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
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“Given our focus on cognitive impairment and dementia rather than movement disorders [16], we recommend a modification of Fig.”
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“‘‘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].”
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“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
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“Region Stain for A /amyloid plaques [57] Stain for NFTs [14,15] Stain for NPs [41] Stain for LBs H&E”
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“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”
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“frequently have phospho-tau immunoreactivity [19, 36, 37, 55].”
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Sorted by citations
NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease
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“It is worthwhile emphasizing that, like the 2012 NIA-AA classification system for AD neuropathic change [105,106], AT(N) scoring of biomarkers is independent from clinical symptoms.”
Self-citationDiagnosis and management of dementia with Lewy bodies: Fourth consensus report of the DLB Consortium
McKeith, I. G., Boeve, B. F., Dickson, D. W., Halliday, G., Taylor, J.-P., Weintraub, D., Aarsland, D., Galvin, J., Attems, J., Ballard, C. G., et al. (2017) · Neurology · doi:10.1212/wnl.0000000000004058 · Cited by 4,476
Self-citationThe neuropathological diagnosis of Alzheimer's disease
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“methods that can detect Alzheimer type neuropathologic change [24], with diagnosis based upon the morphology and density of lesions and their topographic distribution.”
BackgroundMethodInfluentialSelf-citationRevised criteria for diagnosis and staging of Alzheimer's disease: Alzheimer's Association Workgroup
Jack, C. R., Andrews, J. S., Beach, T. G., Buracchio, T., Dunn, B., Graf, A., Hansson, O., Ho, C., Jagust, W., McDade, E., et al. (2024) · Alzheimer's & Dementia · doi:10.1002/alz.13859 · Cited by 2,803
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Self-citationThe spectrum of disease in chronic traumatic encephalopathy
McKee, A. C., Stein, T. D., Nowinski, C. J., Stern, R. A., Daneshvar, D. H., Alvarez, V. E., Lee, H.-S., Hall, G., Wojtowicz, S. M., Baugh, C. M., et al. (2013) · Brain · doi:10.1093/brain/aws307 · Cited by 2,098
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Self-citationDefeating Alzheimer's disease and other dementias: a priority for European science and society
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Pathology of Neurodegenerative Diseases
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“The most recent revision of neuropathological criteria (Montine et al. 2012) includes an assessment of topographic distribution rather than density of amyloid deposits using a staging scheme proposed by Thalet al. (2002).”
BackgroundMethodInfluentialSelf-citationLimbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report
Nelson, P. T., Dickson, D. W., Trojanowski, J. Q., Jack, C. R., Boyle, P. A., Arfanakis, K., Rademakers, R., Alafuzoff, I., Attems, J., Brayne, C., et al. (2019) · Brain · doi:10.1093/brain/awz099 · Cited by 1,547
Self-citationFunctional aspects of meningeal lymphatics in ageing and Alzheimer’s disease
Da Mesquita, S., Louveau, A., Vaccari, A., Smirnov, I., Cornelison, R. C., Kingsmore, K. M., Contarino, C., Onengut-Gumuscu, S., Farber, E., Raper, D., et al. (2018) · Nature · doi:10.1038/s41586-018-0368-8 · Cited by 1,445
Primary age-related tauopathy (PART): a common pathology associated with human aging
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“the current guidelines for AD [64, 102], mild Aβ plaques”
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“The new NIA criteria use this same combination of NPs and Braak stage as the minimum lesion density necessary for attributing the cause of dementia to AD (39, 40).”
BackgroundMethodSelf-citationClinicopathological evaluation of chronic traumatic encephalopathy in players of American football
Mez, J., Daneshvar, D. H., Kiernan, P. T., Abdolmohammadi, B., Alvarez, V. E., Huber, B. R., Alosco, M. L., Solomon, T. M., Nowinski, C. J., McHale, L., et al. (2017) · JAMA · doi:10.1001/jama.2017.8334 · Cited by 1,098
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“Segmental hippocampal neuron loss can be also observed in other pathologic conditions, including dementia, aging, ischemia, and neurodegeneration, but the patterns of neuronal cell loss may differ and usually also involves the subiculum (Nelson et al., 2011; Montine et al., 2012).”
