The DOI matches its Crossref record; 66 of the 66 references it cites were found in a registry or an index; 27 of the 65 sources its claims cite were checked for support.
National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach
Open accessAbstract
We present a practical guide for the implementation of recently revised National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease (AD). Major revisions from previous consensus criteria are: (1) recognition that AD neuropathologic changes may occur in the apparent absence of cognitive impairment, (2) an "ABC" score for AD neuropathologic change that incorporates histopathologic assessments of amyloid β deposits (A), staging of neurofibrillary tangles (B), and scoring of neuritic plaques (C), and (3) more detailed approaches for assessing commonly co-morbid conditions such as Lewy body disease, vascular brain injury, hippocampal sclerosis, and TAR DNA binding protein (TDP)-43 immunoreactive inclusions. Recommendations also are made for the minimum sampling of brain, preferred staining methods with acceptable alternatives, reporting of results, and clinico-pathologic correlations.
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11 No full text of the sources · 9 Partly supported · 4 Supported · 3 Supported so far · 1 Own interpretation · accuracy not yet measured
Every source the paper cites for this claim was checked and supports it.
In the paper
“recognition that AD neuropathologic changes may occur in the apparent absence of cognitive impairment”
- Also stated in: § CLINICO-PATHOLOGIC CORRELATION · plain
“Similar neuropathologic changes, albeit usually at lower levels, also occur in individuals who did not show cognitive or behavioral impairments during life [54].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > Abstract
What the sources say
- Supportedcites [54] Sperling RA, Aisen PS, Beckett LA et al (2011) Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement 7:280–292 source
Section 6 reports that AD-related biomarker abnormalities can be detected before overt clinical symptoms and that Aβ accumulation occurs in clinically normal older adults. Section 2 also notes that some people have diagnostic AD neuropathological features at autopsy without having developed dementia during life. No page numbers are available in our copy. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § CLINICO-PATHOLOGIC CORRELATION · plain
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“LBs may be detected in neurons of medulla, pons and midbrain with hematoxylin and eosin (H&E)-stained sections; however, greater sensitivity can be achieved with immunohistochemistry for α-synuclein and this approach is strongly preferred [3,4,13].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE > Method
What the sources say
- Partly supportedcites [3] Alafuzoff I, Parkkinen L, Al-Sarraj S et al (2008) Assessment of alpha-synuclein pathology: a study of the BrainNet Europe Consortium. J Neuropathol Exp Neurol 67:125–143 sourceExperimental — accuracy not yet measured
The Introduction (p. 125) says consensus guidelines recommend α-synuclein immunohistochemistry for synucleinopathies, supporting the preference for that approach. The paper’s staining results and Discussion assess variation among immunohistochemical methods, but do not establish that immunohistochemistry detects Lewy bodies more sensitively than H&E; searches for H&E and hematoxylin–eosin found no such comparison. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [4] Alafuzoff I, Pikkarainen M, Al-Sarraj S et al (2006) Interlaboratory comparison of assessments of Alzheimer disease-related lesions: a study of the BrainNet Europe Consortium. J Neuropathol Exp Neurol 65:740–757 source
- Partly supportedcites [13] Beach TG, White CL, Hamilton RL et al (2008) Evaluation of alpha-synuclein immunohistochemical methods used by invited experts. Acta Neuropathol 116:277–288 sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) calls α-synuclein immunohistochemistry the method of choice for diagnosing Lewy body disorders, supporting its preferred use. The paper compares immunohistochemical methods with one another, however, and does not establish that they detect Lewy bodies more sensitively than H&E staining. (LLM, conf=0.84)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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- Partly supported
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In the paper
“one MVL identified in standard sections of brain (Table 1 regions shaded green) is of unclear relationship to cognitive function, while multiple MVLs in these regions are associated with increased likelihood of cognitive impairment or dementia [24,52,62].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > CEREBROVASCULAR DISEASE and VASCULAR BRAIN INJURY > Reporting
What the sources say
- Partly supportedcites [24] Gorelick PB, Scuteri A, Black SE et al (2011) Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 42:2672–2713 sourceExperimental — accuracy not yet measured
Section 3.2 (page not available in our copy) reports that some studies associate multiple microscopic infarcts with dementia, even after accounting for macroscopic infarcts. It does not establish the claim for MVLs generally or specify that the lesions were identified in standard brain sections. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites [52] Sonnen JA, Larson EB, Crane PK et al (2007) Pathological correlates of dementia in a longitudinal, population-based sample of aging. Ann Neurol 62:406–413 source
- Not checked — no full text of the sourcecites [62] White L (2009) Brain lesions at autopsy in older Japanese-American men as related to cognitive impairment and dementia in the final years of life: a summary report from the Honolulu-Asia aging study. J Alzheimers Dis 18:713–725 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Clinico-pathologic correlations for individuals without cognitive impairment should indicate that it is possible for AD neuropathologic change to predate onset of symptoms by years [54].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > AD NEUROPATHOLOGIC CHANGE > Reporting
What the sources say
- Supportedcites [54] Sperling RA, Aisen PS, Beckett LA et al (2011) Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement 7:280–292 source
Section 2, “Redefining the earliest stages of AD,” says the pathological cascade may begin a decade or more before clinically evident impairment. Section 6 also describes AD-related abnormalities in cognitively normal individuals, supporting the claim that neuropathologic change can predate symptoms by years. (LLM, conf=0.94)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“one MVL identified in standard sections of brain (Table 1 regions shaded green) is of unclear relationship to cognitive function, while multiple MVLs in these regions are associated with increased likelihood of cognitive impairment or dementia [24,52,62].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > CEREBROVASCULAR DISEASE and VASCULAR BRAIN INJURY > Reporting
What the sources say
- Partly supportedcites [24] Gorelick PB, Scuteri A, Black SE et al (2011) Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 42:2672–2713 sourceExperimental — accuracy not yet measured
Section 3.2 (page unavailable) says the number of infarcts needed for cognitive impairment is difficult to determine and reports that multiple microscopic infarcts may be related to dementia. It does not specifically assess the cognitive significance of one MVL identified in standard brain sections. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites [52] Sonnen JA, Larson EB, Crane PK et al (2007) Pathological correlates of dementia in a longitudinal, population-based sample of aging. Ann Neurol 62:406–413 source
- Not checked — no full text of the sourcecites [62] White L (2009) Brain lesions at autopsy in older Japanese-American men as related to cognitive impairment and dementia in the final years of life: a summary report from the Honolulu-Asia aging study. J Alzheimers Dis 18:713–725 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“this may represent pre-clinical LBD [12,22,31].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE > Reporting
What the sources say
- Supportedcites [12] Beach TG, Adler CH, Sue LI et al (2008) Reduced striatal tyrosine hydroxylase in incidental Lewy body disease. Acta Neuropathol 115:445–451 source
The Introduction defines incidental Lewy body disease as Lewy bodies without clinically documented parkinsonism or dementia. The Results and discussion report reduced striatal tyrosine hydroxylase in these individuals and say this suggests ILBD is likely a precursor to Parkinson’s disease and/or dementia with Lewy bodies, supporting the citing sentence’s qualified “may represent” claim. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites [22] Dickson DW, Fujishiro H, DelleDonne A et al (2008) Evidence that incidental Lewy body disease is pre-symptomatic Parkinson’s disease. Acta Neuropathol 115:437–444 source
- Supportedcites [31] Jicha GA, Schmitt FA, Abner E et al (2010) Prodromal clinical manifestations of neuropathologically confirmed Lewy body disease. Neurobiol Aging 31:1805–1813 source
The Introduction (page unavailable) says Lewy body pathology has been found in autopsied people described as normal and suggests that DLB pathology may predate clinical diagnosis. The Discussion (page unavailable) also says the study’s subjects were cognitively and neurologically normal at enrollment. Together, these support the qualified suggestion that LBD without apparent cognitive or motor deficits may be pre-clinical. (LLM, conf=0.91)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“LBs are frequent in the setting of moderate-to-severe levels of AD neuropathologic change [27,59], including some early-onset familial AD cases [32,33].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE
