD NEUROPATHOLOGIC CHANGE
What the sources say
- Not checked — no full text of the sourcecites [19] DeKosky ST, Scheff SW (1990) Synapse loss in frontal cortex biopsies in Alzheimer’s disease: correlation with cognitive severity. Ann Neurol 27:457–464 source
- Not checked — no full text of the sourcecites [36] Masliah E, Mallory M, Deerinck T et al (1993) Re-evaluation of the structural organization of neuritic plaques in Alzheimer’s disease. J Neuropathol Exp Neurol 52:619–632 source
- Not checked — no full text of the sourcecites [37] Masliah E, Terry RD, Mallory M et al (1990) Diffuse plaques do not accentuate synapse loss in Alzheimer’s disease. Am J Pathol 137:1293–1297
- Not checked — no full text of the sourcecites [55] Terry RD, Masliah E, Salmon DP et al (1991) Physical basis of cognitive alterations in Alzheimer’s disease: synapse loss is the major correlate of cognitive impairment. Ann Neurol 30:572–580 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
Many other neurodegenerative disorders can cause dementia and may be co-morbid with AD neuropathologic change, especially in the elderly.
“There are many other neurodegenerative disorders that can cause dementia in addition to those discussed here, and any may be co-morbid with AD neuropathologic change, especially in the elderly.”
The paper relies on this without support.
Multiple diseases in the cerebrum can conspire to worsen cognitive symptoms.
“Multiple diseases in cerebrum can conspire to worsen cognitive symptoms; however, it often is difficult to judge the extent to which each disease observed at autopsy may have contributed to a given patient’s cognitive state.”
The paper relies on this without support.
Abnormal neuropil and neuronal cytoplasmic α-synuclein immunoreactivity are usually present with Lewy bodies but will not be apparent by H&E; in some instances, these changes occur in the absence of Lewy bodies.
“Abnormal neuropil and neuronal cytoplasmic α-synuclein immunoreactivity are usually present with LBs but will not be apparent by H&E; in some instances, these changes occur in the absence of LBs.”
The paper relies on this without support.
Diffuse white matter injury is a form of VBI but it is more difficult to judge objectively and is not specific to VBI.
“Diffuse white matter injury is a form of VBI but it is more difficult to judge objectively and is not specific to VBI.”
The paper relies on this without support.
Hippocampal sclerosis can be observed in the context of AD neuropathologic change, FTLD, and VBI, likely reflecting a heterogeneous etiology.
“HS can be observed in the context of AD neuropathologic change, frontotemporal lobar degeneration (FTLD), and VBI, likely reflecting a heterogeneous etiology.”
The paper relies on this without support.
Hippocampal sclerosis can be focal, so its absence in the recommended screening section does not rule out the possibility of HS elsewhere in the hippocampal formation.
“HS can be focal, thus its absence in the recommended screening section does not rule out the possibility of HS elsewhere in the hippocampal formation.”
The paper relies on this without support.
Hippocampal sclerosis can occur in several different diseases and has varying clinical implications in different settings.
“Clinico-pathological correlations need to recognize that HS can occur in several different diseases and has varying clinical implications in different settings.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The new NIA criteria use the same combination of NPs and Braak stage as the minimum lesion density necessary for attributing the cause of dementia to AD (39, 40).”
From Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer Disease Centers, 2005–2010 (2012) · cites this paper as [40]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The definitive diagnosis of AD requires microscopic examination of multiple brain regions employing staining methods that can detect Alzheimer type neuropathologic change [24], with diagnosis based upon the morphology and density of lesions and their topographic distribution.”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [24]
The cited source says what the claim attributes to it.
In the citing paper
“This finding is highlighted by the fact that nearly one third of patients with pathological findings of high likelihood Alzheimer’s disease [24] were thought to other disorders, and 3% were considered clinically normal at the time of their last clinical exam (Table 2).”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [24]
The cited source says what the claim attributes to it.
In the citing paper
“However, both Aβ and paired helical filament (PHF) tau deposits are required to fulfill neuropathologic criteria for AD [105,106]”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [105]
The cited source says what the claim attributes to it.
In the citing paper
“Autopsy analyses classified the level of ADNC from “none” to “high” using an established scoring system when available.”
From Automatic classification of AD pathology in FTD phenotypes using natural speech (2024) · cites this paper as [30]
The cited source says what the claim attributes to it.
In the citing paper
“Participants in the Confirmed-AD group (n ¼ 1854) were diagnosed with primary or contributing ADdementia at their last UDS visit before death and met our criteria for ADNC: moderate to frequent neuritic plaques and Braak stages III through VI, which loosely aligns with NIA-AA criteria for intermediate or high ADNC (13).”
From Concordance of Clinical Alzheimer Diagnosis and Neuropathological Features at Autopsy (2020) · cites this paper as [13]
The cited source says what the claim attributes to it.
In the citing paper
“The shortcomings of the NIA-Reagan criteria have been recognized and a revised set of criteria are currently in press (39, 40).”
From Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer Disease Centers, 2005–2010 (2012) · cites this paper as [40]
The cited source says what the claim attributes to it.
In the citing paper
“In the revision of the 1997 criteria, combinations of plaque and tangle pathologies considered sufficient to cause dementia and qualify for the neuropathological diagnosis of AD are explicitly stated (40, 41).”
From Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer Disease Centers, 2005–2010 (2012) · cites this paper as [40]
The cited source says what the claim attributes to it.
In the citing paper
“Neuropathologic diagnosis of AD was in accordance with current NIA-AA guidelines (Hyman et al., 2012; Montine et al., 2012).”