Backgroundthe TBI/CTE group, McKee, A. C., Cairns, N. J., Dickson, D. W., Folkerth, R. D., Dirk Keene, C., Litvan, I., Perl, D. P., Stein, T. D., Vonsattel, J.-P., et al. (2016) · Acta Neuropathologica · doi:10.1007/s00401-015-1515-z · Cited by 885
“Of the NIA-AA sampling guidelines, the following blocks are most valuable for detecting CTE: sulcal depths of the superior and middle frontal gyrus, superior and middle temporal gyrus and inferior parietal gyrus (Fig.”
BackgroundMethodInfluentialSelf-citationParkinson's disease dementia: convergence of α-synuclein, tau and amyloid-β pathologies
Irwin, D. J., Lee, V. M. ‐., & Trojanowski, J. Q. (2013) · Nature reviews. Neuroscience · doi:10.1038/nrn3549 · Cited by 914
Self-citationAlzheimer's disease: experimental models and reality
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“The current consensus guidelines for neuropathological evaluation of AD are ranked on three parameters (Amyloid, Braak and CERAD staging) to obtain an “ABC” score that quantifies both neuritic plaques and NFT pathology [65, 99].”
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Proteopathic tau seeding predicts tauopathy in vivo
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“In 2012, new consensus guidelines for neuropathologic evaluation of AD were adopted (Hyman et al., 2012; Montine et al., 2012).”
Self-citationRobinson, J. L., Lee, E. B., Xie, S. X., Rennert, L., Suh, E., Bredenberg, C., Caswell, C., Van Deerlin, V. M., Yan, N., Yousef, A., et al. (2018) · Brain · doi:10.1093/brain/awy146 · Cited by 729
Self-citationIranzo, Á., Tolosa, E. S., Gelpí, E., Molinuevo, J. L., Valldeoriola, F., Serradell, M., Sánchez‐Valle, R., Vilaseca, I., Lomeña, F., Vilas, D., et al. (2013) · The Lancet Neurology · doi:10.1016/s1474-4422(13)70056-5 · Cited by 747
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New insights into atypical Alzheimer's disease in the era of biomarkers
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Alpha‐synuclein RT ‐Qu IC in the CSF of patients with alpha‐synucleinopathies
Fairfoul, G., McGuire, L. I., Pal, S., Ironside, J. W., Neumann, J., Christie, S., Joachim, C., Esiri, M., Evetts, S. G., Rolinski, M., et al. (2016) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.338 · Cited by 608
“All cases used had been examined histologically and the diagnosis reached using internationally accepted criteria.(18) Initial 10% w/v brain homogenates were prepared using phosphate-buffered saline (PBS) containing 1 mmol/L EDTA, 150 mmol/L NaCl, 0.”
MethodJohnson, K. A., Minoshima, S., Bohnen, N. I., Donohoe, K. J., Foster, N. L., Herscovitch, P., Karlawish, J. H., Rowe, C. C., Carrillo, M. C., Hartley, D. M., et al. (2013) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2013.01.002 · Cited by 603
Irwin, D. J., Grossman, M., Weintraub, D. A., Hurtig, H. I., Duda, J. E., Xie, S. X., Lee, E. B., Deerlin, V. M. V., López, O. L., Kofler, J., et al. (2016) · The Lancet Neurology · doi:10.1016/s1474-4422(16)30291-5 · Cited by 606
Self-citationOssenkoppele, R., Pijnenburg, Y. A. L., Perry, D. C., Cohn-Sheehy, B. I., Scheltens, N. M. E., Vogel, J. W., Kramer, J. H., van der Vlies, A. E., Joie, R. L., Rosen, H. J., et al. (2015) · Brain · doi:10.1093/brain/awv191 · Cited by 548
“All had stage V and thus classified for ‘high’ Alzheimer’s disease neuropathological change according to recently proposed NIA-AA guidelines (Montine et al., 2012).”
BackgroundMethodPreclinical Alzheimer's disease and its outcome: a longitudinal cohort study
Vos, S. J., Xiong, C., Visser, P. J., Jasielec, M. S., Hassenstab, J., Grant, E. A., Cairns, N. J., Morris, J. C., Holtzman, D. M., & Fagan, A. M. (2013) · The Lancet Neurology · doi:10.1016/s1474-4422(13)70194-7 · Cited by 564
Self-citationJohnson, E. C. B., Carter, E. K., Dammer, E. B., Duong, D. M., Gerasimov, E. S., Liu, Y., Liu, J., Betarbet, R., Ping, L., Yin, L., et al. (2022) · Nature Neuroscience · doi:10.1038/s41593-021-00999-y · Cited by 561
“Cases were defined based on a unified classification scheme using semi-quantitative histopathological measures of A β and tau neurofibrillary tangle deposition 12–15 as well as cognitive function near time of death, as previously described 7 .”
