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 101–200 of 2,854
Josephs, K. A., Dickson, D. W., Tosakulwong, N., Weigand, S. D., Murray, M. E., Petrucelli, L., Liesinger, A. M., Senjem, M. L., Spychalla, A. J., Knopman, D. S., et al. (2017) · The Lancet Neurology · doi:10.1016/s1474-4422(17)30284-3 · Cited by 252
Self-citationFrontotemporal lobar degeneration: defining phenotypic diversity through personalized medicine
Irwin, D. J., Cairns, N. J., Grossman, M., McMillan, C. T., Lee, E. B., Deerlin, V. M. V., Lee, V. M. ‐., & Trojanowski, J. Q. (2014) · Acta Neuropathologica · doi:10.1007/s00401-014-1380-1 · Cited by 278
“This distinction is now recognized in the recent National Institute on Aging-Alzheimer’s Association (NIA-AA) diagnostic criteria for AD [159] and thus, since the neuropathology can occur with minimal cognitive symptoms the term “tangle predominant senile dementia” has been replaced with PART [51].”
BackgroundMethodSelf-citationTDP‐43 pathology in Alzheimer's disease, dementia with Lewy bodies and ageing
McAleese, K. E., Walker, L., Erskine, D., Thomas, A. J., McKeith, I. G., & Attems, J. (2016) · Brain Pathology · doi:10.1111/bpa.12424 · Cited by 268
“Fourty-six cases fulfilled neuropathological criteria for high AD neuropathological change according to NIA-AA criteria (26), 15 for DLB (inclusive of DLB and Parkinson’s disease dementia clinical phenotypes) according to McKeith Lewy body criteria (25) [limbic/neocortical Lewy body disease; Braak Lewy body stage, 4 o…”
BackgroundMethodInfluentialSNMMI Procedure Standard/EANM Practice Guideline for Amyloid PET Imaging of the Brain 1.0
Minoshima, S., Drzezga, A. E., Barthel, H., Bohnen, N. I., Djekidel, M., Lewis, D. H., Mathis, C. A., McConathy, J., Nordberg, A. K., Sabri, O., et al. (2016) · Journal of Nuclear Medicine · doi:10.2967/jnumed.116.174615 · Cited by 264
Braak, H., & Del Tredici, K. (2017) · Journal of Parkinson’s Disease · doi:10.3233/jpd-179001 · Cited by 372
Where, when, and in what form does sporadic Alzheimerʼs disease begin?
Braak, H., & Tredici, K. D. (2012) · Current Opinion in Neurology · doi:10.1097/wco.0b013e32835a3432 · Cited by 261
Olsson, B., Portelius, E., Cullen, N. C., Sandelius, Å., Zetterberg, H., Andréasson, U., Höglund, K., Irwin, D. J., Grossman, M., Weintraub, D. A., et al. (2018) · JAMA Neurology · doi:10.1001/jamaneurol.2018.3746 · Cited by 256
“1) 1578 (1287-3104) 210 (167-260) 50 (36-75) 12 (10-19)”
Self-citationLing, H., Morris, H. R., Neal, J. W., Lees, A. J., Hardy, J., Holton, J. L., Revesz, T., & Williams, D. D. R. (2017) · Acta Neuropathologica · doi:10.1007/s00401-017-1680-3 · Cited by 252
18F-MK-6240 PET for early and late detection of neurofibrillary tangles
Pascoal, T. A., Therriault, J., Benedet, A. L., Savard, M., Lussier, F. Z., Chamoun, M., Tissot, C., Qureshi, M. N. I., Kang, M. S., Mathotaarachchi, S. S., et al. (2020) · Brain · doi:10.1093/brain/awaa180 · Cited by 263
Brain-derived tau: a novel blood-based biomarker for Alzheimer’s disease-type neurodegeneration
González‐Ortiz, F., Turton, M., Kac, P. R., Smirnov, D. S., Premi, E., Ghidoni, R., Benussi, L., Cantoni, V., Saraceno, C., Rivolta, J., et al. (2022) · Brain · doi:10.1093/brain/awac407 · Cited by 277
“49 For biomarker – pathology associations, we evaluated comparisons with NIA Reagan, 50 Braak stage 47 and CERAD 48 stages separately.”
Bassil, F., Brown, H. J., Pattabhiraman, S., Iwasyk, J. E., Maghames, C. M., Meymand, E. S., Cox, T. O., Riddle, D. M., Zhang, B., Trojanowski, J. Q., et al. (2019) · Neuron · doi:10.1016/j.neuron.2019.10.010 · Cited by 246
“For human brain analysis, α-syn scores from PD, PDD, DLB patients were pooled and sorted according to Aβ plaque load (Montine et al., 2012).”