From Cholesterol and matrisome pathways dysregulated in astrocytes and microglia (2022) · cites this paper as Montine et al., 2012
In the citing paper
“Neuropathological assessment was performed by 2 authors (T.G.B. and T.J.M.) blinded to clinical and imaging results and using NIA–AA diagnostic scoring guidelines.5,40”
From Positron Emission Tomography Imaging With [ 18 F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [40]
In the citing paper
“Additional changes that may also occur in the brains of AD patients include amyloid angiopathy, age-related brain atrophy, synaptic pathology, white matter rarefaction, granulovacuolar degeneration, neuron loss, TDP-43 proteinopathy, and neuroinflammation (20-26), which may contribute to cognitive impairment; however, these are not considered pathognomonic features of AD (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“In contrast, dense and extensive neocortical NFTs are very consistently associated with dementia and thus, according to new diagnostic criteria, these are required to constitute high burden of AD neuropathologic change (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“The current revision of the National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of AD stipulate that subjects with moderately dense neuritic AβPs may be regarded as having an intermediate level of AD neuropathologic change and that other potential contributors to cognitive impairment and dementia should be sought (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“There is no universally applied rubric for CVD pathologic diagnosis, although the recent National Institute on Aging–Alzheimer’s Association criteria attempted to systematize neuropathologic assessment of this complex form of brain injury (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“Alzheimer's disease cases met criteria for a high likelihood of AD (Montine et al., 2012).”
From Alzheimer's amyloid‐β and tau protein accumulation is associated with decreased expression of the LDL receptor‐associated protein in human brain tissue (2020) · cites this paper as Montine et al., 2012
Citations
Cites
McKhann, G. M., Knopman, D. S., Chertkow, H., Hyman, B. T., Jack, C. R., Kawas, C. H., Klunk, W. E., Koroshetz, W. J., Manly, J. J., Mayeux, R., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.005 · Cited by 18,657 · cited 1×
“‘‘Alzheimer’s disease’’ refers to a constellation of cognitive and behavioral changes that are typical for patients who have substantial amounts of its hallmark lesions [6, 39].”
Self-citationNeuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123 · cited 8×
“‘‘Intermediate’’ or ‘‘High’’ AD neuropathologic change (italicized) is considered sufficient explanation for dementia a NFT stage should be determined by the method of Braak [14, 15] b Ab/amyloid plaque score should be determined by the method of Thal et al.”
InfluentialStaging of brain pathology related to sporadic Parkinson’s disease
Braak, H., Tredici, K. D., Rüb, U., de Vos, R. A. I., Jansen Steur, E. N. H., & Braak, E. (2003) · Neurobiology of Aging · doi:10.1016/s0197-4580(02)00065-9 · Cited by 10,777 · cited 2×
“Given our focus on cognitive impairment and dementia rather than movement disorders [16], we recommend a modification of Fig.”
Albert, M. S., DeKosky, S. T., Dickson, D., Dubois, B., Feldman, H. H., Fox, N. C., Gamst, A., Holtzman, D. M., Jagust, W. J., Petersen, R. C., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.008 · Cited by 10,152 · cited 1×
“‘‘Alzheimer’s disease’’ refers to a constellation of cognitive and behavioral changes that are typical for patients who have substantial amounts of its hallmark lesions [6, 39].”
Self-citationSperling, R. A., Aisen, P. S., Beckett, L. A., Bennett, D. A., Craft, S., Fagan, A. M., Iwatsubo, T., Jack, C. R., Kaye, J., Montine, T. J., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.003 · Cited by 7,155 · cited 2×
“Similar neuropathologic changes, albeit usually at lower levels, also occur in individuals who did not show cognitive or behavioral impairments during life [54].”
Self-citationDiagnosis and management of dementia with Lewy bodies: Third report of the DLB consortium
McKeith, I. G., Dickson, D. W., Lowe, J., Emre, M., O'Brien, J. T., Feldman, H., Cummings, J., Duda, J. E., Lippa, C., Perry, E. K., et al. (2005) · Neurology · doi:10.1212/01.wnl.0000187889.17253.b1 · Cited by 5,069
Self-citationMirra, S. S., Heyman, A., McKeel, D., Sumi, S. M., Crain, B. J., Brownlee, L. M., Vogel, F. S., Hughes, J. P., Belle, G. V., Berg, L., et al. (1991) · Neurology · doi:10.1212/wnl.41.4.479 · Cited by 4,961 · cited 11×
“Region Stain for A /amyloid plaques [57] Stain for NFTs [14,15] Stain for NPs [41] Stain for LBs H&E”
InfluentialSelf-citationDeJesus-Hernandez, M., Mackenzie, I. R., Boeve, B. F., Boxer, A. L., Baker, M., Rutherford, N. J., Nicholson, A. M., Finch, N. A., Flynn, H., Adamson, J., et al. (2011) · Neuron · doi:10.1016/j.neuron.2011.09.011 · Cited by 4,936 · cited 1×
“With the exception of individuals with mutations in TARDBP, GRN, VCP or c9ORF72 [10, 18], it is not clear whether TDP-43 proteinopathy in these other neurodegenerative diseases is”
Self-citationTerry, R. D., Masliah, E., Salmon, D. P., Butters, N., DeTeresa, R., Hill, R., Hansen, L. A., & Katzman, R. (1991) · Annals of Neurology · doi:10.1002/ana.410300410 · Cited by 4,397 · cited 1×
“frequently have phospho-tau immunoreactivity [19, 36, 37, 55].”
Self-citationGorelick, P. B., Scuteri, A., Black, S. E., DeCarli, C., Greenberg, S. M., Iadecola, C., Launer, L. J., Laurent, S., Lopez, O. L., Nyenhuis, D., et al. (2011) · Stroke · doi:10.1161/str.0b013e3182299496 · Cited by 3,811
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Items 1,501–1,600 of 2,854
Leiby, A. C., Scambray, K. A., Nguyen, H. L., Basith, F., Fakhraee, S., Melikyan, Z. A., Bukhari, S. A., Montine, T. J., Corrada, M. M., Kawas, C. H., et al. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230238 · Cited by 14
Self-citationAlteration of Metabolic Profiles during the Progression of Alzheimer’s Disease
Yu, W., Chen, L., Li, X., Han, T.-L., Yang, Y., Hu, C., Yu, W., & Lü, Y. (2023) · Brain Sciences · doi:10.3390/brainsci13101459 · Cited by 15
“All subjects were diagnosed with “probable AD” on the basis of the 2011 National Institute on Aging-Alzheimer’s Association (NIA–AA) criteria [16].”