Self-citationThe preclinical phase of the pathological process underlying sporadic Alzheimer’s disease
Braak, H., & Del Tredici, K. (2015) · Brain · doi:10.1093/brain/awv236 · Cited by 540
“susceptible proteins Aggregates consisting of two different pathological proteins, abnormal tau and amyloid-b, are central to the process underlying Alzheimer’s disease (Duyckaerts et al., 2009; Montine et al., 2012; Nelson et al., 2012; Spillantini and Goedert, 2013).”
BackgroundInfluentialMolecular characterization of selectively vulnerable neurons in Alzheimer’s disease
Leng, K., Li, E., Eser, R., Piergies, A., Sit, R., Tan, M., Neff, N., Li, S. H., Rodriguez, R. D., Suemoto, C. K., et al. (2021) · Nature Neuroscience · doi:10.1038/s41593-020-00764-7 · Cited by 485
Reduced glucocerebrosidase is associated with increased α-synuclein in sporadic Parkinson’s disease
Murphy, K. E., Gysbers, A. M., Abbott, S. K., Tayebi, N., Kim, W. S., Sidransky, E., Cooper, A., Garner, B., & Halliday, G. M. (2014) · Brain · doi:10.1093/brain/awt367 · Cited by 475
An autoradiographic evaluation of AV-1451 Tau PET in dementia
Lowe, V. J., Curran, G., Fang, P., Liesinger, A. M., Josephs, K. A., Parisi, J. E., Kantarci, K., Boeve, B. F., Pandey, M. K., Bruinsma, T., et al. (2016) · Acta Neuropathologica Communications · doi:10.1186/s40478-016-0315-6 · Cited by 474
“To examine binding specificity of AV-1451 to tau we included neuropathologically normal individuals with no NFT or Aβ deposits (n = 3), neuropathologically normal individuals with minimal NFT and substantial Aβ deposits ((“pathological aging” (PA), n = 2), neuropathologically normal individuals with NFT and no Aβ depo…”
BackgroundSelf-citationModeling Alzheimer’s disease with iPSC-derived brain cells
Penney, J., Ralvenius, W. T., & Tsai, L.-H. (2020) · Molecular Psychiatry · doi:10.1038/s41380-019-0468-3 · Cited by 471
Arizona Study of Aging and Neurodegenerative Disorders and Brain and Body Donation Program
Beach, T. G., Adler, C. H., Sue, L. I., Serrano, G., Shill, H. A., Walker, D. G., Lue, L., Roher, A. E., Dugger, B. N., Maarouf, C., et al. (2015) · Neuropathology · doi:10.1111/neup.12189 · Cited by 460
“We are currently engaged in retrospectively rating a subset of past cases for Thal amyloid phase,(86) and re-classifying the same subset according to NIA-AA (National Institute on Aging-Alzheimer’s Association) criteria for AD.(104,105) Paraffin sections stained with IHC for phosphorylated α-synuclein(70,82) are grade…”
MethodInfluentialSelf-citationRare coding variants in the phospholipase D3 gene confer risk for Alzheimer’s disease
Cruchaga, C., Karch, C. M., Jin, S. C., Benitez, B. A., Cai, Y., Guerreiro, R., Harari, O., Norton, J., Budde, J., Bertelsen, S., et al. (2014) · Nature · doi:10.1038/nature12825 · Cited by 461
Self-citationNeuropathologic substrates of Parkinson disease dementia
Irwin, D. J., White, M. T., Toledo, J. B., Xie, S. X., Robinson, J. L., Van Deerlin, V., Lee, V. M. ‐., Leverenz, J. B., Montine, T. J., Duda, J. E., et al. (2012) · Annals of Neurology · doi:10.1002/ana.23659 · Cited by 518
“Cerebrovascular disease (CVD) was defined based on the presence of vascular brain injury (VBI) using modified criteria outlined in the latest National Institute on Aging (NIA)-Alzheimer’s Association (AA) guidelines.(38) Briefly, gross evidence of ischemic or hemorrhagic infarction or 2 or more microvascular lesions (…”