Self-citationDavies, D. S., Ma, J., Jegathees, T., & Goldsbury, C. (2017) · Brain Pathology · doi:10.1111/bpa.12456 · Cited by 251
“on Aging guidelines for the neuropathological assessment of AD (22).”
BackgroundDown Syndrome, Partial Trisomy 21, and Absence of Alzheimer’s Disease: The Role of APP
Doran, E., Keator, D., Head, E., Phelan, M. J., Kim, R., Totoiu, M., Barrio, J. R., Small, G. W., Potkin, S. G., & Lott, I. T. (2017) · Journal of Alzheimer’s Disease · doi:10.3233/jad-160836 · Cited by 244
Molecular pathology of neurodegenerative diseases: principles and practice
Kovács, G. G. (2019) · Journal of Clinical Pathology · doi:10.1136/jclinpath-2019-205952 · Cited by 255
“of AD neuropathological change: not, low, intermediate or high.(53) prion diseases Prion diseases are classified based on the aetiology as idiopathic/sporadic, acquired and genetic forms.”
BackgroundExpanding the spectrum of neuronal pathology in multiple system atrophy
Cykowski, M. D., Coon, E. A., Powell, S. Z., Jenkins, S. M., Benarroch, E. E., Low, P. A., Schmeichel, A. M., & Parisi, J. E. (2015) · Brain · doi:10.1093/brain/awv114 · Cited by 241
Johnson, 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) · Journal of Nuclear Medicine · doi:10.2967/jnumed.113.120618 · Cited by 329
“This process is described in Appendix B. Based on the consensus discussion, the Indication Subcommittee consolidated potential indications and nonindications into 14 scenarios that were subsequently incorporated in a data extraction form used for the evidence assessment (described later).”
Proteomic differences in amyloid plaques in rapidly progressive and sporadic Alzheimer’s disease
Drummond, E., Nayak, S., Faustin, A., Pires, G., Hickman, R. A., Askenazi, M., Cohen, M., Haldiman, T., Kim, C., Han, X., et al. (2017) · Acta Neuropathologica · doi:10.1007/s00401-017-1691-0 · Cited by 239
“At autopsy rpAD patients have similar neuropathology to sAD, although there is a higher prevalence of a low degree of pathology using standard NIA-Alzheimer’s Association guidelines [18, 51].”
BackgroundMethodCorriveau, R. A., Bosetti, F., Emr, M., Gladman, J. T., Koenig, J. I., Moy, C. S., Pahigiannis, K., Waddy, S. P., & Koroshetz, W. (2016) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-016-0334-7 · Cited by 240
Ehrenberg, A. J., Nguy, A. K., Theofilas, P., Dunlop, S. R., Suemoto, C. K., Alho, A. T. D. L., Leite, R. P., Rodriguez, R. D., Mejia, M. B., Rüb, U., et al. (2017) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12387 · Cited by 243
Besser, L. M., Kukull, W. A., Teylan, M. A., Bigio, E. H., Cairns, N. J., Kofler, J. K., Montine, T. J., Schneider, J. A., & Nelson, P. T. (2018) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nly049 · Cited by 224
“The v10 form incorporated the NIA-AA ADNC criteria and sampling recommendations, as well as additional advances to the neuropathologic classification and nomenclature of FTLD (13) and vascular contributions to cognitive impairment and dementia (VCID) (3, 14–18).”
BackgroundMethodInfluentialSelf-citationTredici, K. D., & Braak, H. (2012) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp-2011-301817 · Cited by 251
Emerging Concepts in Alzheimer's Disease
Vinters, H. V. (2014) · Annual Review of Pathology Mechanisms of Disease · doi:10.1146/annurev-pathol-020712-163927 · Cited by 244
Self-citationDiabetes is associated with cerebrovascular but not Alzheimer's disease neuropathology
Abner, E. L., Nelson, P. T., Kryscio, R. J., Schmitt, F. A., Fardo, D. W., Woltjer, R. L., Cairns, N. J., Yu, L., Dodge, H. H., Xiong, C., et al. (2016) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2015.12.006 · Cited by 233
Self-citationMultiple Cerebral Hemorrhages in a Patient Receiving Lecanemab and Treated with t-PA for Stroke
Reish, N. J., Jamshidi, P., Stamm, B. J., Flanagan, M. E., Sugg, E., Tang, M., Donohue, K. L., McCord, M., Krumpelman, C. S., Mesulam, M. M., et al. (2023) · New England Journal of Medicine · doi:10.1056/nejmc2215148 · Cited by 234
Tang, Z., Chuang, K. V., DeCarli, C. S., Jin, L., Beckett, L. A., Keiser, M. J., & Dugger, B. N. (2019) · Nature Communications · doi:10.1038/s41467-019-10212-1 · Cited by 234
“Consequently, studies using limited-range scores or overall pathology burden 3,8,13,24 are powerful but have interrater variability, 4,13 are difficult to adapt to statistically meaningful disease-correlation analysis, or are blind to selected locational vulnerability 20 .”