BackgroundImpact of APOE on amyloid and tau accumulation in argyrophilic grain disease and Alzheimer’s disease
Raulin, A., Doss, S. V., Heckman, M. G., Craver, E. C., Li, Z., Ikezu, T. C., Sekiya, H., Liu, C., Martens, Y. A., Rosenberg, C. L., et al. (2024) · Acta Neuropathologica Communications · doi:10.1186/s40478-024-01731-0 · Cited by 14
“The diagnosis of AD neuropathologic change (ADNC) was conducted using the 2012 NIA-AA criteria [21], a well-established neuropathologic consensus criteria which include examination of AD-related pathologies such as Thal phase for Aβ plaques [34], and Braak NFT stage [1, 2].”
MethodSelf-citationCortical-sparing chronic traumatic encephalopathy (CSCTE): a distinct subtype of CTE
Alexander, A. L., Alvarez, V. E., Huber, B. R., Alosco, M. L., Mez, J., Tripodis, Y., Nicks, R., Katz, D. I., Dwyer, B. C., Daneshvar, D. H., et al. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02690-5 · Cited by 14
“NIA-Reagan criteria were used to diagnose Alzheimer’s disease (AD) [31, 33, 42].”
Tremblay, C., Aslam, S., Walker, J. E., Lorenzini, I., Intorcia, A. J., Arce, R. A., Choudhury, P., Adler, C. H., Shill, H. A., Driver‐Dunckley, E. D., et al. (2024) · Neurobiology of Disease · doi:10.1016/j.nbd.2024.106514 · Cited by 14
“…2002), CERAD neuritic plaque density score (Mirra et al., 1991), AD neuro-pathological change according to the NIA-AA criteria (Hyman et al., 2012; Montine et al., 2012), neuropathological assessment of PD (Dickson et al., 2009) and aSyn stage according to the Unified Staging System for Lewy…”
Self-citationKon, T., Forrest, S. L., Lee, S., Li, J., Chasiotis, H., Nassir, N., Uddin, M. J., Lang, A. E., & Kovács, G. G. (2024) · Neurobiology of Disease · doi:10.1016/j.nbd.2024.106551 · Cited by 14
“…and limbic-predominant age-related TDP-43 encephalopathy was assessed based on consensus criteria for each pathology (Attems et al., 2021; Braak and Braak, 1991; Kovacs et al., 2018; Montine et al., 2012; Nelson et al., 2019; Saito et al., 2004; Thal et al., 2002a; Thal et al., 2002b).”
MethodHamlin, D., Ryall, C., Turner, C. P., Faull, R. L. M., Murray, H. C., & Curtis, M. A. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.13922 · Cited by 16
“2,8 These stages are determined based on labeling for hyperphosphorylated tau using the AT8 antibody, which binds tau phosphorylated at the serine 202 and threonine 205 positions.”
Ramanan, S., Akarca, D., Henderson, S. K., Rouse, M. A., Allinson, K. S. J., Patterson, K. E., Rowe, J. B., & Ralph, M. A. L. (2024) · Brain · doi:10.1093/brain/awae233 · Cited by 14
“48 ( ii) (iv) PSP pathology was coded using the NACCPROG variable.”
Hagihara, H., & Miyakawa, T. (2024) · The International Journal of Neuropsychopharmacology · doi:10.1093/ijnp/pyae047 · Cited by 16
“In the datasets that provided ABC score, scores 1, 2, and 3 in category “B” (representing Braak stage) were treated as stages 1.5, 3.5, and 5.5, respectively, as score 1 encompasses Braak stage I or II, score 2 corresponds to stage III or IV, and score 3 to stages V or VI (Montine et al., 2012).”
MethodInfluentialKatsumata, Y., Wu, X., Aung, K. Z., Fardo, D. W., Woodworth, D. C., Sajjadi, S. A., Tomé, S. O., Thal, D. R., Troncoso, J. C., Chang, K., et al. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02821-y · Cited by 14
Self-citationHiya, S., Maldonado‐Díaz, C., Rohde, S. K., Gonzales, M. M., Canbeldek, L., Mahadevan, L. S. K., Yokoda, R. T., Sullivan, A. C., Parker, A. S., White, C. L., et al. (2024) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlae134 · Cited by 14
Alzheimer's disease‐related plaques in nondemented subjects
El‐Obeid, A., Rantakömi, S. H., Soininen, H. S., & Alafuzoff, I. I. (2014) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2012.12.009 · Cited by 13
“A Braak stagewas given to each case using current criteria [4], and the level of AD neuropathological change was estimated as recommended by the NIA-RI in 1997 and by the NIA-AA in 2012 [3,5,6].”
BackgroundMethodInfluentialBrains for Dementia Research: The Importance of Cohorts in Brain Banking
Francis, P. T., Hayes, G. M., Costello, H., & Whitfield, D. (2019) · Neuroscience Bulletin · doi:10.1007/s12264-018-0327-2 · Cited by 16
FTLD-TDP With and Without GRN Mutations Cause Different Patterns of CA1 Pathology
Mao, Q., Zheng, X., Gefen, T. D., Rogalski, E. J., Spencer, C., Rademakers, R., Fought, A. J., Kohler, M., Weıntraub, S., Xia, H., et al. (2019) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlz059 · Cited by 15
Self-citationYoshida, K., Hata, Y., Ichimata, S., & Nishida, N. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-190196 · Cited by 14
“The pathological hallmarks of Alzheimer’s disease (AD) are neurofibrillary tangles (NFTs), which are phosphorylated tau protein positive intraneuronal inclusions, and extracellular deposits of amyloid-(cid:2) (A (cid:2) ) protein [1].”