MethodSelf-citationKalaria, R. N. (2016) · Acta Neuropathologica · doi:10.1007/s00401-016-1571-z · Cited by 441
Rossi, M., Candelise, N., Baiardi, S., Capellari, S., Giannini, G., Orru, C. D., Antelmi, E., Mammana, A., Hughson, A. G., Buonaura, G. C., et al. (2020) · Acta Neuropathologica · doi:10.1007/s00401-020-02160-8 · Cited by 470
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Self-citationVilleneuve, S., Rabinovici, G. D., Cohn-Sheehy, B. I., Madison, C., Ayakta, N., Ghosh, P. M., La Joie, R., Arthur-Bentil, S. K., Vogel, J. W., Marks, S. M., et al. (2015) · Brain · doi:10.1093/brain/awv112 · Cited by 408
Distinct amyloid-β and tau-associated microglia profiles in Alzheimer’s disease
Gerrits, E., Brouwer, N., Kooistra, S. M., Woodbury, M. E., Vermeiren, Y., Lambourne, M., Mulder, J., Kummer, M., Möller, T., Biber, K., et al. (2021) · Acta Neuropathologica · doi:10.1007/s00401-021-02263-w · Cited by 441
Tau molecular diversity contributes to clinical heterogeneity in Alzheimer’s disease
Dujardin, S., Commins, C., Lathuiliere, A., Beerepoot, P., Fernandes, A. R., Kamath, T. V., De Los Santos, M. B., Klickstein, N., Corjuc, D. L., Corjuc, B. T., et al. (2020) · Nature Medicine · doi:10.1038/s41591-020-0938-9 · Cited by 438
Self-citationSchwarz, A. J., Yu, P., Miller, B. B., Shcherbinin, S., Dickson, J., Navitsky, M., Joshi, A. D., Devous, M. D., & Mintun, M. S. (2016) · Brain · doi:10.1093/brain/aww023 · Cited by 425
“Those guidelines recommend that the 7-level staging scheme is reduced to a 4-level one, with stages I– II, III–IV and V–VI, respectively, combined for improved reliability (Montine et al., 2012).”
BackgroundMethodGroveman, B. R., Orru, C. D., Hughson, A. G., Raymond, L. D., Zanusso, G., Ghetti, B. F., Campbell, K. J., Safar, J., Galasko, D. R., & Caughey, B. W. (2018) · Acta Neuropathologica Communications · doi:10.1186/s40478-018-0508-2 · Cited by 414
“Pathological diagnoses of AD and DLB are made using National Institute on Aging-Alzheimer’s Association (NIA-AA) guidelines [22].”
Multimodal deep learning for Alzheimer's disease dementia assessment
Qiu, S., Miller, M. I., Joshi, P. S., Lee, J. C., Xue, C., Ni, Y., Wang, Y., De Anda-Duran, I., Hwang, P. H., Cramer, J. A., et al. (2022) · Nature Communications · doi:10.1038/s41467-022-31037-5 · Cited by 420
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Cholesterol and matrisome pathways dysregulated in astrocytes and microglia
TCW, J., Qian, L., Pipalia, N. H., Chao, M. J., Liang, S. A., Shi, Y., Jain, B. R., Bertelsen, S. E., Kapoor, M., Marcora, E., et al. (2022) · Cell · doi:10.1016/j.cell.2022.05.017 · Cited by 411
Integrated multimodal cell atlas of Alzheimer’s disease
Gabitto, M. I., Travaglini, K. J., Rachleff, V. M., Kaplan, E. S., Long, B., Ariza, J., Ding, Y., Mahoney, J. T., Dee, N., Goldy, J., et al. (2024) · Nature Neuroscience · doi:10.1038/s41593-024-01774-5 · Cited by 397
“Donors with any level of Lewy body dementia (LBD), vascular pathology or limbic-predominant age-related TDP-43 encephalopathy (LATE) were included because these conditions are common comorbidities in AD 39,40 .”