BackgroundParchi, P., de Boni, L., Saverioni, D., Cohen, M. L., Ferrer, I., Gambetti, P. L., Gelpí, E., Giaccone, G., Hauw, J., Höftberger, R., et al. (2012) · Acta Neuropathologica · doi:10.1007/s00401-012-1002-8 · Cited by 228
“[31] as well as vCJD; and (3) absence of additional significant pathological co-morbidity, such as ‘‘intermediate’’ or ‘‘high’’ Alzheimer’s disease neuropathological changes [19], cerebral haemorrhages or infarcts, or a known history of neurological disorders other than prion disease.”
Jacobs, H. I. L., Becker, J. A., Kwong, K. K., Engels, N., Prokopiou, P. C., Papp, K. V., Properzi, M. J., Hampton, O. L., Uquillas, F. D., Sanchez, J. S., et al. (2021) · Science Translational Medicine · doi:10.1126/scitranslmed.abj2511 · Cited by 236
Cerebrovascular Disease and Mechanisms of Cognitive Impairment
Kalaria, R. N. (2012) · Stroke · doi:10.1161/strokeaha.112.655803 · Cited by 234
Reducing acetylated tau is neuroprotective in brain injury
Shin, M.-K., Vázquez-Rosa, E., Koh, Y., Dhar, M., Chaubey, K., Cintrón-Pérez, C. J., Barker, S., Miller, E., Franke, K., Noterman, M. F., et al. (2021) · Cell · doi:10.1016/j.cell.2021.03.032 · Cited by 226
Walker, L., McAleese, K. E., Thomas, A. J., Johnson, M. A., Martin-Ruiz, C. M., Parker, C., Colloby, S. J., Jellinger, K. A., & Attems, J. (2015) · Acta Neuropathologica · doi:10.1007/s00401-015-1406-3 · Cited by 224
Neuropathologic basis of white matter hyperintensity accumulation with advanced age
Erten‐Lyons, D., Woltjer, R. L., Kaye, J. A., Mattek, N., Dodge, H. H., Green, S., Tran, H. T. D., Howieson, D. B., Wild, K. V., & Silbert, L. C. (2013) · Neurology · doi:10.1212/wnl.0b013e3182a43e45 · Cited by 227
“The frontal watershed area is 1 of the 2 areas recommended by the National Institute on Aging–Alzheimer’s Association guidelines for neuropathologic assessment for CVD.26 In addition, previous studies have shown progression of WMH to be greatest in the anterior white matter.27 Additional sections from the deep gray nu…”
Thal, D. R., Grinberg, L. T., & Attems, J. (2012) · Experimental Gerontology · doi:10.1016/j.exger.2012.05.023 · Cited by 231
Self-citationPlasma biomarkers for Alzheimer’s Disease in relation to neuropathology and cognitive change
Smirnov, D. S., Ashton, N. J., Blennow, K., Zetterberg, H., Simrén, J., Lantero‐Rodriguez, J., Karikari, T. K., Hiniker, A. O., Rissman, R. A., Salmon, D. P., et al. (2022) · Acta Neuropathologica · doi:10.1007/s00401-022-02408-5 · Cited by 231
“Cerebral Amyloid Angiopathy (CAA) was graded from 0 (absent) to 3 (severe) according to procedures described by the NACC Neuropathology Working Group [27].”
MethodXia, Y., Prokop, S., & Giasson, B. I. (2021) · Molecular Neurodegeneration · doi:10.1186/s13024-021-00460-5 · Cited by 227
“Along with Aβ amyloid plaques, neurofibrillary tangles (NFT) made of phosphorylated tau are one of the major pathological hallmarks of AD and are cornerstones of the current NIA criteria for the post-mortem diagnosis of AD neuropathologic change [57, 58].”
BackgroundMorris, G. P., Clark, I. A., & Vissel, B. (2018) · Acta Neuropathologica · doi:10.1007/s00401-018-1918-8 · Cited by 212
“NFTs propagate fairly linearly, as denoted in the Braak staging guidelines [28, 175].”