Hunter, S., Hokkanen, S. R. K., Keage, H. A. D., Fleming, J., Minett, T., Polvikoski, T. M., Allinson, K. S. J., & Brayne, C. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-191093 · Cited by 14
Dai, D., Tropea, T. F., Robinson, J. L., Suh, E. R., Hurtig, H. I., Weintraub, D. A., Deerlin, V. M. V., Lee, E. B., Trojanowski, J. Q., & Chen‐Plotkin, A. S. (2020) · Acta Neuropathologica · doi:10.1007/s00401-020-02199-7 · Cited by 14
Self-citationPatterns of neuronal Rhes as a novel hallmark of tauopathies
Ehrenberg, A. J., Leng, K., Letourneau, K. N., Hernández, I., Lew, C. H., Seeley, W. W., Spina, S., Miller, B. L., Heinsen, H., Kampmann, M., et al. (2021) · Acta Neuropathologica · doi:10.1007/s00401-021-02279-2 · Cited by 14
Tau Isoform Profile in Essential Tremor Diverges From Other Tauopathies
Kim, S. H., Farrell, K. W., Cosentino, S., Vonsattel, J., Faust, P. L., Cortes, E. P., Bennet, D. A., Louis, E. D., & Crary, J. F. (2021) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlab073 · Cited by 13
Ma, W., Yao, Q., Hu, G., Ge, H., Xue, C., Wang, Y., Yan, Y., Xiao, C., Shi, J., & Chen, J. (2021) · NeuroImage Clinical · doi:10.1016/j.nicl.2021.102930 · Cited by 16
“, 2016), and Lewy bodies, the core pathological features of DLB, also are common in some early-onset familial AD cases and neuropathological changes of moderate to severe AD (Robinson et al., 2020; Montine et al., 2012).”
BackgroundNeuropathology and cholinesterase expression in the brains of octogenarians and older
Maxwell, S. P., Cash, M. K., & Darvesh, S. (2022) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2022.110065 · Cited by 15
Moreno, J., Lanau, A. V., Madrigal, L., Pineda, A. Y. B., Hernandez, J. V., Campo, O., Soto-Ospina, A., Marín, P. A., Rishishwar, L., Norris, E. T., et al. (2022) · PLoS ONE · doi:10.1371/journal.pone.0269955 · Cited by 14
“According to the current National Institute for Classification of Aging, this results in a "high change in neuropathology of AD considered as a sufficient explanation for dementia" [85], 2.”
MethodWalter, K. R., Ricketts, D. K., Presswood, B. H., Smith, S. M., & Mooney, S. M. (2022) · The American Journal of Drug and Alcohol Abuse · doi:10.1080/00952990.2022.2119571 · Cited by 17
Cao, Y., Huang, M., Mao, C., Wang, X. L., Xu, Y.-Y., Qian, X., Ma, C., Qiu, W., & Zhu, Y. (2022) · Stroke and Vascular Neurology · doi:10.1136/svn-2022-001924 · Cited by 13
Koga, S., Metrick, M. A., Golbe, L. I., Santambrogio, A., Kim, M., Soto‐Beasley, A. I., Walton, R. L., Baker, M., Castro, C. H. F. D., Deture, M. A., et al. (2023) · Acta Neuropathologica Communications · doi:10.1186/s40478-023-01584-z · Cited by 17
“Braak neurofibrillary tangle stage (NFT) and Thal amyloid phase were assigned by thioflavin S fluorescent microscopy according to published criteria as previously described [5, 22, 28, 32, 40].”
MethodSelf-citationSynthesis and Evaluation of 13N-Labelled Azo Compounds for β-Amyloid Imaging in Mice
Gaja, V., Gómez‐Vallejo, V., Puigivila, M., Pérez‐Campaña, C., Martín, A., García‐Osta, A., Calvo-Fernández, T., Cuadrado‐Tejedor, M., Franco, R., & Llop, J. (2013) · Molecular Imaging and Biology · doi:10.1007/s11307-013-0708-x · Cited by 14
“Moreover, as the neuropathological diagnosis of AD entails a complex regional localization of tau and Aβ aggregates [12,13], the diagnostic validity of these imaging probes has been recently questioned [11]; thus, current Aβ imaging may not be suitable as a stand-alone method for diagnosis of AD, and a combination of…”
BackgroundNeuropathologic Assessment of Dementia Markers in Identical and Fraternal Twins
Iacono, D., Volkmann, I., Nennesmo, I., Pedersen, N. L., Fratiglioni, L., Johansson, B. E. A., Karlsson, D., Winblad, B. G., & Gatz, M. (2014) · Brain Pathology · doi:10.1111/bpa.12127 · Cited by 14
Kovács, G. G., & Gelpí, E. (2012) · Clinical Neuropathology · doi:10.5414/np300512 · Cited by 16
“Indeed, a new guideline has been recently published [8] accompanied by an article on the application of these guidelines in neuropathology practice [9].”
BackgroundFlanagan, M. E., Marshall, D. A., Shofer, J. B., Montine, K. S., Nelson, P. T., Montine, T. J., & Keene, C. D. (2017) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlw104 · Cited by 14
Self-citationLee, K., Seo, S. W., Lim, T. S., Kim, E., Kim, B. C., Kim, Y., Lee, H., Jeon, J. P., Shim, S.-M., Na, D. L., et al. (2017) · Yonsei Medical Journal · doi:10.3349/ymj.2017.58.5.1055 · Cited by 14
“By combining ABC scores, ADNC can be transformed into one of four levels: not, low, intermediate, or high.(6) LBD is a neuropathological term that encompasses the two clinical entities of Parkinson disease and DLB.”
MethodLibard, S., Laurell, K., Cesarini, K. G., & Alafuzoff, I. I. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-170446 · Cited by 16
AD molecular: Imaging tau aggregates with positron emissions tomography
Betthauser, T. J. (2019) · Progress in molecular biology and translational science · doi:10.1016/bs.pmbts.2019.07.007 · Cited by 14
Paasila, P. J., Davies, D., Sutherland, G. T., & Goldsbury, C. S. (2020) · Free Neuropathology · doi:10.17879/freeneuropathology-2020-2845 · Cited by 16
Brain TDP‐43 pathology in corticobasal degeneration: Topographical correlation with neuronal loss
Sainouchi, M., Tada, M., Fitrah, Y. A., Hara, N., Tanaka, K., Idezuka, J., Aida, I., Nakajima, T., Miyashita, A., Akazawa, K., et al. (2021) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12786 · Cited by 14
“In accordance with the ‘ABC’ score for AD neuropathologic change [20], three and seven patients corresponded to ‘Not’ and ‘Low’, respectively.”
