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 401–500 of 2,854
Alzheimer’s Disease Neuropathological Comorbidities are Common in the Younger-Old
Beach, T. G., & Malek‐Ahmadi, M. H. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-201213 · Cited by 88
“Included subject data was restricted to those with dementia and meeting National Institute on Aging-Alzheimer’s Association (NIA-AA) intermediate or high AD Neuropathological Change (ADNC) levels [72,73], considered to be a sufficient cause of cognitive impairment or dementia.”
Self-citationYamamoto, Y., Craggs, L., Watanabe, A., Booth, T. A., Attems, J., Low, R. W. C., Oakley, A. E., & Kalaria, R. N. (2013) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0b013e31829020b5 · Cited by 87
“A diagnosis of AD was made when there was evidence of significant AD-type pathology (Braak stages VYVI and moderate to severe CERAD score) and absence of significant vascular pathology (24).”
MethodWood, L. B., Winslow, A. R., Proctor, E. A., McGuone, D., Mordes, D. A., Frosch, M. P., Hyman, B. T., Lauffenburger, D. A., & Haigis, K. M. (2015) · Scientific Reports · doi:10.1038/srep16622 · Cited by 83
Self-citationHenríquez, G., Gomez, A., Guerrero, E., & Narayan, M. (2020) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.0c00381 · Cited by 83
Longitudinal tau-PET uptake and atrophy in atypical Alzheimer's disease
Sintini, I., Martin, P. R., Graff‐Radford, J., Senjem, M. L., Schwarz, C. G., Machulda, M. M., Spychalla, A. J., Drubach, D. A., Knopman, D. S., Petersen, R. C., et al. (2019) · NeuroImage Clinical · doi:10.1016/j.nicl.2019.101823 · Cited by 87
Neuropathological assessment of the Alzheimer spectrum
Jellinger, K. A. (2020) · Journal of Neural Transmission · doi:10.1007/s00702-020-02232-9 · Cited by 85
The MAPT H1 haplotype is associated with tangle-predominant dementia
Santa‐María, I., Haggiagi, A. M., Liu, X., Wasserscheid, J., Nelson, P. T., Dewar, K., Clark, L. N., & Crary, J. F. (2012) · Acta Neuropathologica · doi:10.1007/s00401-012-1017-1 · Cited by 88
“While the possibility that APP or its catabolites contribute to TPD has not previously been tested experimentally, the consensus criteria require the presence of insoluble Ab deposited in plaques together with NFT for the neuropathological diagnosis of AD [27, 42].”
BackgroundSelf-citationPKR involvement in Alzheimer’s disease
Hugon, J., Mouton‐Liger, F., Dumurgier, J., & Paquet, C. (2017) · Alzheimer s Research & Therapy · doi:10.1186/s13195-017-0308-0 · Cited by 86
“The pathology of AD involves senile plaques made of accumulated Aβ peptide, neurofibrillary tangles with abnormally phosphorylated tau protein, and synaptic and neuronal losses [2].”
BackgroundRinne, J. O., Wong, D. F., Wolk, D. A., Leinonen, V., Arnold, S. E., Buckley, C. J., Smith, A. P. L., McLain, R. W., Sherwin, P. F., Farrar, G., et al. (2012) · Acta Neuropathologica · doi:10.1007/s00401-012-1051-z · Cited by 84
Association of APOE e2 genotype with Alzheimer’s and non-Alzheimer’s neurodegenerative pathologies
Goldberg, T. E., Huey, E. D., & Devanand, D. P. (2020) · Nature Communications · doi:10.1038/s41467-020-18198-x · Cited by 82
Cherry, J. D., Esnault, C. D., Baucom, Z., Tripodis, Y., Huber, B. R., Alvarez, V. E., Stein, T. D., Dickson, D. W., & McKee, A. C. (2021) · Acta Neuropathologica Communications · doi:10.1186/s40478-021-01189-4 · Cited by 85
“Cases were assessed for neurodegenerative disease using well-established criteria for AD [7, 20, 34], neocortical Lewy body disease (LBD) [31], frontal temporal lobar degeneration (FTLD) [27], motor neuron disease (MND) [26], and CTE [1, 6, 29].”