What the sources say
- Supportedcites [32] Leverenz JB, Fishel MA, Peskind ER et al (2006) Lewy body pathology in familial Alzheimer disease: evidence for disease- and mutation-specific pathologic phenotype. Arch Neurol 63:370–376 source
The Results report Lewy body pathology in the amygdala of 24 of 25 familial AD cases with PSEN1 mutations. The section on PSEN1-associated AD reports a mean age at onset of about 43 years in the groups it compares, supporting the early-onset qualifier. The indexed copy provides section labels but no page numbers. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites [33] Lippa CF, Duda JE, Grossman M et al (2007) DLB and PDD boundary issues: diagnosis, treatment, molecular pathology, and biomarkers. Neurology 68:812–819 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Accumulation of Aβ plaques and NFTs follows distinct regional progressions across brain regions as AD advances.”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > AD NEUROPATHOLOGIC CHANGE
What the sources say
- Partly supportedcites [14] Braak H, Alafuzoff I, Arzberger T et al (2006) Staging of Alzheimer disease-associated neurofibrillary pathology using paraffin sections and immunocytochemistry. Acta Neuropathol 112:389–404 sourceExperimental — accuracy not yet measured
The staging-system section describes a predictable regional progression of neurofibrillary pathology, from transentorhinal and entorhinal regions to limbic and then neocortical areas. It does not describe a separate regional progression of Aβ plaques or compare that progression with NFTs. Its references to neuritic plaques occur in the context of tau-immunoreactive pathology, not an Aβ-plaque staging scheme. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [15] Braak H, Braak E (1991) Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol 82:239–259 source
- Not checked — no full text of the sourcecites [57] Thal DR, Rub U, Orantes M, Braak H (2002) Phases of A beta-deposition in the human brain and its relevance for the development of AD. Neurology 58:1791–1800 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“CVD and vascular brain injury (VBI) [50] commonly are encountered in the brains with AD neuropathologic change [25].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > CEREBROVASCULAR DISEASE and VASCULAR BRAIN INJURY
What the sources say
- Partly supportedcites [25] Grinberg LT, Thal DR (2010) Vascular pathology in the aged human brain. Acta Neuropathol 119:277–290 sourceExperimental — accuracy not yet measured
The ‘Cerebral amyloid angiopathy’ section (page unavailable) reports that around 80–100% of AD patients have CAA, supporting the claim that cerebrovascular disease commonly accompanies AD pathology. It identifies infarction and hemorrhage as possible complications of CAA, but does not establish that vascular brain injury itself is commonly found in AD brains. (LLM, conf=0.82)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“LBs are frequent in the setting of moderate-to-severe levels of AD neuropathologic change [27,59], including some early-onset familial AD cases [32,33].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE
What the sources say
- Not checked — no full text of the sourcecites [27] Hamilton RL (2000) Lewy bodies in Alzheimer’s disease: a neuropathological review of 145 cases using alpha-synuclein immunohistochemistry. Brain Pathol 10:378–384 source
- Supportedcites [59] Uchikado H, Lin WL, DeLucia MW, Dickson DW (2006) Alzheimer disease with amygdala Lewy bodies: a distinct form of alpha-synucleinopathy. J Neuropathol Exp Neurol 65:685–697 source
The Materials and Methods section (page unavailable) says all 347 cases met pathologic criteria for AD and had Braak NFT stage IV or greater, indicating advanced AD in almost all cases. The “Frequency of α-Synuclein Pathology in Alzheimer Disease” section (page unavailable) reports Lewy-body pathology in 62 AD/ALB and 149 AD/LBD cases, supporting that Lewy bodies are frequent in this setting. (LLM, conf=0.90)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 2
- Probably not a substantial claim. 1
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Relatively isolated HS may occur in very old individuals, and in this context it is associated with TDP-43-immunoreactive inclusions and with cognitive impairment [45,47].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > HIPPOCAMPAL SCLEROSIS and TAR DNA BINDING PROTEIN (TDP)-43 INCLUSIONS > Reporting
What the sources say
- Partly supportedcites [45] Nelson PT, Abner EL, Schmitt FA et al (2010) Modeling the association between 43 different clinical and pathological variables and the severity of cognitive impairment in a large autopsy cohort of elderly persons. Brain Pathol 20:66–79 sourceExperimental — accuracy not yet measured
The Discussion reports that hippocampal sclerosis (HS) was associated with lower MMSE scores and states that HS is associated with TDP-43 proteinopathy. The Results describe TDP-43-positive inclusions. Neither passage establishes these associations specifically for relatively isolated HS in very old individuals. (LLM, conf=0.86)
- Supportedcites [47] Nelson PT, Schmitt FA, Lin Y et al (2011) Hippocampal sclerosis in advanced age: clinical and pathological features. Brain 134:1506–1518 source
The Introduction describes hippocampal sclerosis in older individuals as unrelated to Alzheimer’s pathology and associated with significant cognitive dysfunction. The Discussion reports aberrant TDP-43 staining in approximately 90% of patients with hippocampal sclerosis, and Table 7 describes HS-Ageing as most prevalent in the oldest-old and associated with dementia. The association is not universal, but the citing sentence does not claim that it is. (LLM, conf=0.92)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
In the paper
“Although not part of this classification scheme, it is important to realize that LBD also occurs frequently in the olfactory bulb in older adults and should be sampled when possible [20].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE > Method
What the sources say
- Not checked — no full text of the sourcecites [20] Del Tredici K, Rub U, De Vos RA et al (2002) Where does Parkinson disease pathology begin in the brain? J Neuropathol Exp Neurol 61:413–426 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“A subset of senile plaques called neuritic plaques appear closely associated with neuronal injury and are characterized by the occurrence of dystrophic neurites that frequently have phospho-tau immunoreactivity [19,36,37,55].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > AD NEUROPATHOLOGIC CHANGE
What the sources say
- Not checked — no full text of the sourcecites [19] DeKosky ST, Scheff SW (1990) Synapse loss in frontal cortex biopsies in Alzheimer’s disease: correlation with cognitive severity. Ann Neurol 27:457–464 source
- Not checked — no full text of the sourcecites [36] Masliah E, Mallory M, Deerinck T et al (1993) Re-evaluation of the structural organization of neuritic plaques in Alzheimer’s disease. J Neuropathol Exp Neurol 52:619–632 source
- Not checked — no full text of the sourcecites [37] Masliah E, Terry RD, Mallory M et al (1990) Diffuse plaques do not accentuate synapse loss in Alzheimer’s disease. Am J Pathol 137:1293–1297
- Not checked — no full text of the sourcecites [55] Terry RD, Masliah E, Salmon DP et al (1991) Physical basis of cognitive alterations in Alzheimer’s disease: synapse loss is the major correlate of cognitive impairment. Ann Neurol 30:572–580 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
Many other neurodegenerative disorders can cause dementia and may be co-morbid with AD neuropathologic change, especially in the elderly.
“There are many other neurodegenerative disorders that can cause dementia in addition to those discussed here, and any may be co-morbid with AD neuropathologic change, especially in the elderly.”
The paper relies on this without support.
Multiple diseases in the cerebrum can conspire to worsen cognitive symptoms.
“Multiple diseases in cerebrum can conspire to worsen cognitive symptoms; however, it often is difficult to judge the extent to which each disease observed at autopsy may have contributed to a given patient’s cognitive state.”
The paper relies on this without support.
Abnormal neuropil and neuronal cytoplasmic α-synuclein immunoreactivity are usually present with Lewy bodies but will not be apparent by H&E; in some instances, these changes occur in the absence of Lewy bodies.
“Abnormal neuropil and neuronal cytoplasmic α-synuclein immunoreactivity are usually present with LBs but will not be apparent by H&E; in some instances, these changes occur in the absence of LBs.”
The paper relies on this without support.
Diffuse white matter injury is a form of VBI but it is more difficult to judge objectively and is not specific to VBI.
“Diffuse white matter injury is a form of VBI but it is more difficult to judge objectively and is not specific to VBI.”
The paper relies on this without support.
Hippocampal sclerosis can be observed in the context of AD neuropathologic change, FTLD, and VBI, likely reflecting a heterogeneous etiology.
“HS can be observed in the context of AD neuropathologic change, frontotemporal lobar degeneration (FTLD), and VBI, likely reflecting a heterogeneous etiology.”
The paper relies on this without support.
Hippocampal sclerosis can be focal, so its absence in the recommended screening section does not rule out the possibility of HS elsewhere in the hippocampal formation.
“HS can be focal, thus its absence in the recommended screening section does not rule out the possibility of HS elsewhere in the hippocampal formation.”