BackgroundMethodCopper pathology in vulnerable brain regions in Parkinson's disease
Davies, K. M., Bohic, S., Carmona, A., Ortega, R., Cottam, V., Hare, D. J., Finberg, J. P. M., Reyes, S., Halliday, G. M., Mercer, J. F. B., et al. (2014) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2013.09.034 · Cited by 244
“…Lewy Body disease (ILBD), identified according to the diagnostic criteria of Dickson et al. (Dickson et al., 2009), and from Alzheimer’s disease (AD) and age-matched controls, identified according to the diagnostic criteria of Montine et al. (Montine et al., 2012) (Supplementary Tables 1, 2 and 3).”
MethodSpecific associations between plasma biomarkers and postmortem amyloid plaque and tau tangle loads
Salvadó, G., Ossenkoppele, R., Ashton, N. J., Beach, T. G., Serrano, G. E., Reiman, E. M., Zetterberg, H., Mattsson‐Carlgren, N., Janelidze, S., Blennow, K., et al. (2023) · EMBO Molecular Medicine · doi:10.15252/emmm.202217123 · Cited by 205
Self-citationNeuropathologic Correlates of Psychiatric Symptoms in Alzheimer’s Disease
Ehrenberg, A. J., Suemoto, C. K., Resende, E. D. P. F., Petersen, C., Leite, R. E. P., Rodriguez, R. D., Ferretti‐Rebustini, R. E. D. L., You, M. Y., Oh, J. Y., Nitríni, R., et al. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180688 · Cited by 233
“AD is characterized by the accumulation of neurofibrillary tangles (NFT) and amyloid-(cid:2) plaques, as well as neuron loss [2].”
Parkinson’s disease and multiple system atrophy have distinct α-synuclein seed characteristics
Yamasaki, T. R., Holmes, B. B., Furman, J. L., Dhavale, D. D., Su, B. W., Song, E.-S., Cairns, N. J., Kotzbauer, P. T., & Diamond, M. I. (2018) · Journal of Biological Chemistry · doi:10.1074/jbc.ra118.004471 · Cited by 221
“We obtained control brain samples from identical regions of patients with similar degrees of Alzheimer disease neuropathology (53) (Table 1).”
Self-citationWhite-matter integrity on DTI and the pathologic staging of Alzheimer’s disease
Kantarci, K., Murray, M. E., Schwarz, C. G., Reid, R. I., Przybelski, S. A., Lesnick, T., Zuk, S. M., Raman, M. R., Senjem, M. L., Gunter, J. L., et al. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.04.024 · Cited by 205
Self-citationAPOE ε4 is associated with severity of Lewy body pathology independent of Alzheimer pathology
Dickson, D. W., Heckman, M. G., Murray, M. E., Soto, A. I., Walton, R. L., Diehl, N. N., van Gerpen, J. A., Uitti, R. J., Wszolek, Z. K., Ertekin-Taner, N., et al. (2018) · Neurology · doi:10.1212/wnl.0000000000006212 · Cited by 210
Self-citationMiners, J. S., Schulz, I., & Love, S. (2018) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1177/0271678x17690761 · Cited by 208
“In those from patients with AD, the diagnosis had been made according to the NIA-AA guidelines.(40) Control brains were from people with no 104 Journal of Cerebral Blood Flow & Metabolism 38(1)”
Altered Proteins in the Aging Brain
Elobeid, A., Libard, S., Leino, M., Popova, S. N., & Alafuzoff, I. (2016) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlw002 · Cited by 202
“Level of Alzheimer Disease Pathology, Applying 2012 National Institute of Aging and Alzheimer’s Association (NIA-AA) Recommendations (38, 39)”
Prevalence and clinical phenotype of quadruple misfolded proteins in older adults
Karanth, S., Nelson, P. T., Katsumata, Y., Kryscio, R. J., Schmitt, F. A., Fardo, D. W., Cykowski, M. D., Jicha, G. A., Van Eldik, L. J., & Abner, E. L. (2020) · JAMA Neurology · doi:10.1001/jamaneurol.2020.1741 · Cited by 206
Self-citationThe role of noradrenaline in cognition and cognitive disorders
Holland, N., Robbins, T. W., & Rowe, J. B. (2021) · Brain · doi:10.1093/brain/awab111 · Cited by 216
Deep clinical and neuropathological phenotyping of P ick disease
Irwin, D. J., Brettschneider, J., McMillan, C. T., Cooper, F. I., Olm, C. A., Arnold, S. E., Deerlin, V. M. V., Seeley, W. W., Miller, B. L., Lee, E. B., et al. (2015) · Annals of Neurology · doi:10.1002/ana.24559 · Cited by 219
“) using previously described methods(9) and diagnostic criteria.(3,10) Two cases (1 previously reported(11)) had a p.”