MethodSelf-citationVermeiren, Y., Dam, D. V., Aerts, T., Engelborghs, S., & Deyn, P. P. D. (2014) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2014.05.031 · Cited by 83
Macdonald, I. R., Maxwell, S. P., Reid, G. A., Cash, M. K., DeBay, D. R., & Darvesh, S. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-170164 · Cited by 85
Somatic variants in autosomal dominant genes are a rare cause of sporadic Alzheimer’s disease
Nicolas, G., Acuña‐Hidalgo, R., Keogh, M. J., Quenez, O., Steehouwer, M., Lelieveld, S., Rousseau, S., Richard, A., Oud, M. S., Marguet, F., et al. (2018) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2018.06.3056 · Cited by 81
“, high AD neuropathologic change according to National Institute on Aging– Alzheimer’s Association criteria [17]) and a negative family history, one positive control carrying a pathogenic PSEN1 variant, and 52 cognitively normal controls.”
The effects of cerebral amyloid angiopathy on integrity of the blood-brain barrier
Magaki, S., Tang, Z., Tung, S., Williams, C. K., Lo, D., Yong, W. H., Khanlou, N., & Vinters, H. V. (2018) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2018.06.004 · Cited by 93
Self-citationPredictors of cognitive impairment in primary age-related tauopathy: an autopsy study
Iida, M. A., Farrell, K. W., Walker, J. M., Richardson, T. E., Marx, G. A., Bryce, C., Purohit, D. P., Ayalon, G., Beach, T. G., Bigio, E. H., et al. (2021) · Acta Neuropathologica Communications · doi:10.1186/s40478-021-01233-3 · Cited by 80
Self-citationThe Use of Tau PET to Stage Alzheimer Disease According to the Braak Staging Framework
Macedo, A. C., Tissot, C., Therriault, J., Servaes, S., Wang, Y.-T., Arias, J. F., Rahmouni, N., Lussier, F. Z., Vermeiren, M. R., Bezgin, G., et al. (2023) · Journal of Nuclear Medicine · doi:10.2967/jnumed.122.265200 · Cited by 99
“In 2012, this staging systemwas integrated into the AD neuropathologic diagnostic criteria (9,10).”
MethodClusterin levels are increased in A lzheimer's disease and influence the regional distribution of Aβ
Miners, J. S., Clarke, P., & Love, S. (2016) · Brain Pathology · doi:10.1111/bpa.12392 · Cited by 83
“According to the NIA-AA guidelines AD neuropathological change was considered an adequate explanation for the dementia in all cases in the AD group (32).”
MethodNelson, P. T., Jicha, G. A., Wang, W., Ighodaro, E. T., Artiushin, S., Nichols, C. G., & Fardo, D. W. (2015) · Ageing Research Reviews · doi:10.1016/j.arr.2015.07.007 · Cited by 85
Self-citationStandardized Operational Protocol for Human Brain Banking in China
Qiu, W., Zhang, H., Bao, A., Zhu, K., Huang, Y. M., Yan, X., Zhang, J., Zhong, C., Shen, Y., Zhou, J., et al. (2018) · Neuroscience Bulletin · doi:10.1007/s12264-018-0306-7 · Cited by 81
Bourassa, P., Tremblay, C., Schneider, J. A., Bennett, D. A., & Calon, F. (2019) · Acta Neuropathologica · doi:10.1007/s00401-019-01967-4 · Cited by 80
Self-citationAl‐Shaikh, F. S. H., Duara, R., Crook, J. E., Lesser, E. R., Schaeverbeke, J. M., Hinkle, K. M., Ross, O. A., Ertekin‐Taner, N., Pedraza, O., Dickson, D. W., et al. (2019) · JAMA Neurology · doi:10.1001/jamaneurol.2019.3606 · Cited by 82
Self-citationDiagnostic Accuracy of Amyloid versus FDG PET in Patients with Cognitive Impairment and Autopsy
Lesman‐Segev, O. H., Joie, R. L., Iaccarino, L., Lobach, I. V., Rosen, H. J., Seo, S. W., Janabi, M., Baker, S. L., Edwards, L., Pham, J. Q., et al. (2019) · Annals of Neurology · doi:10.1002/ana.25968 · Cited by 82
Paladugu, L., Gharaibeh, A., Kolli, N., Learman, C. R., Hall, T. C., Li, L., Rossignol, J., Maiti, P., & Dunbar, G. L. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22020860 · Cited by 79
“Although the definitive diagnosis of AD was originally made only through autopsy [19,20], pathological changes in the brain can happen long before behavioral symptoms appear.”