COVID-19 neuropathology at Columbia University Irving Medical Center/New York Presbyterian Hospital
Thakur, K. T., Miller, E. H., Glendinning, M. D., Al‐Dalahmah, O., Banu, M. A., Boehme, A. K., Boubour, A., Bruce, S. S., Chong, A. M., Claassen, J., et al. (2021) · Brain · doi:10.1093/brain/awab148 · Cited by 396
Melanopsin retinal ganglion cell loss in A lzheimer disease
Morgia, C. L., Ross‐Cisneros, F. N., Koronyo, Y., Hannibal, J., Gallassi, R., Cantalupo, G., Sambati, L., Pan, B. X., Tozer, K. R., Barboni, P., et al. (2015) · Annals of Neurology · doi:10.1002/ana.24548 · Cited by 400
Dementia with Lewy bodies: an update and outlook
Outeiro, T. F., Koss, D. J., Erskine, D., Walker, L., Kurzawa-Akanbi, M., Burn, D., Donaghy, P., Morris, C., Taylor, J.-P., Thomas, A., et al. (2019) · Molecular Neurodegeneration · doi:10.1186/s13024-019-0306-8 · Cited by 381
“Unsurprisingly, such cases usually show additional high levels of AD neuropathological change [24, 25].”
BackgroundSystematic Review on Resting-State EEG for Alzheimer’s Disease Diagnosis and Progression Assessment
Cassani, R., Estarellas, M., San-Martin, R., Fraga, F. J., & Falk, T. H. (2018) · Disease Markers · doi:10.1155/2018/5174815 · Cited by 415
“Additionally, other disorders that also lead to dementia as vascular brain injury, Lewy body diseases, and Parkinson disease in some cases are also comorbid to AD [25].”
BackgroundNeuropathology of Alzheimer's Disease
Trejo‐Lopez, J. A., Yachnis, A. T., & Prokop, S. (2021) · Neurotherapeutics · doi:10.1007/s13311-021-01146-y · Cited by 419
“1 3 Braak stages were condensed into a 3-tier system with “B1” corresponding to Braak stages I and II, “B2” corresponding to Braak stages III and IV, and “B3” encompassing Braak stages V and VI [9, 10].”
BackgroundMethodInfluentialBrickman, A. M., Manly, J. J., Honig, L. S., Sanchez, D., Reyes‐Dumeyer, D., Lantigua, R. A., Lao, P. J., Stern, Y., Vonsattel, J. P., Teich, A. F., et al. (2021) · Alzheimer's & Dementia · doi:10.1002/alz.12301 · Cited by 387
Updated TDP-43 in Alzheimer’s disease staging scheme
Josephs, K. A., Murray, M. E., Whitwell, J. L., Tosakulwong, N., Weigand, S. D., Petrucelli, L., Liesinger, A. M., Petersen, R. C., Parisi, J. E., & Dickson, D. W. (2016) · Acta Neuropathologica · doi:10.1007/s00401-016-1537-1 · Cited by 382
“The basal forebrain and insula cortex, for example, are well known to be affected by tau immunoreactive neurofibrillary tangle pathology in Alzheimer’s disease [9, 34].”
Self-citationAPOE4 homozygosity represents a distinct genetic form of Alzheimer’s disease
Fortea, J., Pegueroles, J., Alcolea, D., Belbin, O., Dols-Icardo, O., Vaqué-Alcázar, L., Videla, L., Gispert, J. D., Suárez-Calvet, M., Johnson, S. C., et al. (2024) · Nature Medicine · doi:10.1038/s41591-024-02931-w · Cited by 369
Prevalence of mixed pathologies in the aging brain
Rahimi, J., & Kovács, G. G. (2014) · Alzheimer s Research & Therapy · doi:10.1186/s13195-014-0082-1 · Cited by 382
Structural imaging of hippocampal subfields in healthy aging and Alzheimer’s disease
de Florès, R., Joie, R. L., & Chételat, G. (2015) · Neuroscience · doi:10.1016/j.neuroscience.2015.08.033 · Cited by 387
Kovács, G. G., Milenković, I., Wöehrer, A., Höftberger, R., Gelpí, E., Haberler, C., Hönigschnabl, S., Reiner‐Concin, A., Heinzl, H., Jungwirth, S., et al. (2013) · Acta Neuropathologica · doi:10.1007/s00401-013-1157-y · Cited by 380
“28), the BB stages of neurofibrillary degeneration, CERAD score, and the level of AD-neuropathologic change [64] (for all Spearman correlation, p < 0.”