MethodSelf-citationAβ Amyloid Pathology Affects the Hearts of Patients With Alzheimer’s Disease
Troncone, L., Luciani, M., Coggins, M., Wilker, E. H., Ho, C.-Y., Codispoti, K. E., Frosch, M. P., Kayed, R., & del Monte, F. (2016) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2016.08.073 · Cited by 204
Self-citationKehoe, P. G., Wong, S., AL Mulhim, N., Palmer, L. E., & Miners, J. S. (2016) · Alzheimer's Research & Therapy · doi:10.1186/s13195-016-0217-7 · Cited by 203
“Brains had been subjected to detailed neuropathological assessment according to the National Institute on Aging-Alzheimer’s Association guidelines [40], and AD pathology was a sufficient explanation for the dementia in these cases.”
MethodDendritic spines provide cognitive resilience against Alzheimer's disease
Boros, B. D., Greathouse, K. M., Gentry, E. G., Curtis, K. A., Birchall, E. L., Gearing, M., & Herskowitz, J. H. (2017) · Annals of Neurology · doi:10.1002/ana.25049 · Cited by 198
“The Amyloid Braak CERAD score was used as a global measure of AD pathology.(17)”
MethodNicoll, J. A. R., Buckland, G. R., Harrison, C. H., Page, A. M., Harris, S., Love, S., Neal, J., Holmes, C., & Boche, D. (2019) · Brain · doi:10.1093/brain/awz142 · Cited by 213
“National Institute on Aging-Alzheimer’s Association guidelines for the neuropathological assessment of Alzheimer’s disease were used (Hyman et al., 2012; Montine et al., 2012).”
MethodTau-positron emission tomography correlates with neuropathology findings.
Lowe, V. J., Lundt, E. S., Albertson, S. M., Min, H., Fang, P., Przybelski, S. A., Senjem, M. L., Schwarz, C. G., Kantarci, K., Boeve, B., et al. (2020) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2019.09.079 · Cited by 203
“Mean (SD) 18 (8) 29 24 27 (2) 22 (6) 28 (1) 26 (4) 21 22 (7) GMWMPVCNPiB SUVR†”
Self-citationRapidly progressive Alzheimer’s disease features distinct structures of amyloid-β
Cohen, M. L., Kim, C., Haldiman, T., ElHag, M., Mehndiratta, P., Termsarasab, P., Lissemore, F. M., Shea, M., Cohen, Y., Chen, W., et al. (2015) · Brain · doi:10.1093/brain/awv006 · Cited by 206
“Neuropathological evaluation according to the National Institutes of Aging – Alzheimer’s Association guidelines (Montine et al., 2012) suggested a trend toward more cases with less severe pathology in the rapidly progressive Alzheimer’s disease group but the difference was not statistically significant (Fig 1C and D).”
BackgroundMethodInfluentialThe development and convergence of co-pathologies in Alzheimer’s disease
Robinson, J. L., Richardson, H., Xie, S. X., Suh, E., Van Deerlin, V. M., Alfaro, B., Loh, N., Porras-Paniagua, M., Nirschl, J. J., Wolk, D., et al. (2021) · Brain · doi:10.1093/brain/awaa438 · Cited by 203
Self-citationBlevins, B. L., Vinters, H. V., Love, S., Wilcock, D. M., Grinberg, L. T., Schneider, J. A., Kalaria, R. N., Katsumata, Y., Gold, B. T., Wang, D. J. J., et al. (2020) · Acta Neuropathologica · doi:10.1007/s00401-020-02235-6 · Cited by 212
Self-citationThe role of gut microbiota in pathogenesis of Alzheimer's disease
Bostancıklıoğlu, M. (2019) · Journal of Applied Microbiology · doi:10.1111/jam.14264 · Cited by 210
Chen, J. J., Nathaniel, D. L., Raghavan, P., Nelson, M., Tian, R., Tse, E., Hong, J. Y., See, S. K., Mok, S.-A., Hein, M. Y., et al. (2019) · Journal of Biological Chemistry · doi:10.1074/jbc.ra119.009432 · Cited by 170
Biomarker-based staging of Alzheimer disease: rationale and clinical applications
Therriault, J., Schindler, S. E., Salvadó, G., Pascoal, T. A., Benedet, A. L., Ashton, N. J., Karikari, T. K., Apostolova, L. G., Murray, M. E., Verberk, I. M. W., et al. (2024) · Nature Reviews Neurology · doi:10.1038/s41582-024-00942-2 · Cited by 225
“Braak stages III–IV and above, accompanied by significant Aβ and neuritic plaques (together indicating intermediate or high AD neuropathological change), are considered sufficient to explain dementia 3,22 .”