BackgroundRetractedNeuropathology of Anti-Amyloid-β Immunotherapy: A Case Report
Castellani, R. J., Shanes, E. D., McCord, M., Reish, N. J., Flanagan, M. E., Mesulam, M. M., & Jamshidi, P. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-221305 · Cited by 85
“AD neuropathologic change was assessed as ‘high’ (A3, B3, C3) according to NIA-AA 2012 consensus guidelines [15].”
Bjorklund, N. L., Reese, L. C., Sadagoparamanujam, V.-M., Ghirardi, V., Woltjer, R. L., & Taglialatela, G. (2012) · Molecular Neurodegeneration · doi:10.1186/1750-1326-7-23 · Cited by 98
“Notably, the National Institute of Health/National Institute on Aging and the Alzheimer’s Association have recently included such individuals in their joint official guidelines for neuropathologic assessment of AD and classified them as individuals who have AD neuropathologic changes in the absence of cognitive impair…”
Nanoscale structure of amyloid-β plaques in Alzheimer’s disease
Querol‐Vilaseca, M., Colom‐Cadena, M., Pegueroles, J., Núñez‐Llaves, R., Luque-Cabecerans, J., Muñoz, L., Andilla, J., Belbin, O., Spires‐Jones, T. L., Gelpí, E., et al. (2019) · Scientific Reports · doi:10.1038/s41598-019-41443-3 · Cited by 81
An update on the interactions between Alzheimer's disease, autophagy and inflammation
Bostancıklıoğlu, M. (2019) · Gene · doi:10.1016/j.gene.2019.04.040 · Cited by 78
Relevance of biomarkers across different neurodegenerative diseases
Ehrenberg, A. J., Khatun, A., Coomans, E. M., Betts, M. J., Capraro, F., Thijssen, E. H., Senkevich, K. A., Bharucha, T., Jafarpour, M., Young, P. N. E., et al. (2020) · Alzheimer s Research & Therapy · doi:10.1186/s13195-020-00601-w · Cited by 81
“terized by the accumulation of tau neurofibrillary tangles and extracellular Aβ plaques [5].”
BackgroundRegional Overlap of Pathologies in Lewy Body Disorders
Colom‐Cadena, M., Grau‐Rivera, O., Planellás, L., Cerquera‐Cleves, C., Morenas‐Rodríguez, E., Helgueta, S., Muñoz, L., Kulisevsky, J., Martı́, M. J., Tolosa, E. S., et al. (2017) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlx002 · Cited by 80
“The National Institute on Aging-Alzheimer’s Association Guidelines for neuropathologic assessment of AD were applied and a final ABC score was assigned (50).”
MethodDrummond, E. S., Nayak, S., Ueberheide, B., & Wisniewski, T. (2015) · Scientific Reports · doi:10.1038/srep15456 · Cited by 78
Voorhees, J. R., Remy, M. T., Cintrón-Pérez, C. J., El Rassi, E., Khan, M. Z., Dutca, L. M., Yin, T. C., McDaniel, L. N., Williams, N. S., Brat, D. J., et al. (2018) · Biological Psychiatry · doi:10.1016/j.biopsych.2017.10.023 · Cited by 78
“When tau becomes hyperphosphorylated, it forms intracellular NFTs predominantly in large pyramidal neurons of the entorhinal cortex, hippocampus, association cortex, and other cortical regions as the disease advances (4, 5).”