The paper relies on this without support.
Hippocampal sclerosis can occur in several different diseases and has varying clinical implications in different settings.
“Clinico-pathological correlations need to recognize that HS can occur in several different diseases and has varying clinical implications in different settings.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The new NIA criteria use the same combination of NPs and Braak stage as the minimum lesion density necessary for attributing the cause of dementia to AD (39, 40).”
From Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer Disease Centers, 2005–2010 (2012) · cites this paper as [40]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The definitive diagnosis of AD requires microscopic examination of multiple brain regions employing staining methods that can detect Alzheimer type neuropathologic change [24], with diagnosis based upon the morphology and density of lesions and their topographic distribution.”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [24]
The cited source says what the claim attributes to it.
In the citing paper
“This finding is highlighted by the fact that nearly one third of patients with pathological findings of high likelihood Alzheimer’s disease [24] were thought to other disorders, and 3% were considered clinically normal at the time of their last clinical exam (Table 2).”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [24]
The cited source says what the claim attributes to it.
In the citing paper
“However, both Aβ and paired helical filament (PHF) tau deposits are required to fulfill neuropathologic criteria for AD [105,106]”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [105]
The cited source says what the claim attributes to it.
In the citing paper
“Autopsy analyses classified the level of ADNC from “none” to “high” using an established scoring system when available.”
From Automatic classification of AD pathology in FTD phenotypes using natural speech (2024) · cites this paper as [30]
The cited source says what the claim attributes to it.
In the citing paper
“Participants in the Confirmed-AD group (n ¼ 1854) were diagnosed with primary or contributing ADdementia at their last UDS visit before death and met our criteria for ADNC: moderate to frequent neuritic plaques and Braak stages III through VI, which loosely aligns with NIA-AA criteria for intermediate or high ADNC (13).”
From Concordance of Clinical Alzheimer Diagnosis and Neuropathological Features at Autopsy (2020) · cites this paper as [13]
The cited source says what the claim attributes to it.
In the citing paper
“The shortcomings of the NIA-Reagan criteria have been recognized and a revised set of criteria are currently in press (39, 40).”
From Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer Disease Centers, 2005–2010 (2012) · cites this paper as [40]
The cited source says what the claim attributes to it.
In the citing paper
“In the revision of the 1997 criteria, combinations of plaque and tangle pathologies considered sufficient to cause dementia and qualify for the neuropathological diagnosis of AD are explicitly stated (40, 41).”
From Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer Disease Centers, 2005–2010 (2012) · cites this paper as [40]
The cited source says what the claim attributes to it.
In the citing paper
“Neuropathologic diagnosis of AD was in accordance with current NIA-AA guidelines (Hyman et al., 2012; Montine et al., 2012).”
From Cholesterol and matrisome pathways dysregulated in astrocytes and microglia (2022) · cites this paper as Montine et al., 2012
In the citing paper
“Neuropathological assessment was performed by 2 authors (T.G.B. and T.J.M.) blinded to clinical and imaging results and using NIA–AA diagnostic scoring guidelines.5,40”
From Positron Emission Tomography Imaging With [ 18 F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [40]
In the citing paper
“Additional changes that may also occur in the brains of AD patients include amyloid angiopathy, age-related brain atrophy, synaptic pathology, white matter rarefaction, granulovacuolar degeneration, neuron loss, TDP-43 proteinopathy, and neuroinflammation (20-26), which may contribute to cognitive impairment; however, these are not considered pathognomonic features of AD (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“In contrast, dense and extensive neocortical NFTs are very consistently associated with dementia and thus, according to new diagnostic criteria, these are required to constitute high burden of AD neuropathologic change (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“The current revision of the National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of AD stipulate that subjects with moderately dense neuritic AβPs may be regarded as having an intermediate level of AD neuropathologic change and that other potential contributors to cognitive impairment and dementia should be sought (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“There is no universally applied rubric for CVD pathologic diagnosis, although the recent National Institute on Aging–Alzheimer’s Association criteria attempted to systematize neuropathologic assessment of this complex form of brain injury (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“Alzheimer's disease cases met criteria for a high likelihood of AD (Montine et al., 2012).”
From Alzheimer's amyloid‐β and tau protein accumulation is associated with decreased expression of the LDL receptor‐associated protein in human brain tissue (2020) · cites this paper as Montine et al., 2012
Citations
Cites
McKhann, G. M., Knopman, D. S., Chertkow, H., Hyman, B. T., Jack, C. R., Kawas, C. H., Klunk, W. E., Koroshetz, W. J., Manly, J. J., Mayeux, R., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.005 · Cited by 18,657 · cited 1×
“‘‘Alzheimer’s disease’’ refers to a constellation of cognitive and behavioral changes that are typical for patients who have substantial amounts of its hallmark lesions [6, 39].”
Self-citationNeuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123 · cited 8×
“‘‘Intermediate’’ or ‘‘High’’ AD neuropathologic change (italicized) is considered sufficient explanation for dementia a NFT stage should be determined by the method of Braak [14, 15] b Ab/amyloid plaque score should be determined by the method of Thal et al.”
InfluentialStaging of brain pathology related to sporadic Parkinson’s disease
Braak, H., Tredici, K. D., Rüb, U., de Vos, R. A. I., Jansen Steur, E. N. H., & Braak, E. (2003) · Neurobiology of Aging · doi:10.1016/s0197-4580(02)00065-9 · Cited by 10,777 · cited 2×
“Given our focus on cognitive impairment and dementia rather than movement disorders [16], we recommend a modification of Fig.”
Albert, M. S., DeKosky, S. T., Dickson, D., Dubois, B., Feldman, H. H., Fox, N. C., Gamst, A., Holtzman, D. M., Jagust, W. J., Petersen, R. C., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.008 · Cited by 10,152 · cited 1×
“‘‘Alzheimer’s disease’’ refers to a constellation of cognitive and behavioral changes that are typical for patients who have substantial amounts of its hallmark lesions [6, 39].”
Self-citationSperling, R. A., Aisen, P. S., Beckett, L. A., Bennett, D. A., Craft, S., Fagan, A. M., Iwatsubo, T., Jack, C. R., Kaye, J., Montine, T. J., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.003 · Cited by 7,155 · cited 2×
“Similar neuropathologic changes, albeit usually at lower levels, also occur in individuals who did not show cognitive or behavioral impairments during life [54].”
Self-citationDiagnosis and management of dementia with Lewy bodies: Third report of the DLB consortium
McKeith, I. G., Dickson, D. W., Lowe, J., Emre, M., O'Brien, J. T., Feldman, H., Cummings, J., Duda, J. E., Lippa, C., Perry, E. K., et al. (2005) · Neurology · doi:10.1212/01.wnl.0000187889.17253.b1 · Cited by 5,069
Self-citationMirra, S. S., Heyman, A., McKeel, D., Sumi, S. M., Crain, B. J., Brownlee, L. M., Vogel, F. S., Hughes, J. P., Belle, G. V., Berg, L., et al. (1991) · Neurology · doi:10.1212/wnl.41.4.479 · Cited by 4,961 · cited 11×
“Region Stain for A /amyloid plaques [57] Stain for NFTs [14,15] Stain for NPs [41] Stain for LBs H&E”
InfluentialSelf-citationDeJesus-Hernandez, M., Mackenzie, I. R., Boeve, B. F., Boxer, A. L., Baker, M., Rutherford, N. J., Nicholson, A. M., Finch, N. A., Flynn, H., Adamson, J., et al. (2011) · Neuron · doi:10.1016/j.neuron.2011.09.011 · Cited by 4,936 · cited 1×
“With the exception of individuals with mutations in TARDBP, GRN, VCP or c9ORF72 [10, 18], it is not clear whether TDP-43 proteinopathy in these other neurodegenerative diseases is”
Self-citationTerry, R. D., Masliah, E., Salmon, D. P., Butters, N., DeTeresa, R., Hill, R., Hansen, L. A., & Katzman, R. (1991) · Annals of Neurology · doi:10.1002/ana.410300410 · Cited by 4,397 · cited 1×
“frequently have phospho-tau immunoreactivity [19, 36, 37, 55].”