AMPK activation: Role in the signaling pathways of neuroinflammation and neurodegeneration
Peixoto, C. A., Oliveira, W. H. D., Araújo, S. M. D. R., & Nunes, A. K. S. (2017) · Experimental Neurology · doi:10.1016/j.expneurol.2017.08.013 · Cited by 196
Early neurone loss in Alzheimer’s disease: cortical or subcortical?
Arendt, T., Brückner, M. K., Morawski, M., Jäger, C., & Gertz, H. (2015) · Acta Neuropathologica Communications · doi:10.1186/s40478-015-0187-1 · Cited by 210
“The diagnosis of AD was made on the basis of both clinical and neuropathological evidence according to the criteria of the International Working Group (IWG) for New Research Criteria for the diagnosis of AD [57,58] in the revision of 2014 (IWG-2) [59], the NIA-AA diagnostic criteria in the revision of 2011 [3,60-62] a…”
MethodCoras, R., Pauli, E., Li, J., Schwarz, M., Rössler, K., Buchfelder, M., Hamer, H. M., Stefan, H., & Blümcke, I. (2014) · Brain · doi:10.1093/brain/awu100 · Cited by 198
Hippocampal sclerosis of aging, a prevalent and high-morbidity brain disease
Nelson, P. T., Smith, C. D., Abner, E. L., Wilfred, B. R., Wang, W., Neltner, J. H., Baker, M., Fardo, D. W., Kryscio, R. J., Scheff, S. W., et al. (2013) · Acta Neuropathologica · doi:10.1007/s00401-013-1154-1 · Cited by 201
“Astrocytosis—astrocyte hypertrophy and hyperplasia— is a histopathologic feature of HS-Aging [72], with the caveat that astrocytosis is also seen in innumerable other”
Self-citationSander, K., Lashley, T., Gami, P., Gendron, T., Lythgoe, M. F., Rohrer, J. D., Schott, J. M., Revesz, T., Fox, N. C., & Årstad, E. (2016) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2016.01.003 · Cited by 187
“according to the Consortium to Establish a Registry for Alzheimer’s Disease, Braak and Braak tau stage VI, and Thal phase 5 amyloid plaque pathology) using the National Institute on Aging-Alzheimer’s Association guidelines [13–16].”
MethodThe cerebellum ages slowly according to the epigenetic clock
Horvath, S., Mah, V., Lu, A. T., Woo, J. S., Choi, O.-W., Jasinska, A. J., Riancho, J. A., Tung, S., Coles, N. S., Braun, J., et al. (2015) · Aging · doi:10.18632/aging.100742 · Cited by 191
“Neuropathologic findings were those of Alzheimer's disease, Braak stage IV-V, NIA-AA stage A2B2C2 [57].”
Self-citationThomas, T. L., Miners, J. S., & Love, S. (2015) · Brain · doi:10.1093/brain/awv025 · Cited by 194
“…Diagnostic and Statistical Manual of Mental Disorders Fourth Edition (DSM-IV), and a high likelihood that Alzheimer's disease neuropathological changes were a sufficient explanation for the dementia, according to National Institute on Aging-Alzheimer's Association guidelines (Montine et al., 2012).”
MethodAmadoru, S., Doré, V., McLean, C. A., Hinton, F., Shepherd, C. E., Halliday, G. M., Leyton, C. E., Yates, P. A., Hodges, J. R., Masters, C. L., et al. (2020) · Alzheimer's Research & Therapy · doi:10.1186/s13195-020-00587-5 · Cited by 181
Confluence of α-Synuclein, Tau, and β-Amyloid Pathologies in Dementia With Lewy Bodies
Colom‐Cadena, M., Gelpí, E., Charif, S., Belbin, O., Blesa, R., Martí, M. J., Clarimón, J., & Lleó, A. (2013) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0000000000000018 · Cited by 188
Understanding the Amyloid Hypothesis in Alzheimer’s Disease
Paroni, G., Bisceglia, P., & Seripa, D. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-180802 · Cited by 194
“However, both A (cid:2) and τ deposits are necessary to fulfill neuropathologic crite-G ria for AD diagnosis, which suggests that evidence of abnormalities in both A (cid:2) and pathologic τ biomarkers should be present to apply the label “Alzheimer’s disease” in a living person [54, 181].”