ResultAutomatic classification of AD pathology in FTD phenotypes using natural speech
Cho, S., Olm, C. A., Ash, S., Shellikeri, S., Agmon, G., Cousins, K. A. Q., Irwin, D. J., Grossman, M., Liberman, M., & Nevler, N. (2024) · Alzheimer's & Dementia · doi:10.1002/alz.13748 · Cited by 13
“Patients were included if they had either a post mortem neuropathologic diagnosis or an in vivo CSF analyte profile suggestive of the underlying neuropathology based on cut-offs previously validated in autopsy series.”
MethodTheoretical impact of the AT(N) framework on dementia using a community autopsy sample
Burke, B. T., Latimer, C., Keene, C. D., Sonnen, J. A., McCormick, W., Bowen, J. D., McCurry, S. M., Larson, E. B., & Crane, P. K. (2021) · Alzheimer's & Dementia · doi:10.1002/alz.12348 · Cited by 13
Longitudinal Evolution of Posterior Cortical Atrophy
Shir, D., Lee, N. A., McCarter, S. J., Ramanan, V. K., Botha, H., Knopman, D. S., Petersen, R. C., Boeve, B. F., Day, G. S., Graff‐Radford, N. R., et al. (2025) · Neurology · doi:10.1212/wnl.0000000000213559 · Cited by 14
Self-citationMitochondrial Dysfunction in Aging: Future Therapies and Precision Medicine Approaches
Jia, L., Wei, Z., Luoqian, J., Wang, X., & Huang, C. (2025) · MedComm – Future Medicine · doi:10.1002/mef2.70026 · Cited by 14
Serrano‐Pozo, A., Escott‐Price, V., Grinberg, L. T., Pascoal, T. A., Suárez‐Calvet, M., Dubois, B., & Sperling, R. A. (2026) · The Lancet · doi:10.1016/s0140-6736(26)00198-4 · Cited by 20
Histopathological Analysis of Cerebrovascular Lesions Associated With Aging
Dallaire‐Théroux, C., Saïkali, S., Richer, M., Potvin, O., & Duchesne, S. (2021) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlab125 · Cited by 16
Iwasaki, Y. (2022) · Neuropathology · doi:10.1111/neup.12787 · Cited by 13
“[6] Lateral and third ventricles include the lining and choroid plexus.”
BackgroundPlasma Exchange in Alzheimer's Disease
Rohrer, L., Yünce, M., Montine, T. J., & Shan, H. (2022) · Transfusion Medicine Reviews · doi:10.1016/j.tmrv.2022.09.005 · Cited by 14
Self-citationKatzeff, J. S., Lok, H. C., Bhatia, S., Fu, Y., Halliday, G. M., & Kim, W. S. (2022) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2022.1043127 · Cited by 13
“, 2010) or no significant neuropathology (controls; Hyman et al., 2012; Montine et al., 2012).”
BackgroundFerrer‐Raventós, P., Puertollano‐Martín, D., Querol‐Vilaseca, M., Sánchez‐Aced, É., Valle‐Tamayo, N., González, A. C., Núñez‐Llaves, R., Pegueroles, J., Dols‐Icardo, O., Iulita, M. F., et al. (2023) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12879 · Cited by 13
The unique neuropathological vulnerability of the human brain to aging
Ferrer, I. (2023) · Ageing Research Reviews · doi:10.1016/j.arr.2023.101916 · Cited by 15
Mi, Z., Abrahamson, E. E., Ryu, A. Y., Malek‐Ahmadi, M. H., Kofler, J., Fish, K. N., Sweet, R. A., Villemagne, V. L., Schneider, J. A., Mufson, E. J., et al. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-221063 · Cited by 15
Self-citationLoss of TDP-43 function contributes to genomic instability in amyotrophic lateral sclerosis
Fang, M., Deibler, S. K., Nana, A. L., Vatsavayai, S. C., Banday, S., Zhou, Y., Almeida, S., Weiss, A., Brown, R. H., Seeley, W. W., et al. (2023) · Frontiers in Neuroscience · doi:10.3389/fnins.2023.1251228 · Cited by 17
Almeida, F., Jesus, T., Coelho, A., Quintas-Neves, M., Gauthreaux, K. M., Teylan, M., Mock, C., Kukull, W. A., Crary, J. F., & Oliveira, T. G. (2024) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2024.02.013 · Cited by 14
Silbert, L. C., Roese, N. E., Krajbich, V., Hurworth, J., Lahna, D. L., Schwartz, D. L., Dodge, H. H., & Woltjer, R. L. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.13816 · Cited by 13
“35 Established criteria were used for the neuropathological diagnosis of primary age-related tauopathy (PART) and vascular cognitive impairment and dementia.”
MethodDistinct transcriptional alterations distinguish Lewy body disease from Alzheimer’s disease
Olney, K. C., Rabichow, B. E., Wojtas, A., Deture, M. A., McLean, P. J., Dickson, D. W., Chang, R. R., Ross, O. A., & Fryer, J. D. (2024) · Brain · doi:10.1093/brain/awae202 · Cited by 14
Self-citationJackson, R. J., Melloni, A. N., Fykstra, D. P., Serrano‐Pozo, A., Shinobu, L. A., & Hyman, B. T. (2024) · Acta Neuropathologica Communications · doi:10.1186/s40478-024-01844-6 · Cited by 13
Self-citationBurgueño‐García, I., López-Martínez, M. J., Uceda‐Heras, A., García‐Carracedo, L., Zea‐Sevilla, M. A., Rodrigo-Lara, H., Rego-García, I., Saiz-Aúz, L., Ruiz-Valderrey, P., López‐González, F. J., et al. (2024) · Journal of Clinical Medicine · doi:10.3390/jcm13226755 · Cited by 13
“…neurodegenerative and cerebral vascular pathologies at CIEN-TB are as follows: • Alzheimer’s disease neuropathological change (ADNC): The ABC system proposed by the National Institute on Aging—Alzheimer’s Association for the classification of Alzheimer’s type pathology is employed here [26].”