Self-citationGorelick, P. B., Scuteri, A., Black, S. E., DeCarli, C., Greenberg, S. M., Iadecola, C., Launer, L. J., Laurent, S., Lopez, O. L., Nyenhuis, D., et al. (2011) · Stroke · doi:10.1161/str.0b013e3182299496 · Cited by 3,811
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Items 1,001–1,100 of 2,854
Distribution Patterns of Astrocyte Populations in the Human Cortex
Forrest, S. L., Kim, J. H., Crockford, D. R., Huynh, K., Cheong, R., Knott, S., Kane, M. A., Ittner, L. M., Halliday, G. M., & Kril, J. J. (2022) · Neurochemical Research · doi:10.1007/s11064-022-03700-2 · Cited by 34
“Four cases had low level AD neuropathological change, one case had intermediate level AD neuropathological change, and five cases had no AD neuropathological change [24].”
BackgroundGauthreaux, K. M., Mock, C., Teylan, M., Culhane, J. E., Chen, Y., Chan, K. C. G., Katsumata, Y., Nelson, P. T., & Kukull, W. A. (2022) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlac093 · Cited by 29
Self-citationCryptic exon inclusion is a molecular signature of LATE-NC in aging brains
Chung, M., Carter, E. K., Veire, A. M., Dammer, E. B., Chang, J., Duong, D. M., Raj, N., Bassell, G. J., Glass, J. D., Gendron, T. F., et al. (2024) · Acta Neuropathologica · doi:10.1007/s00401-023-02671-0 · Cited by 31
“Stage-based diagnoses of LATE-NC, ADNC, and other pathologies used consensus-based criteria [3, 11, 28, 34].”
MethodSelf-citationPostupna, N. O., Keene, C. D., Latimer, C. S., Sherfield, E., Gelder, R. D. V., Ojemann, J. G., Montine, T. J., & Darvas, M. (2014) · Laboratory Investigation · doi:10.1038/labinvest.2014.103 · Cited by 31
“We used consensus neuropathological criteria to stratify cases (24, 25).”
MethodSelf-citationNho, K. T., Initiative, A. D. N., Saykin, A. J., & Nelson, P. T. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160077 · Cited by 30
“Hippocampal sclerosis in aged individuals is diagnosed at autopsy, according to consensus-based criteria [45], when neuron loss and astrocytosis are observed in the hippocampal formation, out of proportion to AD-type plaques and tangles in the same structure.”
Self-citationNanotechnology in the diagnostic and therapy for Alzheimer's disease
Panghal, A., & Flora, S. J. S. (2024) · Biochimica et Biophysica Acta (BBA) - General Subjects · doi:10.1016/j.bbagen.2024.130559 · Cited by 31
Progress Update: Fluid and Imaging Biomarkers in Alzheimer’s Disease
Sutphen, C. L., Fagan, A. M., & Holtzman, D. M. (2014) · Biological Psychiatry · doi:10.1016/j.biopsych.2013.07.031 · Cited by 31
Concurrent tau pathologies in frontotemporal lobar degeneration with TDP‐43 pathology
Koga, S., Zhou, X., Murakami, A., Fernandez De Castro, C., Baker, M. C., Rademakers, R., & Dickson, D. W. (2022) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12778 · Cited by 30
Self-citationFreiburghaus, T., Pawlik, D., Hauer, K. O., Ossenkoppele, R., Strandberg, O. T., Leuzy, A., Rittmo, J. Ö., Tremblay, C., Serrano, G. E., Pontecorvo, M. J., et al. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02801-2 · Cited by 34
“Specific diagnoses were made according to published criteria [10, 11, 13, 16, 25, 28, 30, 33].”
MethodSelf-citationColloby, S. J., McAleese, K. E., Walker, L., Erskine, D., Toledo, J. B., Donaghy, P. C., McKeith, I. G., Thomas, A. J., Attems, J., & Taylor, J. (2024) · Brain · doi:10.1093/brain/awae372 · Cited by 33
Tsering, W., de la Rosa, A., Ruan, I. Y., Philips, J. L., Bathe, T., Villareal, J. A. B., & Prokop, S. (2024) · Journal of Neurochemistry · doi:10.1111/jnc.16275 · Cited by 33
“…ADNC—“low AD” ( n = 10), “Intermediate AD” ( n = 10), and “high AD” ( n = 20) based on the NIA-AA guideline for pathological diagnosis which constitutes the Thal phase of A β plaques (A), Braak and Braak NFT stage (B), and CERAD neuritic plaque score (C)—“ABC” score (Montine et al., 2012 ).”
Autophagy and Cellular Senescence in Alzheimer's Disease: Key Drivers of Neurodegeneration
Hussain, M. S., Agrawal, N., Ilma, B., Rekha, M. M., Nayak, P. P., Kaur, M., Khachi, A., Goyal, K., Rekha, A., Gupta, S., et al. (2025) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.70503 · Cited by 35
Cousins, K. A. Q., Korecka, M., Wan, Y., Vulaj, A., Brown, C. D., Tropea, T. F., Lee, E. B., Tosun, D., Landau, S. M., Okonkwo, O. C., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70469 · Cited by 35
Changes to the lateral geniculate nucleus in A lzheimer's disease but not dementia with L ewy bodies
Erskine, D., Taylor, J., Firbank, M., Patterson, L., ONOFRJ, M. C., O'Brien, J. T., McKeith, I. G., Attems, J., Thomas, A. J., Morris, C. M., et al. (2015) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12249 · Cited by 30
Pathogenesis and Treatment of Vascular Cognitive Impairment
Jellinger, K. A. (2014) · Neurodegenerative Disease Management · doi:10.2217/nmt.14.37 · Cited by 30
Brain Capillaries in Alzheimer’s Disease
Balogiannis, S. (2015) · Journal of Neurology & Stroke · doi:10.15406/jnsk.2015.02.00069 · Cited by 31
“Tau pathology consisted of intracellular accumulation of neurofibrillary tangles of hyperphosphorilated tau protein and accumulation of Aβ-peptide’s deposits, defined as neuritic plaques, are the principal neuropathological diagnostic criteria of the disease [4].”
BackgroundWijesinghe, P., Shankar, S. K., Yasha, T. C., Gorrie, C. A., Amaratunga, D., Hulathduwa, S., Kumara, K. S., Samarasinghe, K., Suh, Y., Steinbusch, H. W. M., et al. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160425 · Cited by 30
“As per NIA-AA [27] Co-morbid cerebrovascular and neurodegenerative pathologies that are commonly detected in the elderly Sri Lankan brains (Fig.”
Chong, J. R., Chai, Y. L., Lee, J. H., Howlett, D., Attems, J., Ballard, C. G., Aarsland, D., Francis, P. T., Chen, C. P., & Lai, M. K. P. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160781 · Cited by 28
Three VCP Mutations in Patients with Frontotemporal Dementia
Wong, T. H., Pottier, C. P., Hondius, D., Meeter, L. H. H., van Rooij, J., Melhem, S., bank, T. N. B., van Minkelen, R., van Duijn, C. M., Rozemüller, A. J. M., et al. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180301 · Cited by 33
Hippocampal LMNA Gene Expression is Increased in Late-Stage Alzheimer’s Disease
Méndez-López, I., Blanco‐Luquin, I., de Gordoa, J. S., Urdánoz‐Casado, A., Roldán, M., Acha, B., Echávarri, C., Zelaya, M. V., Jericó, I., & Mendióroz, M. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20040878 · Cited by 30
Neuropathological Changes in Dementia With Lewy Bodies and the Cingulate Island Sign
Patterson, L., Firbank, M., Colloby, S. J., Attems, J., Thomas, A. J., & Morris, C. M. (2019) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlz047 · Cited by 30
“Of note, 4 DLB patients also fulfilled the neuropathological criteria for high AD neuropathological change and could therefore be classified as neuropathologically mixed AD/DLB with a Lewy body disease (LBD) clinical phenotype (20, 21).”
BackgroundTuzzi, E., Balla, D. Z., Loureiro, J. R., Neumann, M., Laske, C., Pohmann, R., Preische, O., Scheffler, K., & Hagberg, G. E. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-190424 · Cited by 30
Arena, J. D., Johnson, V. E., Lee, E. B., Gibbons, G. S., Smith, D. H., Trojanowski, J. Q., & Stewart, W. B., Jr. (2020) · Brain Communications · doi:10.1093/braincomms/fcaa210 · Cited by 31
“Alzheimer’s disease cases had no documented history of TBI or participation in contact sport, and met neuropathological criteria for the diagnosis of Alzheimer’s disease (n=6; 4 high and 2 intermediate Alzhemier’s disease neuropathologic changes (ADNC) (Montine et al., 2012)).”