Josephs, K. A., Martin, P. R., Weigand, S. D., Tosakulwong, N., Buciuc, M., Murray, M. E., Petrucelli, L., Senjem, M. L., Spychalla, A. J., Knopman, D. S., et al. (2020) · Brain · doi:10.1093/brain/awaa299 · Cited by 76
“, 1991) scoring of neuritic plaques in neocortex: C0 = no neuritic plaques; C1 = sparse neuritic plaques; C2 = moderate neuritic plaques; and C3 = frequent neuritic plaques (Hyman et al., 2012; Montine et al., 2012).”
BackgroundMethodInfluentialSelf-citationSystemic infection exacerbates cerebrovascular dysfunction in Alzheimer’s disease
Asby, D. J., Boche, D., Allan, S. M., Love, S., & Miners, J. S. (2021) · Brain · doi:10.1093/brain/awab094 · Cited by 83
Cho, H., Mundada, N. S., Apostolova, L. G., Carrillo, M. C., Shankar, R. P., Amuiri, A. N., Zeltzer, E., Windon, C., Soleimani‐Meigooni, D. N., Tanner, J. A., et al. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.13453 · Cited by 81
“∙ Among EOAD patients, younger onset and female sex were associated with higher tau-PET.”
BackgroundIrwin, D. J., Lleó, A., Xie, S. X., McMillan, C. T., Wolk, D. A., Lee, E. B., Van Deerlin, V. M., Shaw, L. M., Trojanowski, J. Q., & Grossman, M. (2017) · Annals of Neurology · doi:10.1002/ana.24996 · Cited by 67
“Both staining methods are considered equivalent for AD neuropathological diagnostic criteria.(22)”
MethodSelf-citationA 2-Step Cerebrospinal Algorithm for the Selection of Frontotemporal Lobar Degeneration Subtypes
Lleó, A., Irwin, D. J., Illán-Gala, I., McMillan, C. T., Wolk, D. A., Lee, E. B., Van Deerlin, V. M., Shaw, L. M., Trojanowski, J. Q., & Grossman, M. (2018) · JAMA Neurology · doi:10.1001/jamaneurol.2018.0118 · Cited by 71
Self-citationMicroglial activation occurs late during preclinical Alzheimer's disease
Streit, W. J., Braak, H., Del Tredici, K., Leyh, J., Lier, J., Khoshbouei, H., Eisenlöffel, C., Müller, W., & Bechmann, I. (2018) · Glia · doi:10.1002/glia.23510 · Cited by 98
A Luminex Assay Detects Amyloid β Oligomers in Alzheimer’s Disease Cerebrospinal Fluid
Herskovits, A. Z., Locascio, J. J., Peskind, E. R., Li, G., & Hyman, B. T. (2013) · PLoS ONE · doi:10.1371/journal.pone.0067898 · Cited by 77
Self-citationDo anti-amyloid beta protein antibody cross reactivities confound Alzheimer disease research?
Hunter, S., & Brayne, C. (2017) · Journal of Negative Results in BioMedicine · doi:10.1186/s12952-017-0066-3 · Cited by 80
“Evidence relating to Aβ from autosomal dominant genetic mutations in the amyloid precursor protein (APP) and presenilins (PS) in familial AD (FAD) [9, 10], coupled with the neuropathological diagnostic value associated with the presence of deposits of Aβ in the brain in both FAD and sporadic AD (SAD) [11, 12], has bee…”
BackgroundBejanin, A., Murray, M. E., Martin, P. R., Botha, H., Tosakulwong, N., Schwarz, C. G., Senjem, M. L., Chételat, G., Kantarci, K., Jack, C. R., et al. (2019) · Brain · doi:10.1093/brain/awz277 · Cited by 75
Self-citationIturria‐Medina, Y., Khan, A. F., Adewale, Q., Shirazi, A. H., & Initiative, T. A. D. N. (2019) · Brain · doi:10.1093/brain/awz400 · Cited by 79
“…assessments of amyl- oid-b deposits, staging of neurofibrillary tangles, scoring of neuritic plaques and assessments of co-morbid conditions such as Lewy body disease, vascular brain injury, hippocampal sclerosis, and TAR DNA-binding protein (TDP) immunoreactive inclusions (Montine et al. , 2012).”