BackgroundMethodPathology and pathogenesis of vascular cognitive impairment—a critical update
Jellinger, K. A. (2013) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2013.00017 · Cited by 353
Corces, M. R., Shcherbina, A., Kundu, S., Gloudemans, M. J., Frésard, L., Granja, J. M., Louie, B. H., Eulalio, T., Shams, S., Bagdatli, S. T., et al. (2020) · Nature Genetics · doi:10.1038/s41588-020-00721-x · Cited by 358
Self-citationPhosphorylation of different tau sites during progression of Alzheimer’s disease
Neddens, J., Temmel, M., Flunkert, S., Kerschbaumer, B., Hoeller, C., Loeffler, T., Niederkofler, V., Daum, G., Attems, J., & Hutter-Paier, B. (2018) · Acta Neuropathologica Communications · doi:10.1186/s40478-018-0557-6 · Cited by 384
“internationally accepted criteria [31] (Table 1).”
Phosphorylated tau interactome in the human Alzheimer's disease brain
Drummond, E., Pires, G., MacMurray, C., Askenazi, M., Nayak, S., Bourdon, M., Safar, J., Ueberheide, B., & Wisniewski, T. (2020) · Brain · doi:10.1093/brain/awaa223 · Cited by 357
Olfactory bulb involvement in neurodegenerative diseases
Attems, J., Walker, L., & Jellinger, K. A. (2014) · Acta Neuropathologica · doi:10.1007/s00401-014-1261-7 · Cited by 341
Murray, M. E., Lowe, V. J., Graff-Radford, N. R., Liesinger, A. M., Cannon, A., Przybelski, S. A., Rawal, B., Parisi, J. E., Petersen, R. C., Kantarci, K., et al. (2015) · Brain · doi:10.1093/brain/awv050 · Cited by 324
“…brains by retrospectively assessing senile plaque quantification of neocortex (i.e. midfrontal, inferior parietal or superior temporal cortex) and hippocampus using thioflavin-S staining results as supported in the latest NIA-AA recommendations (Hyman et al., 2012; Montine et al., 2012).”
BackgroundMethodInfluentialSelf-citationImmune Signaling in Neurodegeneration
Hammond, T. R., Marsh, S. E., & Stevens, B. (2019) · Immunity · doi:10.1016/j.immuni.2019.03.016 · Cited by 336
“tau, although both eventually heavily impact neocortical, entorhinal cortex, and hippocampal regions (for review and further description see (Braak and Braak, 1991; Montine et al., 2012)).”
BackgroundMesulam, M.-M., Weintraub, S., Rogalski, E. J., Wieneke, C., Geula, C., & Bigio, E. H. (2014) · Brain · doi:10.1093/brain/awu024 · Cited by 334
Self-citationPrognosis and neuropathologic correlation of clinical subtypes of Parkinson disease
De Pablo-Fernández, E., Lees, A. J., Holton, J. L., & Warner, T. T. (2019) · JAMA Neurology · doi:10.1001/jamaneurol.2018.4377 · Cited by 332
Moloney, C. M., Lowe, V. J., & Murray, M. E. (2021) · Alzheimer s & Dementia · doi:10.1002/alz.12321 · Cited by 358
de la Monte, S. M. (2017) · Drugs · doi:10.1007/s40265-016-0674-0 · Cited by 331
Bieniek, K. F., Cairns, N. J., Crary, J. F., Dickson, D. W., Folkerth, R. D., Keene, C. D., Litvan, I., Perl, D. P., Stein, T. D., Vonsattel, J., et al. (2021) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlab001 · Cited by 345
Self-citationKovács, G. G. (2016) · International Journal of Molecular Sciences · doi:10.3390/ijms17020189 · Cited by 346
“Together with the classical semiquantitative scoring of neuritic plaques [68], the Braak stages and Thal phases are included in the recent NIA-AA neuropathological criteria for AD [69].”
BackgroundSkrobot, O. A., Attems, J., Esiri, M. M., Hortobágyi, T., Ironside, J. W., Kalaria, R. N., King, A., Lammie, G. A., Mann, D. M. A., Neal, J., et al. (2016) · Brain · doi:10.1093/brain/aww214 · Cited by 331
“…to identify and categorize different types of cerebrovascular pathology in relation to dementia (Esiri et al., 1997; Chalmers et al., 2003; Kalaria et al., 2004; Love, 2005; Strozyk et al., 2010; Deramecourt et al., 2012; Montine et al., 2012; Richardson et al., 2012; Smallwood et al., 2012).”