BackgroundSelf-citationOxysterols and Oxysterol Sulfates in Alzheimer’s Disease Brain and Cerebrospinal Fluid
Dias, I. H. K., Shokr, H., Shephard, F., & Chakrabarti, L. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220083 · Cited by 30
Conte, C., Ingrassia, A. M. T., Brevé, J. J. P., Bol, J. G. J. M., Huisman, E., van Dam, A., Beccari, T., & van de Berg, W. D. J. (2023) · Cells · doi:10.3390/cells12101368 · Cited by 33
“Braak neurofibrillary tangle (NFT) stages [37], CERAD neuritic plaque scores [39] and levels of AD-type pathology were determined according to NIA-AA consensus criteria [40] Additionally, the presence of aging-related tau astrogliopathy (ARTAG) [41] microvascular lesions and hippocampal sclerosis was assessed.”
MethodCortical pyroglutamate amyloid-β levels and cognitive decline in Alzheimer's disease
Pivtoraiko, V. N., Abrahamson, E. E., Leurgans, S. E., DeKosky, S. T., Mufson, E. J., & Ikonomović, M. D. (2014) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2014.06.021 · Cited by 32
“Application of the new National Institute on Aging-Alzheimer’s Association guidelines (Hyman et al., 2012; Montine et al., 2012) to the RROS cohort is currently ongoing.”
MethodA comparison of Aβ amyloid pathology staging systems and correlation with clinical diagnosis
Boluda, S., Toledo, J. B., Irwin, D. J., Raible, K. M., Byrne, M., Lee, E. B., Lee, V. M. ‐., & Trojanowski, J. Q. (2014) · Acta Neuropathologica · doi:10.1007/s00401-014-1308-9 · Cited by 31
“Because of the variability of TAP scores in cases with CerAD C1, the staining of the six sections proposed in Alafuzoff et al. [2] is suggested as it was shown that the evaluation of these sole regions gave similar results in agreement rate and assessment results as the use of more numerous brain sections as suggested…”
BackgroundMethodResultInfluentialSelf-citationSierra, M., Gelpí, E., Martı́, M. J., & Compta, Y. (2016) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12308 · Cited by 30
Elevated medial temporal lobe and pervasive brain tau‐PET signal in normal participants
Lowe, V. J., Bruinsma, T. J., Min, H.-K. P., Lundt, E. S., Fang, P., Senjem, M. L., Boeve, B. F., Josephs, K. A., Pandey, M. K., Murray, M. E., et al. (2018) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1016/j.dadm.2018.01.005 · Cited by 32
“Braak NFT staging is strongly associated with cognitive impairment [1,3–6] and is one of the two hallmark pathological criteria for the diagnosis of AD [7,8].”
Pathologic correlates of supranuclear gaze palsy with parkinsonism
Martin, W. R. W., Hartlein, J. M., Racette, B. A., et al. (2017) · Parkinsonism & Related Disorders · doi:10.1016/j.parkreldis.2017.02.027 · Cited by 29
Self-citationKurihara, M., Matsubara, T., Morimoto, S., Arakawa, A., Ohse, K., Kanemaru, K., Iwata, A., Murayama, S., & Saito, Y. (2024) · Acta Neuropathologica Communications · doi:10.1186/s40478-024-01758-3 · Cited by 29
“Neuropathologic diagnoses and stagings were performed according to internationally accepted neuro-pathologic criteria for the diagnosis of AD [32, 33], Lewy body disease [31, 34, 35], PSP [36], CBD [37], frontotemporal lobar degeneration with TDP-43 proteinopathy [38], argyrophilic grain disease…”
Methodde Vries, L. E., Jongejan, A., Fortes, J. M., Balesar, R. A., Rozemüller, A. J. M., Moerland, P. D., Huitinga, I., Swaab, D. F., & Verhaagen, J. (2024) · Acta Neuropathologica Communications · doi:10.1186/s40478-024-01760-9 · Cited by 29
“…including neuropathological classification according to Braak [18], CERAD [19] and the National Institute on Aging–Alzheimer’s Association guidelines [20], cerebrovascular diseases, Lewy bodies (LBs), hippocampal sclerosis (HS), limbic-predominant age-related (LATE) TDP-43 and ubiquitin (P62).”
Shi, H., Mirzaei, N., Koronyo, Y., Davis, M. R., Robinson, E., Braun, G. M., Jallow, O., Rentsendorj, A., Ramanujan, V. K., Fert‐Bober, J., et al. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02760-8 · Cited by 33
Self-citationOno, D., Dickson, D. W., & Koga, S. (2024) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12997 · Cited by 32
Self-citationReddy, J. S., Heath, L., Linden, A. V., Allen, M., Lopes, K. D. P., Seifar, F., Wang, E., Ma, Y., Poehlman, W. L., Quicksall, Z. S., et al. (2024) · Alzheimer's & Dementia · doi:10.1002/alz.14208 · Cited by 29
Self-citationArendt, T., Morawski, M., Gärtner, U., Fröhlich, N., Schulze, F., Wohmann, N., Jäger, C., Eisenlöffel, C., Gertz, H., Mueller, W. C., et al. (2016) · Brain Pathology · doi:10.1111/bpa.12442 · Cited by 28
Walker, L., McAleese, K. E., Johnson, M. A., Khundakar, A. A., Erskine, D., Thomas, A. J., McKeith, I. G., & Attems, J. (2017) · Journal of Neural Transmission · doi:10.1007/s00702-017-1702-2 · Cited by 29
“…underwent standard neuropathological assessment using internationally accepted criteria including neuritic Braak stages (Alafuzoff et al. 2008), Thal amyloid phases (Thal et al. 2002), CERAD scores (Mirra et al. 1991), NIA-AA scores (Montine et al. 2012) and McKeith criteria (McKeith et al. 2005).”
MethodAlegro, M., Theofilas, P., Nguy, A. K., Castruita, P. A., Seeley, W. W., Heinsen, H., Ushizima, D. M., & Grinberg, L. T. (2017) · Journal of Neuroscience Methods · doi:10.1016/j.jneumeth.2017.03.002 · Cited by 29
“All subjects showed variable degree of Alzheimers disease pathology staged according to the new NIA-AA guidelines [21].”
MethodDatta, A., Chai, Y. L., Tan, J. M., Lee, J. H., Francis, P. T., Chen, C., Sze, S. K., & Lai, M. K. P. (2017) · Molecular Brain · doi:10.1186/s13041-017-0316-9 · Cited by 28
Modified amyloid variants in pathological subgroups of β‐amyloidosis
Gerth, J., Kumar, S., Upadhaya, A. R., Ghebremedhin, E., Arnim, C. A. F. V., Thal, D. R., & Walter, J. (2018) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.577 · Cited by 30
Self-citationStevens, C. H., Guthrie, N. J., van Roijen, M., Halliday, G. M., & Ooi, L. (2019) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlz041 · Cited by 28
Xu, G. M., Fromholt, S., Chakrabarty, P., Zhu, F., Liu, X., Pace, M. C., Koh, J., Golde, T. E., Levites, Y., Lewis, J. M., et al. (2020) · Acta Neuropathologica Communications · doi:10.1186/s40478-020-00911-y · Cited by 29
“These types of plaques are referred to as neuritic plaques (NPs) and a semiquantitative assessment of this pathology is used in the pathological diagnosis of AD [12, 30].”
Alzheimer and Purinergic Signaling: Just a Matter of Inflammation?
Merighi, S., Poloni, T. E., Terrazzan, A., Moretti, E., Gessi, S., & Ferrari, D. (2021) · Cells · doi:10.3390/cells10051267 · Cited by 30
11C-PiB PET can underestimate brain amyloid-β burden when cotton wool plaques are numerous
Abrahamson, E. E., Kofler, J., Becker, C. R., Price, J. C., Newell, K. L., Ghetti, B. F., Murrell, J. R., McLean, C., López, O. L., Mathis, C. A., et al. (2021) · Brain · doi:10.1093/brain/awab434 · Cited by 28
Primary age‐related tauopathy in a Finnish population‐based study of the oldest old (Vantaa 85+)
Savola, S. E., Kaivola, K., Raunio, A., Kero, M., Mäkelä, M., Pärn, K., Palta, P., Tanskanen, M., Tuimala, J., Polvikoski, T. M., et al. (2021) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12788 · Cited by 29
“In addition to the lack of Aβ plaques, PART also differs neuropathologically from AD in regard to the extent of HPtau pathology [1, 6, 7].”