Friedberg, J. S., Aytan, N., Cherry, J. D., Xia, W., Standring, O. J., Alvarez, V. E., Nicks, R., Svirsky, S. E., Meng, G., Jun, G., et al. (2020) · Scientific Reports · doi:10.1038/s41598-020-59869-5 · Cited by 82
Iaccarino, L., Burnham, S. C., Dell’Agnello, G., Dowsett, S. A., & Epelbaum, S. (2023) · The Journal of Prevention of Alzheimer s Disease · doi:10.14283/jpad.2023.43 · Cited by 87
“Additional performance data are provided in a study of 114 participants that showed a significant correlation between INNOTEST CSF P-tau181 and Braak stage (Montine score B (89)), with Spearman ρ of 0.”
MethodString Vessel Formation is Increased in the Brain of Parkinson Disease
Yang, P., Pavlovic, D., Waldvogel, H. J., Dragunow, M., Synek, B. J., Turner, C. P., Faull, R. L. M., & Guan, J. (2015) · Journal of Parkinson s Disease · doi:10.3233/jpd-140454 · Cited by 77
Mapping of SARS-CoV-2 Brain Invasion and Histopathology in COVID-19 DiseasePreprint
Serrano, G. E., Walkera, J., Arce, R., Glass, M. J., Vargas, D., Sue, L. I., Intorcia, A. J., Nelson, C. M., Oliver, J., Papa, J. D., et al. (2021) · medRxiv · doi:10.1101/2021.02.15.21251511 · Cited by 81
Self-citationPeet, B. T., Spina, S., Mundada, N., & La Joie, R. (2021) · Neurotherapeutics · doi:10.1007/s13311-021-01101-x · Cited by 74
Primary Tau Pathology, Not Copathology, Correlates With Clinical Symptoms in PSP and CBD
Robinson, J. L., Yan, N., Caswell, C., Xie, S. X., Suh, E. R., Deerlin, V. M. V., Gibbons, G. S., Irwin, D. J., Grossman, M., Lee, E. B., et al. (2019) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlz141 · Cited by 78
Self-citationRöhr, D., Boon, B. D. C., Schuler, M., Kremer, K., Hoozemans, J. J. M., Bouwman, F. H., El-Mashtoly, S. F., Nabers, A., Großerueschkamp, F., Rozemuller, A. J. M., et al. (2020) · Acta Neuropathologica Communications · doi:10.1186/s40478-020-01091-5 · Cited by 77
“AD cases (n = 5) were selected when clinical and neuropathological information fulfilled the criteria of the National Institute on Aging-Alzheimer’s Association (NIA-AA) for AD and no other neurodegenerative or psychiatric disease was present [51].”
MethodMastenbroek, S. E., Vogel, J. W., Collij, L. E., Serrano, G. E., Tremblay, C., Young, A. L., Arce, R. A., Shill, H. A., Driver‐Dunckley, E. D., Mehta, S. H., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-49402-x · Cited by 82
Self-citationAsymmetry of post-mortem neuropathology in behavioural-variant frontotemporal dementia
Irwin, D. J., McMillan, C. T., Xie, S. X., Rascovsky, K., Deerlin, V. M. V., Coslett, H. B., Hamilton, R. H., Aguirre, G. K., Lee, E. B., Lee, V. M. ‐., et al. (2017) · Brain · doi:10.1093/brain/awx319 · Cited by 78
“Neuropathological diagnosis was performed by expert neuropathologists (J.Q.T., E.B.L.) using formal criteria (Mackenzie et al., 2010; Montine et al., 2012).”