BackgroundJack, C. R., Therneau, T. M., Weigand, S. D., Wiste, H. J., Knopman, D. S., Vemuri, P., Lowe, V. J., Mielke, M. M., Roberts, R. O., Machulda, M. M., et al. (2019) · JAMA Neurology · doi:10.1001/jamaneurol.2019.1971 · Cited by 300
PART is part of Alzheimer disease
Duyckaerts, C. J., Braak, H., Brion, J., Buée, L., Tredici, K. D., Goedert, M., Halliday, G. M., Neumann, M., Spillantini, M. G., Tolnay, M., et al. (2015) · Acta Neuropathologica · doi:10.1007/s00401-015-1390-7 · Cited by 329
“In conclusion, both Aβ and tau pathologies are necessary for the diagnosis of AD according to current criteria [17, 22].”
BackgroundMethodInfluentialSelf-citationLewczuk, P., Riederer, P. F., O’Bryant, S. E., Verbeek, M. M., Dubois, B., Visser, P. J., Jellinger, K. A., Engelborghs, S., Ramírez, A., Parnetti, L., et al. (2017) · The World Journal of Biological Psychiatry · doi:10.1080/15622975.2017.1375556 · Cited by 318
“The recent NIA-AA guidelines consider levels of AD pathology regardless of the clinical history (Montine et al. 2012).”
BackgroundSelf-citationWu, Z., Guo, Z., Gearing, M., & Chen, G. (2014) · Nature Communications · doi:10.1038/ncomms5159 · Cited by 306
Suspected non-Alzheimer disease pathophysiology — concept and controversy
Jack, C. R., Knopman, D. S., Chételat, G., Dickson, D. W., Fagan, A. M., Frisoni, G. B., Jagust, W. J., Mormino, E. C., Petersen, R. C., Sperling, R. A., et al. (2016) · Nature Reviews Neurology · doi:10.1038/nrneurol.2015.251 · Cited by 313
“Third, the neuropathological definition of AD requires both Aβ and tau pathology 58,59 .”
Self-citationHall, H., Reyes, S., Landeck, N., Bye, C. R., Leanza, G., Double, K. L., Thompson, L. H., Halliday, G. M., & Kirik, D. (2014) · Brain · doi:10.1093/brain/awu193 · Cited by 315
“For this purpose, we selected cases not reaching current neuropathological criteria for any neurodegenerative condition other than Parkinson’s disease (Hyman et al., 2012; Montine et al., 2012) and analysed in detail selected brain regions in post-mortem material obtained from longitudinally followed demented and non-…”
BackgroundMethodBiomarker modeling of Alzheimer’s disease using PET-based Braak staging
Therriault, J., Pascoal, T. A., Lussier, F. Z., Tissot, C., Chamoun, M., Bezgin, G., Servaes, S., Benedet, A. L., Ashton, N. J., Karikari, T. K., et al. (2022) · Nature Aging · doi:10.1038/s43587-022-00204-0 · Cited by 308
“Unique (2) the correspondence with existing gold-standard histopathological frameworks for AD diagnosis 6,7 .”
InfluentialTesta, G., Staurenghi, E., Zerbinati, C., Gargiulo, S., Iuliano, L., Giaccone, G., Fantò, F., Poli, G., Leonarduzzi, G., & Gamba, P. (2016) · Redox Biology · doi:10.1016/j.redox.2016.09.001 · Cited by 270
“Definitive diagnosis requires post-mortem evaluation of NFT and senile plaques in the brain [9,10].”
De Schepper, S., Ge, J. Z., Sierksma, A., Crowley, G., Ferreira, L. S. S., Garceau, D., Toomey, C. E., Sokolova, D., Rueda-Carrasco, J., Shin, S.-H., et al. (2023) · Nature Neuroscience · doi:10.1038/s41593-023-01257-z · Cited by 295
“The level of AD pathology in all cases was assessed using current diagnostic consensus criteria 79,80 .”