BackgroundMethodLloyd, G. M., Sorrentino, Z. A., Quintin, S. S., Gorion, K.-M. M., Bell, B. M., Paterno, G., Long, B., Prokop, S., & Giasson, B. I. (2022) · Acta Neuropathologica · doi:10.1007/s00401-022-02425-4 · Cited by 28
“Post-mortem neuro-pathological staging and diagnoses were made according to the current guidelines and criteria proposed by the National Institute of Aging-Alzheimer’s Association, the Dementia with Lewy Bodies Consortium [36, 52], and the Neuropathology Working Group on MSA [27].”
MethodGatto, R. G., Martin, P. R., Ali, F., Clark, H. M., Duffy, J. R., Utianski, R. L., Botha, H., Machulda, M. M., Dickson, D. W., Josephs, K. A., et al. (2022) · NeuroImage Clinical · doi:10.1016/j.nicl.2022.103030 · Cited by 29
“…identical neuroimaging: 1) a disease control cohort that consisted of 10 patients with speech/language problems but with AD pathology at autopsy (Montine et al., 2012) (diagnosed clinically with logopenic progressive aphasia (AD-LPA) (Botha et al., 2015; Gorno-Tempini et al., 2008)) and 2) 10…”
MethodResultSelf-citationTREM2 risk variants are associated with atypical Alzheimer’s disease
Kim, B., Suh, E. R., Nguyen, A. T., Prokop, S., Mikytuck, B., Olatunji, O. A., Robinson, J. L., Grossman, M., Phillips, J. S., Irwin, D. J., et al. (2022) · Acta Neuropathologica · doi:10.1007/s00401-022-02495-4 · Cited by 30
“1 3 and PHF1-positive Aβ, neurofibrillary tangles, and neuritic plaques were evaluated to determine the level of Alzheimer’s disease neuropathologic change (ADNC) [31].”
BackgroundSelf-citationMontero‐Calle, A., Coronel, R., Garranzo‐Asensio, M., Solís‐Fernández, G., Rábano, A., Ríos, V. D. L., Fernández‐Aceñero, M. J., Mendes, M. L., Martínez‐Useros, J., Megías, D., et al. (2023) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-023-04791-y · Cited by 32
“Alzheimer’s histopathological changes were assessed following NIAAA guidelines [40].”
MethodRetinal Alterations Predict Early Prodromal Signs of Neurodegenerative Disease
Casciano, F., Zauli, E., Celeghini, C., Caruso, L., Gonelli, A., Zauli, G., & Pignatelli, A. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25031689 · Cited by 34
“…without clinical symptoms; mild cognitive impairment, also referred to as the prodromal stage of AD (intermediate), where noticeable memory/thinking problems appear; and Alzheimer’s dementia (late), the advanced stage of the disease that significantly impacts the person’s independence [151,152].”
BackgroundAssociation Between the Prevalence of Learning Disabilities and Primary Progressive Aphasia
Rogalski, E. J., RADEMAKER, A. W., Wieneke, C., Bigio, E. H., Weıntraub, S., & Mesulam, M. M. (2014) · JAMA Neurology · doi:10.1001/jamaneurol.2014.2805 · Cited by 30
Self-citationTatsumi, S., Uchihara, T., Aiba, I., Iwasaki, Y., Mimuro, M., Takahashi, R., & Yoshida, M. (2014) · Acta Neuropathologica Communications · doi:10.1186/s40478-014-0161-3 · Cited by 31
“The diagnoses of AD and CBD were based on the current diagnostic criteria [6,21].”
MethodMultimodal imaging evidence of pathology-mediated disease distribution in corticobasal syndrome
McMillan, C. T., Boyd, C. D., Gross, R. G., Weinstein, J., Firn, K., Toledo, J. B., Rascovsky, K., Shaw, L. M. J., Wolk, D. A., Irwin, D. J., et al. (2016) · Neurology · doi:10.1212/wnl.0000000000003119 · Cited by 31
“) using previously described immunohistochemical methods(12) and diagnostic criteria.(13,14) Nonautopsied patients were classified as CBS–non-AD and CBSAD on the basis of either genetic status or CSF analyses.”
MethodSelf-citationRose, S. E., Frankowski, H., Knupp, A., Berry, B. J., Martinez, R. A., Dinh, S. Q., Bruner, L. T., Willis, S. L., Crane, P. K., Larson, E. B., et al. (2018) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nly013 · Cited by 29
“NPTMT Core autopsies include rapid dissection of 1 hemisphere and collection of 60 or more fresh frozen samples and comprehensive neuropathologic evaluation according to the latest consensus guidelines (9).”
MethodHaytural, H., Mermelekas, G., Emre, C., Nigam, S. M., Carroll, S. L., Winblad, B. G., Bogdanović, N., Barthet, G., Granholm, A., Orre, L. M., et al. (2019) · Molecular & Cellular Proteomics · doi:10.1074/mcp.ra119.001737 · Cited by 30
Synthesizing images of tau pathology from cross-modal neuroimaging using deep learning
Lee, J., Burkett, B. J., Min, H.-K. P., Senjem, M. L., Dicks, E., Corriveau‐Lecavalier, N., Mester, C. T., Wiste, H. J., Lundt, E. S., Murray, M. E., et al. (2023) · Brain · doi:10.1093/brain/awad346 · Cited by 32
“52,53”
Integrative Single-Plaque Analysis Reveals Signature Aβ and Lipid Profiles in the Alzheimer’s Brain
Enzlein, T., Lashley, T., Sammour, D. A., Hopf, C., & Chávez‐Gutiérrez, L. (2024) · Analytical Chemistry · doi:10.1021/acs.analchem.3c05557 · Cited by 28
Limbic-predominant age-related TDP-43 encephalopathy in the oldest old: a population-based study
Mikhailenko, E., Colangelo, K., Tuimala, J., Kero, M., Savola, S. E., Raunio, A., Kok, E., Tanskanen, M., Mäkelä, M., Puttonen, H. A. J., et al. (2024) · Brain · doi:10.1093/brain/awae212 · Cited by 30
“30 and Hyman et al .”
Moszczynski, A. J., Yang, W., Hammond, R. R., Ang, L. C., & Strong, M. J. (2017) · Acta Neuropathologica Communications · doi:10.1186/s40478-016-0406-4 · Cited by 30
IgM response against amyloid-beta in aging: a potential peripheral protective mechanism
Agrawal, S., Abud, E. M., Snigdha, S., & Agrawal, A. (2018) · Alzheimer s Research & Therapy · doi:10.1186/s13195-018-0412-9 · Cited by 29
Tobacco Smoking and Dementia in a Kentucky Cohort: A Competing Risk Analysis
Abner, E. L., Nelson, P. T., Jicha, G. A., Cooper, G. E., Fardo, D. W., Schmitt, F. A., & Kryscio, R. J. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-181119 · Cited by 27
Self-citationLibard, S., & Alafuzoff, I. I. (2019) · Acta Neuropathologica Communications · doi:10.1186/s40478-019-0748-9 · Cited by 29
Alexandris, A. S., Walker, L., Liu, A. K. L., McAleese, K. E., Johnson, M., Pearce, R. K. B., Gentleman, S., & Attems, J. (2019) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12577 · Cited by 28
on behalf of the Cognitive Function and Ageing Neuropathology Study Group, Wharton, S. B., Wang, D. Y. Q., Parikh, C. R., Matthews, F. E., Brayne, C., & Ince, P. G. (2019) · Acta Neuropathologica Communications · doi:10.1186/s40478-019-0858-4 · Cited by 32
CSF SerpinA1 in Creutzfeldt–Jakob disease and frontotemporal lobar degeneration
Abu‐Rumeileh, S., Halbgebauer, S., Steinacker, P., et al. (2020) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.50980 · Cited by 28
Hippocampal sclerosis, TDP‐43, and the duration of the symptoms of dementia of AD patients
López, O. L., Kofler, J., Chang, Y., Berman, S., Becker, J. T., Sweet, R. A., Nadkarni, N. K., Patira, R., Kamboh, M. I., Cohen, A. D., et al. (2020) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.51135 · Cited by 28
Yamazaki, D. A. D. S., Rozada, A. M. F., Baréa, P., Reis, E. C., Basso, E. A., Sarragiotto, M. H., Seixas, F. A. V., & Gauze, G. F. (2021) · Bioorganic & Medicinal Chemistry · doi:10.1016/j.bmc.2020.115991 · Cited by 29
Borrego‐Écija, S., Turón‐Sans, J., Ximelis, T., Aldecoa, I., Molina‐Porcel, L., Povedano, M., Rubio, M. Á., Gámez, J., Cano, A., Paré, M., et al. (2021) · Brain Pathology · doi:10.1111/bpa.12942 · Cited by 29
“The National Institute on AgingAlzheimer’s Association (NIAA) Guidelines for neuropathologic assessment of AD were applied and a final ABC score was assigned (27).”