Calcium Dyshomeostasis in Alzheimer’s Disease Pathogenesis
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APOE ε2 is associated with milder clinical and pathological Alzheimer disease
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“This is of critical importance, because up to 30% of subjects diagnosed with probable AD in US NIA-funded ADCs have other neuropathological diagnoses causing or contributing to their cognitive deficits, or insufficient AD neuropathological changes at autopsy to fulfill current AD neuropathological diagnostic criteria.…”
BackgroundSelf-citationVeitch, D. P., Weiner, M. W., Aisen, P. S., Beckett, L. A., DeCarli, C., Green, R. C., Harvey, D., Jack, C. R., Jagust, W., Landau, S. M., et al. (2022) · Alzheimer's & Dementia · doi:10.1002/alz.12422 · Cited by 184
Self-citationRegional protein expression in human Alzheimer’s brain correlates with disease severity
Xu, J., Patassini, S., Rustogi, N., Riba‐Garcia, I., Hale, B. D., Phillips, A. M., Waldvogel, H. J., Haines, R., Bradbury, P., Stevens, A., et al. (2019) · Communications Biology · doi:10.1038/s42003-018-0254-9 · Cited by 182
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PM2.5 exposure in association with AD-related neuropathology and cognitive outcomes
Thiankhaw, K., Chattipakorn, N., & Chattipakorn, S. C. (2021) · Environmental Pollution · doi:10.1016/j.envpol.2021.118320 · Cited by 180
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“In addition, all cases were rated (ABC level) for Alzheimer’s disease neuropathological change by assessment of amyloid-b plaques (A), neurofibrillary tangles (B) and neuritic plaques (C) scores (Montine et al., 2012).”
BackgroundVilas, D., Iranzo, Á., TOLOSA, E. S., Aldecoa, I., Berenguer, J., Vilaseca, I., Martí, C. D., Serradell, M., Lomeña, F., Alós, L., et al. (2016) · The Lancet Neurology · doi:10.1016/s1474-4422(16)00080-6 · Cited by 179
Transmission of tauopathy strains is independent of their isoform composition
He, Z., McBride, J. D., Xu, H. W., Changolkar, L. N., Kim, S., Zhang, B., Narasimhan, S., Gibbons, G. S., Guo, J., Kozak, M., et al. (2020) · Nature Communications · doi:10.1038/s41467-019-13787-x · Cited by 183
Self-citationPathological combinations in neurodegenerative disease are heterogeneous and disease-associated
Robinson, J. L., Xie, S. X., Baer, D. R., Suh, E. R., Deerlin, V. M. V., Loh, N., Irwin, D. J., McMillan, C. T., Wolk, D. A., Chen‐Plotkin, A. S., et al. (2023) · Brain · doi:10.1093/brain/awad059 · Cited by 186
“sures to diagnosis the level of Alzheimer’s disease neuropathological change according to NIA-AA criteria.(18) In addition, 29 were missing arteriolosclerosis or infarct measures to diagnosis cerebro-”
Self-citationToledo, J. B., Gopal, P., Raible, K., Irwin, D. J., Brettschneider, J., Sedor, S., Waits, K., Boluda, S., Grossman, M., Van Deerlin, V. M., et al. (2016) · Acta Neuropathologica · doi:10.1007/s00401-015-1526-9 · Cited by 184
“Both staining approaches are still recognized by the most current AD neuropathological diagnostic criteria [26, 36].”
Self-citationAmyloid and tau imaging biomarkers explain cognitive decline from late middle-age
Betthauser, T. J., Koscik, R. L., Jonaitis, E. M., Allison, S. L., Cody, K. A., Erickson, C. M., Rowley, H. A., Stone, C. K., Mueller, K. D., Clark, L. R., et al. (2019) · Brain · doi:10.1093/brain/awz378 · Cited by 176
“Definitive adjudication of Alzheimer’s disease is reserved for post-mortem neuropathology based on the presence of neurofibrillary tangles composed of aggregated microtubule associated tau protein, and amyloid-b plaques (Montine et al. , 2012).”
Soleimani‐Meigooni, D. N., Iaccarino, L., Joie, R. L., Baker, S. L., Bourakova, V., Boxer, A. L., Edwards, L., Eser, R. A., Gorno‐Tempini, M., Jagust, W. J., et al. (2020) · Brain · doi:10.1093/brain/awaa276 · Cited by 186
Nelson, P. T., Brayne, C., Flanagan, M. E., Abner, E. L., Agrawal, S., Attems, J., Castellani, R. J., Corrada, M. M., Cykowski, M. D., Di, J., et al. (2022) · Acta Neuropathologica · doi:10.1007/s00401-022-02444-1 · Cited by 187
“Brain autopsies of persons with documented amnestic dementia often reveal evidence of Alzheimer’s disease neuropathologic change (ADNC) [69], limbic predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) [81], or both.”