Genetics and Neuropathology of Neurodegenerative Dementias
Scholz, S. W., & Cobos, I. (2024) · CONTINUUM Lifelong Learning in Neurology · doi:10.1212/con.0000000000001505 · Cited by 13
Hayes, C. A., Young, C. B., Ruiz, C. A., Reeves, A. N., Odden, M. C., Nirschl, J., Crane, P. K., Poston, K. L., Mormino, E. C., & Younes, K. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70059 · Cited by 16
“25,26 The consensus guidelines for LBD corresponded to the National Institute on Aging–Alzheimer’s Association (NIA-AA) Lewy body score of 0 (none), 1 (brainstem), 2 (limbic/transitional), or 3 (neocortical diffuse).”
Armstrong, R. A., McKee, A. C., Stein, T. D., Alvarez, V. E., & Cairns, N. J. (2018) · Neurological Sciences · doi:10.1007/s10072-018-3686-6 · Cited by 13
Self-citationFreitas, R. S., Roque, C. R., Matos, G. A., Belayev, L., de Azevedo, O. G. R., Alvarez-Leite, J. I., Guerrant, R. L., & Oriá, R. B. (2021) · Nutrition Reviews · doi:10.1093/nutrit/nuab063 · Cited by 13
Monoranu, C.-M., Hartmann, T., Strobel, S., Heinsen, H., Riederer, P., Distel, L. V., & Bohnert, S. (2021) · Journal of Alzheimer s Disease Reports · doi:10.3233/adr-210052 · Cited by 14
Kawakatsu, S., Kobayashi, R., Hayashi, H., Morioka, D., Utsunomiya, A., Kabasawa, T., Ohe, R., & Otani, K. (2021) · Neuropathology · doi:10.1111/neup.12765 · Cited by 12
DeChellis-Marks, M. R., Wei, Y., Ding, Y., Wolfe, C. M., Krivinko, J. M., MacDonald, M. L., López, O. L., Sweet, R. A., & Kofler, J. (2022) · Frontiers in Neurology · doi:10.3389/fneur.2022.778419 · Cited by 13
Urdánoz‐Casado, A., de Gordoa, J. S., Robles, M., Roldán, M., Zelaya, M. V., Blanco‐Luquin, I., & Mendióroz, M. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23147682 · Cited by 13
“ABC score combines histopathologic assessments of Aβ deposits determined by the method of Thal (A) [76], staging of neurofibrillary tangles by Braak and Braak classification (B) [77], and”
MethodMinogue, G., Kawles, A., Zouridakis, A., Keszycki, R. M., Macomber, A. J., Lubbat, V., Gill, N. P., Mao, Q., Flanagan, M. E., Zhang, H., et al. (2023) · Annals of Neurology · doi:10.1002/ana.26762 · Cited by 15
Self-citationFornicola, W., Pelcovits, A., Li, B.-X., Heath, J., Perry, G. L., & Castellani, R. J. (2014) · The Open Neurology Journal · doi:10.2174/1874205x01408010022 · Cited by 14
Dekker, A. D., Vermeiren, Y., Carmona‐Iragui, M., Benejam, B., Videla, L., Gelpí, E., Aerts, T., Dam, D. V., Fernández, S., Lleó, A., et al. (2017) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1016/j.dadm.2017.11.001 · Cited by 15
“Intermediate and high signify the diagnosis of AD [25].”
BackgroundMethodInfluentialDominguez, S., Rodríguez, G., Fazelinia, H., Ding, H., Spruce, L. A., Seeholzer, S. H., & Dong, H. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-191009 · Cited by 12
“Despite AD being a disease that increases in severity with age, disease pathogenesis begins in affected individuals well before symptom presentation [24].”
Edler, M. K., Johnson, C. T., Ahmed, H. S., & Richardson, J. R. (2020) · The Journal of Comparative Neurology · doi:10.1002/cne.25089 · Cited by 14
“…Alzheimer's disease (AD), is characterized pathologically by senile plaques containing amyloid-beta (Aβ) protein, neurofibrillary tangles (NFT), selective neuronal loss, and neuroinflammation (Association, 2018; Bussière et al., 2003; Montine et al., 2012; Selkoe, 2000; Wisniewski et al., 1989).”
BackgroundBrůžová, M., Rusina, R., Stejskalova, Z., & Matěj, R. (2021) · Scientific Reports · doi:10.1038/s41598-021-90366-5 · Cited by 13
Tau seeding in chronic traumatic encephalopathy parallels disease severity
Kaufman, S. K., Svirsky, S. E., Cherry, J. D., McKee, A. C., & Diamond, M. I. (2021) · Acta Neuropathologica · doi:10.1007/s00401-021-02373-5 · Cited by 14
“Neuropathological diagnosis of AD was based on National Institute on Aging-Alzheimer’s Association guidelines [31].”
MethodBaiardi, S., Mammana, A., Rossi, M., Ladogana, A., Carlà, B., Gambetti, P. L., Capellari, S., & Parchi, P. (2022) · Viruses · doi:10.3390/v14020367 · Cited by 13
“We detected CAA and a low burden of AD neuropathologic change [37] in the older patients (129MV and VV).”
BackgroundÁlvarez‐Mora, M. I., Blanco-Palmero, V. A., Quesada‐Espinosa, J. F., Arteche‐López, A., Velasco, S. L., Milla, C. P., Rosales, J. M. L., Gómez-Manjón, I., Hernández‐Laín, A., Almonacid, J. J., et al. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23084230 · Cited by 13
“AD evaluation included the Braak and Braak stage, the Thal phases, and the Consortium to Establish a Registry for Alzheimer Disease (CERAD) plaque score, using the Diagnostic Criteria for the Neuropathological Assessment of Alzheimer’s Disease, following the recommendation by the National Institute on Aging-Alzheimer’…”
MethodSerrano, G. E., Intorcia, A. J., Carew, J., Chiarolanza, G., Hidalgo, J. A., Sue, L. I., Dugger, B. N., Saxon‐LaBelle, M., Filon, J. R., Scroggins, A., et al. (2015) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0000000000000235 · Cited by 13
“Q2 105 (73) 75 (52) 103 (72) 64 (46) 37 (26) 58 (40) NA”
Self-citationKelley, A. R., Perry, G. L., Bethea, C., Castellani, R. J., & Bach, S. B. H. (2016) · The Open Neurology Journal · doi:10.2174/1874205x01610010088 · Cited by 13
“The hippocampus is located toward the bottom of the tissue slice and it is known that the hippocampus is less amyloid-beta rich than the adjacent cortex of the brains of AD patients [27].”