MethodMartínez-Valbuena, I., Valenti‐Azcarate, R., Amat, I., Marcilla, I., Martí‐Andrés, G., Caballero, M. C., Riverol, M., Tuñon, M.-T., Fraser, P. E., & Luquín, M. R. (2021) · Acta Neuropathologica Communications · doi:10.1186/s40478-021-01171-0 · Cited by 30
“Specific consensus diagnostic criteria for PD [1, 9] DLB [9, 42], incidental Lewy body disease (ILBD) [7] and AD [29, 43] were used to establish the neuropathological diagnosis.”
MethodSingle-synapse analyses of Alzheimer’s disease implicate pathologic tau, DJ1, CD47, and ApoE
Phongpreecha, T., Gajera, C. R., Liu, C. C., Vijayaragavan, K., Chang, A. L., Becker, M., Fallahzadeh, R., Fernandez, R., Postupna, N. O., Sherfield, E., et al. (2021) · Science Advances · doi:10.1126/sciadv.abk0473 · Cited by 28
Self-citationAdmixture Mapping of Alzheimer’s disease in Caribbean Hispanics identifies a new locus on 22q13.1
Kızıl, Ç., Sariya, S., Kim, Y. A., Rajabli, F., Martin, E. R., Reyes‐Dumeyer, D., Vardarajan, B. N., Maldonado, A., Haines, J. L., Mayeux, R. P., et al. (2022) · Molecular Psychiatry · doi:10.1038/s41380-022-01526-6 · Cited by 28
“Interestingly, two main mechanisms have been proposed to explain methylglyoxal and methylglyoxal-derived advanced glycation end products (AGEs) neurotoxicity in LOAD: (a) AGEs induced cross-linking of cytoskeletal proteins promoting neuronal dysfunction and cell death and (b) AGEs inducing accumulation of Aβ42, one of…”
BackgroundArezoumandan, S., Xie, S. X., Cousins, K. A. Q., Mechanic-Hamilton, D. J., Peterson, C. S., Huang, C. Y., Ohm, D. T., Ittyerah, R., McMillan, C. T., Wolk, D. A., et al. (2022) · Acta Neuropathologica · doi:10.1007/s00401-022-02472-x · Cited by 29
Self-citationPagnotti, R. M. B., Pudumjee, S. B., Cross, C. L., & Miller, J. B. (2023) · Neurology · doi:10.1212/wnl.0000000000207159 · Cited by 37
“Because these autopsies are conducted at ADRCs across the country, there are a minimum number of recommended brain regions to be assessed.(15) ADRCs conduct autopsies based on the established criteria for the assessment of AD, Lewy body disease (LBD), FTLD, cerebrovascular disease, and rarer neurologic pathologies.”
BackgroundMethodCampos, H. C., Ribeiro, D. E., Hashiguchi, D., Glaser, T., Milanis, M. D. S., Gimenes, C., Suchecki, D., Arida, R. M., Ulrich, H., & Longo, B. M. (2023) · Frontiers in Neuroscience · doi:10.3389/fnins.2023.1132825 · Cited by 30
“The extracellular plaque formation leads to increased neuroinflammation and neuronal loss, which evolves cognitive impairment and clinical symptoms (Braak and Braak, 1991; Montine et al., 2012).”
BackgroundCai, X., Qian, G., Wang, F., Zhang, M., Da, Y., & Liang, J. (2023) · Frontiers in Neuroscience · doi:10.3389/fnins.2023.1221990 · Cited by 31
“the National Institute of Aging Alzheimer’s Association (NIAAA), the Diagnostic and Statistical Manual of Mental Disorders (DSM), and Petersen’s criteria (Montine et al., 2012; Battle, 2013; Petersen et al., 2018); (2) articles were cross-sectional, cohort, and case–control studies, without language restrictions; (3)…”
MethodDetection of TDP‐43 oligomers in frontotemporal lobar degeneration–TDP
Kao, P. F., Chen, Y., Liu, X., DeCarli, C. S., Seeley, W. W., & Jin, L. (2015) · Annals of Neurology · doi:10.1002/ana.24431 · Cited by 28
TDP-43: A new player on the AD field?
Youmans, K. L., & Wolozin, B. L. (2012) · Experimental Neurology · doi:10.1016/j.expneurol.2012.05.018 · Cited by 28
George, D. R., Qualls, S. H., Camp, C. J., & Whitehouse, P. J. (2012) · The Gerontologist · doi:10.1093/geront/gns096 · Cited by 28
“For full versions of the guidelines, readers are referred to earlier recommendations from the NIA–AA workgroups on diagnostic guidelines for Alzheimer’s disease published in summer 2011 (Albert et al., 2011; Jack et al., 2011; McKhann et al., 2011; Sperling et al., 2011; these articles and accompanying commentaries ca…”
BackgroundBerge, G., Sando, S. B., Albrektsen, G., Lauridsen, C., Møller, I., Grøntvedt, G. R., Bråthen, G., & White, L. R. (2016) · BMC Neurology · doi:10.1186/s12883-016-0706-0 · Cited by 29
“Classical AD neuropathology demonstrates amyloid plaques and neurofibrillary tangles [2, 3], and cerebrospinal fluid (CSF) levels of amyloid-β 1–42 (Aβ42), total tau (t-tau), and phosphorylated tau (p-tau) are promising”
BackgroundVisual discrimination and reversal learning in aged common marmosets (Callithrix jacchus)
Munger, E. L., Takemoto, A., Raghanti, M. A., et al. (2017) · Neuroscience Research · doi:10.1016/j.neures.2017.06.002 · Cited by 28
Evans, S., McRae‐McKee, K., Wong, M. M., Hadjichrysanthou, C., de Wolf, F., & Anderson, R. M. (2018) · European Journal of Epidemiology · doi:10.1007/s10654-018-0381-0 · Cited by 27
Gray, S. L., Anderson, M. L., Hanlon, J. T., Dublin, S., Walker, R. L., Hubbard, R. A., Yu, O., Montine, T. J., Crane, P. K., Sonnen, J. A., et al. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-171174 · Cited by 31
Self-citationPLD3 epigenetic changes in the hippocampus of Alzheimer’s disease
Blanco‐Luquin, I., Altuna, M., de Gordoa, J. S., Urdánoz‐Casado, A., Roldán, M., Cámara, M. S., Zelaya, M. V., Erro, M. E., Echávarri, C., & Mendióroz, M. (2018) · Clinical Epigenetics · doi:10.1186/s13148-018-0547-3 · Cited by 30
Relative neuron loss in hippocampal sclerosis of aging and Alzheimer's disease
Ihara, R., Vincent, B. D., Baxter, M. R., Franklin, E. E., Hassenstab, J. J., Xiong, C., Morris, J. C., & Cairns, N. J. (2018) · Annals of Neurology · doi:10.1002/ana.25344 · Cited by 28
“In several neurodegenerative diseases, there may be extensive neuron loss and gliosis in multiple fields of the hippocampus, but in HS-Aging the neuron loss is restricted mainly to the CA1 field and subiculum.(9) The coexistence of multiple pathologies and the focal nature of HS-Aging raise two difficulties for the pr…”
BackgroundSelf-citationCoughlin, D. G., Petrovitch, H., White, L. R., Noorigian, J. V., Masaki, K., Ross, G. W., & Duda, J. E. (2019) · Parkinsonism & Related Disorders · doi:10.1016/j.parkreldis.2019.03.023 · Cited by 28
Morgello, S. (2018) · Handbook of clinical neurology · doi:10.1016/b978-0-444-63849-6.00002-5 · Cited by 28
Alavi, A. A., Barrio, J. R., Werner, T. J., Khosravi, M., Newberg, A. B., & Høilund‐Carlsen, P. F. (2019) · European Journal of Nuclear Medicine and Molecular Imaging · doi:10.1007/s00259-019-04564-5 · Cited by 28
Concomitant progressive supranuclear palsy and chronic traumatic encephalopathy in a boxer
Ling, H., Kara, E., Revesz, T., Lees, A. J., Plant, G. T., Martino, D., Houlden, H., Hardy, J., & Holton, J. L. (2014) · Acta Neuropathologica Communications · doi:10.1186/2051-5960-2-24 · Cited by 27
Biomarker-based signature of alzheimer's disease in pre-MCI individuals
Chipi, E., Salvadori, N., Farotti, L., & Parnetti, L. (2019) · Brain Sciences · doi:10.3390/brainsci9090213 · Cited by 27
“Autoptic confirmation of AD pathology has been associated with in vivo evidences of subtle longitudinal decline in different cognitive domains [38,39].”