Neuropathology and biochemistry of Aβ and its aggregates in Alzheimer’s disease
Thal, D. R., Walter, J., Saido, T. C., & Fändrich, M. (2015) · Acta Neuropathologica · doi:10.1007/s00401-014-1375-y · Cited by 319
Self-citationMonoaminergic neuropathology in Alzheimer’s disease
Šimić, G., Leko, M. B., Wray, S., Harrington, C. R., Delalle, I., Milošević, N. J., Bažadona, D., Buée, L., de Silva, R., Giovanni, G. D., et al. (2016) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2016.04.001 · Cited by 297
“The fourth part of the NIA/AA guidelines (Hyman et al., 2012; Montine et al., 2012) updated the 1997 NIA/Reagan Institute neuropathological criteria for AD (Hyman and Trojanowski, 1997).”
InfluentialBeta-amyloid deposition in chronic traumatic encephalopathy
Stein, T. D., Montenigro, P. H., Alvarez, V. E., Xia, W., Crary, J. F., Tripodis, Y., Daneshvar, D. H., Mez, J., Solomon, T., Meng, G., et al. (2015) · Acta Neuropathologica · doi:10.1007/s00401-015-1435-y · Cited by 291
“Subjects with AD changes had a low degree of neuropathological change as defined by the ABC score [15, 34].”
BackgroundComorbid neuropathological diagnoses in early versus late-onset Alzheimer's disease
Spina, S., La Joie, R., Petersen, C., Nolan, A. L., Cuevas, D., Cosme, C., Hepker, M., Hwang, J.-H., Miller, Z. A., Huang, E. J., et al. (2021) · Brain · doi:10.1093/brain/awab099 · Cited by 278
Xia, C., Makaretz, S. J., Caso, C., McGinnis, S. M., Gomperts, S. N., Sepulcre, J., Gómez‐Isla, T., Hyman, B. T., Schultz, A. P., Vasdev, N., et al. (2017) · JAMA Neurology · doi:10.1001/jamaneurol.2016.5755 · Cited by 288
Self-citationAttems, J., Toledo, J. B., Walker, L., Gelpí, E., Gentleman, S., Halliday, G. M., Hortobágyi, T., Jellinger, K. A., Kovács, G. G., Lee, E. B., et al. (2021) · Acta Neuropathologica · doi:10.1007/s00401-020-02255-2 · Cited by 295
Self-citationMcAleese, K. E., Walker, L., Graham, S., Moya, E. L. J., Johnson, M. A., Erskine, D., Colloby, S. J., Dey, M., Martin-Ruiz, C. M., Taylor, J., et al. (2017) · Acta Neuropathologica · doi:10.1007/s00401-017-1738-2 · Cited by 280
“1 3 (NIA-AA) criteria [44] that included assessment of Thal phases of Aβ deposition [57], Braak staging of neurofibrillary pathology [10] and Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) scoring [43].”
MethodTherriault, J., Vermeiren, M. R., Servaes, S., Tissot, C., Ashton, N. J., Benedet, A. L., Karikari, T. K., Lantero‐Rodriguez, J., Brum, W. S., Lussier, F. Z., et al. (2022) · JAMA Neurology · doi:10.1001/jamaneurol.2022.4485 · Cited by 278
Duration of American Football Play and Chronic Traumatic Encephalopathy
Mez, J., Daneshvar, D. H., Abdolmohammadi, B., Chua, A. S., Alosco, M. L., Kiernan, P. T., Evers, L., Marshall, L., Martin, B. M., Palmisano, J. N., et al. (2020) · Annals of Neurology · doi:10.1002/ana.25611 · Cited by 271
“Concussion definition provided 45 (12-150) 0 47.”
Novel advances in shotgun lipidomics for biology and medicine
Wang, M., Wang, C., Han, R. H., & Han, X. (2015) · Progress in Lipid Research · doi:10.1016/j.plipres.2015.12.002 · Cited by 274
“AD is characterized clinically by progressive cognitive impairment [174] and neuropathologically by the appearance of diffusible amyloid-beta (Aβ), neuritic plaques, and intraneuronal neurofibrillary tangles [175].”
BackgroundUnger, M. S., Li, E., Scharnagl, L., Poupardin, R., Altendorfer, B., Mrowetz, H., Hutter-Paier, B., Weiger, T. M., Heneka, M. T., Attems, J., et al. (2020) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2020.05.070 · Cited by 248
Aging, Cellular Senescence, and Alzheimer’s Disease
Liu, R.-M. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23041989 · Cited by 267
“Accumulation of β-amyloid (Aβ) peptides in the brain is a pathological feature of AD [44,45].”
BackgroundInfluential
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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