Fardo, D. W., Katsumata, Y., Kauwe, J. S. K., Deming, Y. K., Harari, O., Cruchaga, C., & Nelson, P. T. (2017) · Experimental Gerontology · doi:10.1016/j.exger.2017.01.025 · Cited by 12
“HS-Aging is diagnosed at autopsy when neuron loss and astrocytosis are observed in the hippocampal formation, out of proportion to AD-type plaques and tangles (Amador-Ortiz et al., 2007a; Montine et al., 2012; Nelson et al., 2013).”
Self-citationSchrötter, A., Oberhaus, A., Kolbe, K., Seger, S., Mastalski, T., Magraoui, F. E., Hoffmann-Posorske, E., Bohnert, M., Deckert, J., Braun, C., et al. (2017) · Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics · doi:10.1016/j.bbapap.2017.03.013 · Cited by 14
Integrated neurodegenerative disease autopsy diagnosis
Lee, E. B. (2018) · Acta Neuropathologica · doi:10.1007/s00401-018-1827-x · Cited by 13
“An integrated diagnostic approach does not alter or supersede any of the existing or future neurodegenerative disease neuropathology criteria such as the NIA-AA or Brain Net Europe criteria for Alzheimer’s disease [1, 6, 19].”
Titze-de-Almeida, S. S., Marina, C. L., Ramos, M. V., Silva, L. D. D. S., Brandão, P. R. D. P., Bispo, D. D. D. C., von Glehn, F., & Titze‐de‐Almeida, R. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26178246 · Cited by 13
Castellani, R. J., Smith, M. C., Bailey, K., Perry, G. L., & deJong, J. L. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-190782 · Cited by 12
“FollowingH&Einterpretation,immuno-histochemicalassessmentsgenerallyfollowedthe 2016 NINDS/NIBIB recommendations for sport-implicated geographic tauopathy [15], and modified NIA-AA 2012 consensus guidelines for assessment of AD neuropathologic change [16].”
Salcedo‐Arellano, M. J., Sanchez, D., Wang, J. Y., McLennan, Y. A., Clark, C. J., Juárez, P., Schneider, A., Tassone, F., Hagerman, R. J., & Martínez‐Cerdeño, V. (2021) · Frontiers in Neuroscience · doi:10.3389/fnins.2021.720253 · Cited by 13
“Our sampling deviated from the current recommendation for the evaluation of AD changes (Montine et al., 2012); since we did not include the middle frontal gyrus and the superior temporal gyrus in our analysis.”
MethodYokota, O., Miki, T., Ishizu, H., Haraguchi, T., Kishimoto, Y., Takenoshita, S., Hara, N., Miyashita, A., Ikeuchi, T., Terada, S., et al. (2022) · Neuropathology · doi:10.1111/neup.12820 · Cited by 12
Jiang, J., Yang, C. G., Ai, J.-Q., Zhang, Q., Cai, X.-L., Tu, T., Wan, L., Wang, X., Wang, H., Pan, A., et al. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.926904 · Cited by 11
“Aβ and pTau have served as neuropathological and imaging/biofluid markers for the diagnosis or risk assessment of AD, and are also being tested as mechanism-based therapeutical targets (Montine et al., 2012; Johnson et al., 2016; Buckley et al., 2017; Grothe et al., 2017; Jack et al., 2018; Schwarz et al., 2018; Long…”
BackgroundWu, W. D., Yu, J., Qian, X., et al. (2022) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2022.09.005 · Cited by 12
Thioflavin S Staining and Amyloid Formation Are Unique to Mixed Tauopathies
Fiock, K. L., Betters, R. K., & Hefti, M. M. (2023) · Journal of Histochemistry & Cytochemistry · doi:10.1369/00221554231158428 · Cited by 13
White Matter Hyperintensity as a Vascular Contribution to the AT(N) Framework
Ng, K. P., shen, J., Chiew, H. J., Ng, A., Kandiah, N., Rosa‐Neto, P., & Gauthier, S. G. (2023) · The Journal of Prevention of Alzheimer s Disease · doi:10.14283/jpad.2023.53 · Cited by 12
“showed that the mean WMH volume in the occipital regions was higher among patients with pathologically proven AD (37, 38) compared to controls (468 mm3 vs 420 mm3, p<0.”
BackgroundResultLok, H. C., Katzeff, J. S., Hodges, J. R., Piguet, O., Fu, Y., Halliday, G. M., & Kim, W. S. (2023) · Scientific Reports · doi:10.1038/s41598-023-35945-4 · Cited by 12
Shades of gray in human white matter
Zouridakis, A., Ayala, I. A. D. L., Minogue, G., Kawles, A., Keszycki, R. M., Macomber, A. J., Bigio, E. H., Geula, C., Mesulam, M. M., & Gefen, T. D. (2023) · The Journal of Comparative Neurology · doi:10.1002/cne.25512 · Cited by 12
“%) for cryoprotection, and stored in 40% sucrose with 0.02% sodium azide at 4 ◦ C. Pathologic diagnoses of AD participants were rendered using criteria set by Montine et al. (2012).”
MethodInfluentialSelf-citationHeterogeneity of cortical pTDP-43 inclusion morphologies in amyotrophic lateral sclerosis
Tan, R. H., McCann, H., Shepherd, C. E., Pinkerton, M., Mazumder, S., Devenney, E. M., Adler, G. L., Rowe, D. B., Kril, J. J., Halliday, G. M., et al. (2023) · Acta Neuropathologica Communications · doi:10.1186/s40478-023-01670-2 · Cited by 12
“An intermediate level of Alzheimer’s disease (AD) neuropathological change, which is considered adequate explanation for cognitive impairment [22] was identified in 5% of cases (n = 3) and Lewy body disease (LBD) ≥ Braak stage IV pathology, which is adequate explanation for clinical parkinsonism or…”
BackgroundLiquid Biopsy in Alzheimer’s Disease Patients Reveals Epigenetic Changes in the PRLHR Gene
Macías, M., Acha, B., Corroza, J., Urdánoz‐Casado, A., Roldán, M., Robles, M., de Gordoa, J. S., Erro, M. E., Jericó, I., Blanco‐Luquin, I., et al. (2023) · Cells · doi:10.3390/cells12232679 · Cited by 11
“AD staging was performed by using the ABC score according to the updated National Institute on Aging-Alzheimer’s Association guidelines [28].”