BackgroundTosun, D., Yardibi, O., Benzinger, T. L. S., Kukull, W. A., Masters, C. L., Perrin, R. J., Weiner, M. W., Simen, A. A., Schwarz, A. J., & Initiative, A. D. N. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.13447 · Cited by 27
Burnham, S. C., Iaccarino, L., Pontecorvo, M. J., Fleisher, A., Lu, M., Collins, E. C., & Devous, M. D. (2023) · Brain Communications · doi:10.1093/braincomms/fcad305 · Cited by 30
“37 Majority read of the visual evaluation by five raters found that flortaucipir had a sensitivity of 92.3% and specificity of 80.0% for identifying Braak Stages V and VI NFT pathology as well as a sensitivity of 94.7% and specificity of 80.8% for identifying high ADNC.”
BackgroundMethodInfluentialThe influence of APOEε4 on the pTau interactome in sporadic Alzheimer’s disease
Thierry, M., Ponce, J., Martá-Ariza, M., Askenazi, M., Faustin, A., Leitner, D., Pires, G., Kanshin, E., Drummond, E., Ueberheide, B. M., et al. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02744-8 · Cited by 27
“This observation cannot be explained by the inclusion of differing stages of AD pathology among APOE groups, as this study was conducted on an homogenous selection of sporadic cases diagnosed with an advanced AD pathology at autopsy (A3, B3, C3 scores [55]).”
BackgroundMethodResultBaiardi, S., Hansson, O., Levin, J., & Parchi, P. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.14039 · Cited by 27
Neuropathological hallmarks in the post-mortem retina of neurodegenerative diseases
de Ruyter, F. J. H., Evers, M. J. A. P., Morrema, T. H. J., Dijkstra, A. A., den Haan, J., Twisk, J. W. R., de Boer, J. F., Scheltens, P., Bouwman, F. H., Verbraak, F. D., et al. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02769-z · Cited by 27
“…according to the guidelines of the BrainNet Europe Consortium [1, 4], including assessment of Alzheimer’s disease neuropathological changes (ADNC) [39], i.e. Thal phase for Aβ [22, 57], Braak stage for NFTs (Braak NFT stage) [7], CERAD score for neuritic plaque pathology [37], and Braak stage for…”
MethodBavarsad, M. S., Spina, S., Oehler, A., Allen, I. E., Suemoto, C. K., Leite, R. E. P., Seeley, W. S., Green, A., Jagust, W., Rabinovici, G. D., et al. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02816-9 · Cited by 29
Alzheimer's Disease and the “Valley of Death”: Not Enough Guidance from Human Brain Tissue?
Beach, T. G. (2012) · Journal of Alzheimer s Disease · doi:10.3233/jad-2012-129020 · Cited by 28
“According to a recent study of data from all National Institute on Aging AD Centers [59], the sensitivity of the clinical diagnosis of AD, as compared to new consensus autopsy criteria [60], may be about 80%.”
Self-citationCopy Number Variants in miR-138 as a Potential Risk Factor for Early-Onset Alzheimer’s Disease
Boscher, E., Husson, T., Quenez, O., Laquerrière, A., Marguet, F., Cassinari, K., Wallon, D., Martinaud, O., Charbonnier, C., Nicolas, G., et al. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-180940 · Cited by 27
“Based on macroscopy, histology, and immunohistochemistry, a diagnosis of AD including Braak & BraakstageV-VIwasmade[36](SupplementaryFig-ure 2).”
The long-term consequences of repetitive head impacts: Chronic traumatic encephalopathy
Alosco, M. L., & Stern, R. A. (2019) · Handbook of clinical neurology · doi:10.1016/b978-0-12-804766-8.00018-2 · Cited by 28
Apolipoprotein D: a potential biomarker for cerebral amyloid angiopathy
Kuiperij, H. B., Hondius, D., Kersten, I., Versleijen, A. A. M., Rozemüller, A. J. M., Greenberg, S. M., Schreuder, F. H. B. M., Klijn, C. J. M., & Verbeek, M. M. (2019) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12595 · Cited by 26
Adams, J. W., Alosco, M. L., Mez, J., Alvarez, V. E., Huber, B. R., Tripodis, Y., Adler, C. H., Kubilius, C., Cormier, K., Mathais, R., et al. (2020) · Acta Neuropathologica · doi:10.1007/s00401-020-02206-x · Cited by 29
“The National Institute of Aging-Reagan criteria were used to diagnose Alzheimer disease (AD), which included intermediate or high probability [28, 52].”
Method
Metadata
- Authors
- Montine, T. J., Phelps, C. H., Beach, T. G., Bigio, E. H., Cairns, N. J., Dickson, D. W., Duyckaerts, C., Frosch, M. P., Masliah, E., Mirra, S. S., Nelson, P. T., Schneider, J. A., Thal, D. R., Trojanowski, J. Q., Vinters, H. V., & Hyman, B. T.
- Affiliations
- University of Washington (US)
- National Institutes of Health (US)
- Banner Sun Health Research Institute (US)
- Northwestern University (US)
- Washington University in St. Louis (US)
- Mayo Clinic (US)
- Pitié-Salpêtrière Hospital (FR)
- Harvard University (US)
- University of California San Diego (US)
- SUNY Downstate Health Sciences University (US)
- University of Kentucky (US)
- Rush University Medical Center (US)
- Universität Ulm (DE)
- University of Pennsylvania (US)
- University of California, Los Angeles (US)
- Corresponding author
- Montine, Thomas J.
- ORCID
- Venue
- Acta Neuropathologica
- Published
- 2011-11-20
- Volume
- 123
- Issue
- 1
- Pages
- 1-11
- ISSN
- 0001-6322 (ISSN-L)
- 1432-0533
- PMC
- PMC3268003
- OpenAlex
- W2128228199
- Cited by
- 2,894
- References
- 66
- Citations by year
- 2026: 254 · 2025: 290 · 2024: 329 · 2023: 251 · 2022: 284 · 2021: 257 · 2020: 244 · 2019: 183 · 2018: 164 · 2017: 148 · 2016: 144 · 2015: 136 · 2014: 92 · 2013: 69 · 2012: 46
- FWCI
- 39.19
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Acta Neuropathologica (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5u01ag024904-10)
- National Institute on Aging (U01-AG-024904, R01AG017917, AG18840, AG-15819, R01AG015866, P30AG028383, R01AG042210, R01AG018440, U01AG016976, P50AG005131, P50AG016570, P01AG003949, P30AG010124, R01AG015819, P30AG010161, AG24904, P50AG005681, P30AG019610, P01AG003991, P50AG005136, P50AG005134, P30AG013854, U19AG010483, RF1AG015819, P01AG012435, U19AG024904, P30AG062421)
- National Institute of Neurological Disorders and Stroke (P50NS062684)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, amyloid-beta deposition, neurofibrillary tangles, neuritic plaques, ABC score, Lewy body disease, vascular brain injury, hippocampal sclerosis, TDP-43 inclusions, staining techniques, clinicopathological correlation, preclinical Alzheimer's disease
- MeSH terms
- Alzheimer Disease, Brain, Cerebrovascular Disorders, DNA-Binding Proteins, Hippocampus, Humans, Sclerosis, United States, Cerebrovascular Trauma, Lewy Body Disease, National Institute on Aging (U.S.)
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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