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“…at facilitating the neuropathological assessment of AD recommend the selection of certain areas and staining of sections to cover AD-related changes and concomitant pathologies such as vascular disease, Lewy body diseases, TDP-43 inclusions, and mesial sclerosis as well (Montine et al., 2012).”
BackgroundBrenowitz, W. D., Nelson, P. T., Besser, L. M., Heller, K., & Kukull, W. A. (2015) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2015.06.028 · Cited by 176
Self-citationPART, a distinct tauopathy, different from classical sporadic Alzheimer disease.
Jellinger, K. A., Alafuzoff, I., Attems, J., Beach, T. G., Cairns, N. J., Crary, J. F., Dickson, D. W., Hof, P. R., Hyman, B. T., Jack, C. R., et al. (2015) · Acta Neuropathologica · doi:10.1007/s00401-015-1407-2 · Cited by 171
“PART cases that lack any Aβ do not meet formal criteria for sporadic AD according to the NIA–AA guidelines [35].”
MethodSelf-citationPerry, E. K., Johnson, M. A., Ekonomou, A., Perry, R. H., Ballard, C. G., & Attems, J. (2012) · Neurobiology of Disease · doi:10.1016/j.nbd.2012.03.033 · Cited by 169
“This has been indicated by Shruster et al. (2010) in relation to amyloidosis.”
BackgroundPortelius, E., Olsson, B., Höglund, K., Cullen, N. C., Kvartsberg, H., Andréasson, U., Zetterberg, H., Sandelius, Å., Shaw, L. M. J., Lee, V. M. ‐., et al. (2018) · Acta Neuropathologica · doi:10.1007/s00401-018-1851-x · Cited by 171
“An ABC score that incorporates histopathologic assessments of Aβ deposits (A), staging of neurofibrillary tangles (B), and scoring of neuritic plaques (C) was calculated as described [37].”
BackgroundMethodInfluentialSelf-citationNeuroprotective effects of CD4+CD25+Foxp3+ regulatory T cells in a 3xTg-AD Alzheimer's disease model
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Synaptic Change in the Posterior Cingulate Gyrus in the Progression of Alzheimer's Disease
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Clinical and multimodal biomarker correlates of ADNI neuropathological findings
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“The neuropathological diagnosis for each case was determined in accordance with previously described criteria [7,42] for the pathological diagnosis of AD using the diagnostic nomenclature of the National Alzheimer’s Coordinating Center for diagnostic neuropathology [43] (DAT refers to the clinical diagnosis, whereas A…”
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Local and distant relationships between amyloid, tau and neurodegeneration in Alzheimer's Disease
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“All AD cases meet the criteria of high level of AD neuropathological change based on the ABC scores according to the National Institute on AgingAlzheimer’s Association guidelines for the neuropathological assessment of Alzheimer’s disease [58].”
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“With standardized neuropathological assessments for AD and related disorders [64,65] there is increasing recognition of mixed or multiple pathologies in LBD and other neurodegenerative diseases, along with the non-demented aging spectrum.”
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“The National Institute on AgingAlzheimer’s Association Guidelines for neuropathologic assessment of AD was also applied [24].”
Non-Alzheimer’s contributions to dementia and cognitive resilience in The 90+ Study
Robinson, J. L., Corrada, M. M., Kovács, G. G., Dominique, M. A., Caswell, C., Xie, S. X., Lee, V. M. ‐., Kawas, C. H., & Trojanowski, J. Q. (2018) · Acta Neuropathologica · doi:10.1007/s00401-018-1872-5 · Cited by 166
Self-citationInsights from multi-omics integration in complex disease primary tissues
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Daneshvar, D. H., Nair, E. S., Baucom, Z., Rasch, A., Abdolmohammadi, B., Uretsky, M., Saltiel, N. A., Shah, A., Jarnagin, J., Baugh, C. M., et al. (2023) · Nature Communications · doi:10.1038/s41467-023-39183-0 · Cited by 176
“Well-established criteria were used for the neuropathologic diagnosis of neurodegenerative diseases, including Alzheimer ’ s disease (NIA-Reagan criteria of high or intermediate likelihood) 63 , Lewy body disease 64 , frontotemporal lobar degeneration 65,66 , and motor neuron disease 67 .”
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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