MethodTau maturation in the clinicopathological spectrum of Lewy body and Alzheimer's disease
Arezoumandan, S., Cousins, K. A. Q., Ohm, D. T., Lowe, M., Chen, M., Gee, J. C., Phillips, J. S., McMillan, C. T., Luk, K. C., Deik, A., et al. (2024) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.51988 · Cited by 13
“Our findings are consistent with pathological diagnostic criteria 25,45 suggesting higher ADNC pathology lowers diagnostic accuracy of DLB, 46 and a recent in vivo bio-marker work finding a lower frequency of DLB clinical features associated with tau positivity.”
MethodResultKhoo, S. C., Zhang, N., Luang‐In, V., Goh, M. S., Sonne, C., & Ling, N. (2024) · Environmental Research · doi:10.1016/j.envres.2024.118441 · Cited by 13
Dysregulation of the renin‐angiotensin system in vascular dementia
Tayler, H. M., Skrobot, O. A., Baron, D. H., Kehoe, P. G., & Miners, J. S. (2024) · Brain Pathology · doi:10.1111/bpa.13251 · Cited by 15
“Alzheimer ’ s disease cases were classified according to National Institute on Ageing-Alzheimer ’ s Association (NIA-AA) guidelines [23].”
Yuchen-Zhang, Du, M., Zhang, Q.-Y., Yang, S., Chen, J., Dan, C.-M., Lian, L., & Wang, J. (2024) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2024.133035 · Cited by 13
Evaluating the updated LATE‐NC staging criteria using data from NACC
Woodworth, D. C., Nguyen, K. M., Sordo, L., Scambray, K. A., Head, E., Kawas, C. H., Corrada, M. M., Nelson, P. T., & Sajjadi, S. A. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.14262 · Cited by 14
“20,21 For variables with multiple levels, we analyzed dichotomized as well as ordinal versions.”
Self-citationTedeschi, V., Nele, V., Valsecchi, V., Anzilotti, S., Vinciguerra, A., Zucaro, L., Sisalli, M. J., Cassiano, C., Iesu, N. D., Pignataro, G., et al. (2024) · Pharmacological Research · doi:10.1016/j.phrs.2024.107491 · Cited by 13
Tremblay, C., Adler, C. H., Shill, H. A., Driver‐Dunckley, E. D., Mehta, S. H., Choudhury, P., Belden, C. M., Shprecher, D., Lee‐Iannotti, J. K., Atri, A., et al. (2024) · Movement Disorders Clinical Practice · doi:10.1002/mdc3.14244 · Cited by 12
Self-citationYang, H., Byun, M. S., Ha, N.-Y., Yang, J., Park, S., Park, J. E., Yi, D., Chang, Y., Jung, W. S., Kim, J. Y., et al. (2024) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2024.117721 · Cited by 14
Zedde, M., Piazza, F., & Pascarella, R. (2025) · Biomedicines · doi:10.3390/biomedicines13040881 · Cited by 12
“The assessment and scoring of CAA were conducted following the methodology outlined by Vonsattel et al. on a semi-quantitative scale from 0 to 3, based on the extent of A β deposition within blood vessels using A β immunohistochemistry [102].”
Postupna, N. O., Latimer, C. S., Larson, E. B., Sherfield, E., Paladin, J., Shively, C. A., Jorgensen, M. J., Andrews, R. N., Kaplan, J. R., Crane, P. K., et al. (2017) · American Journal Of Pathology · doi:10.1016/j.ajpath.2016.12.010 · Cited by 12
Self-citationMiki, T., Yokota, O., Takenoshita, S., Mori, Y., Yamazaki, K., Ozaki, Y., Ueno, S., Haraguchi, T., Ishizu, H., Kuroda, S., et al. (2017) · Neuropathology · doi:10.1111/neup.12441 · Cited by 12
“Minimal NFTs with Braak stage I were found only in the entorhinal cortex,(31) and no Aβ deposit was observed in any anatomical region,(32) being classified as a low level of AD pathology according to the pathological criteria.(33) The Gallyas method and AT8 immunohistochemistry did Fig.”
MethodNeuropathologic basis of in vivo cortical atrophy in the aphasic variant of Alzheimer's disease
Ohm, D. T., Fought, A. J., RADEMAKER, A. W., Kım, G., Sridhar, J., Coventry, C., Gefen, T. D., Weıntraub, S., Bigio, E. H., Mesulam, M. M., et al. (2019) · Brain Pathology · doi:10.1111/bpa.12783 · Cited by 14
“© 2019 International Society of Neuropathology 334 of “high” AD neuropathologic change based on the published consensus criteria (33, 55).”
BackgroundSelf-citationGenetic risk for Alzheimer’s disease influences neuropathology via multiple biological pathways
Hannon, E. J., Shireby, G. L., Brookes, K. J., Attems, J., Sims, R., Cairns, N. J., Love, S., Thomas, A. J., Morgan, K., Francis, P. T., et al. (2020) · Brain Communications · doi:10.1093/braincomms/fcaa167 · Cited by 14
“78) across 612 individuals and neuritic plaque density was scored using the CERAD classification (Mirra et al., 1991; Montine et al., 2012) with a mean value of 1.”
Self-citationCoexisting Lewy body disease and clinical parkinsonism in amyotrophic lateral sclerosis
Forrest, S. L., Kim, J. H., Sousa, C. D., Cheong, R., Crockford, D. R., Sheedy, D. L., Stevens, J., McCrossin, T., Tan, R. H., McCann, H., et al. (2021) · European Journal of Neurology · doi:10.1111/ene.14849 · Cited by 13
“Cases were assigned an 'ABC' score corresponding to the level of AD neuropathological change as none, low, intermediate or high according to consensus recommendations [24].”
BackgroundMethodInfluential
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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