MethodSelf-citationPublic Knowledge about Dementia in China: A National WeChat-Based Survey
Liu, D., Cheng, G., An, L., Gan, X.-G., Wu, Y., Zhang, B., Hu, S. H., Zeng, Y., & Wu, L. (2019) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph16214231 · Cited by 79
“AD, people think it is possible to improve the patients’ quality of life through an active management of dementia [56].”
BackgroundLimbic-predominant age-related TDP-43 encephalopathy differs from frontotemporal lobar degeneration
Robinson, J. L., Porta, S., Garrett, F. G., Zhang, P., Xie, S. X., Suh, E. R., Deerlin, V. M. V., Abner, E. L., Jicha, G. A., Barber, J. M., et al. (2020) · Brain · doi:10.1093/brain/awaa219 · Cited by 77
Self-citationData-driven neuropathological staging and subtyping of TDP-43 proteinopathies
Young, A. L., Vogel, J. W., Robinson, J. L., McMillan, C. T., Ossenkoppele, R., Wolk, D. A., Irwin, D. J., Elman, L. B., Grossman, M., Lee, V. M. ‐., et al. (2023) · Brain · doi:10.1093/brain/awad145 · Cited by 84
“26 A secondary neuropathological diagnosis of LATE-AD+ was made if individuals showed a primary diagnosis of Alzheimer’s disease (using NIA-AA criteria), did not have a secondary diagnosis of FTLD or ALS, and also had evidence of TDP-43.”
del Campo, M., Vermunt, L., Peeters, C. F. W., Sieben, A., Hok‐A‐Hin, Y. S., Lleó, A., Alcolea, D. A., van Nee, M. M., Engelborghs, S., van Alphen, J. L., et al. (2023) · Nature Communications · doi:10.1038/s41467-023-41122-y · Cited by 82
“The neuro-pathological validation cohort included cases with a de fi nite diagnosis according to international neuropathological examination guidelines for DLB 31,70 and AD 72 .”
Is sporadic Alzheimer′s disease a developmental disorder?
Arendt, T., Stieler, J., & Ueberham, U. (2017) · Journal of Neurochemistry · doi:10.1111/jnc.14036 · Cited by 76
Impaired hepatic amyloid-beta degradation in Alzheimer’s disease
Maarouf, C. L., Walker, J. E., Sue, L. I., Dugger, B. N., Beach, T. G., & Serrano, G. E. (2018) · PLoS ONE · doi:10.1371/journal.pone.0203659 · Cited by 73
Self-citationMichno, W., Nyström, S., Wehrli, P. M., Lashley, T., Brinkmalm, G., Guérard, L., Syvänen, S., Sehlin, D., Kaya, I., Brinet, D., et al. (2019) · Journal of Biological Chemistry · doi:10.1074/jbc.ra118.006604 · Cited by 75
“standard diagnostic criteria were used for the neuropathological diagnosis of AD (67-69).”
MethodAssociation of APOE Genotype With Heterogeneity of Cognitive Decline Rate in Alzheimer Disease
Qian, J., Betensky, R. A., Hyman, B. T., & Serrano-Pozo, A. (2021) · Neurology · doi:10.1212/wnl.0000000000011883 · Cited by 71
“Participants can donate their brain on death for research purposes, including a standardized neuropathologic evaluation.(27) The NACCNeuropathology database was interrogated for UDS visits conducted between September 2005 and November 2018.”
Self-citationNeocortical origin and progression of gray matter atrophy in nonamnestic Alzheimer's disease
Phillips, J. S., Da Re, F., Dratch, L., Xie, S. X., Irwin, D. J., McMillan, C. T., Vaishnavi, S. N., Ferrarese, C., Lee, E. B., Shaw, L. M., et al. (2018) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.11.008 · Cited by 74
“These ordinal ratings assessed phosphorylated tau (evaluated using anti-PHF1 antibody), β-amyloid plaques (stained with thioflavin-s), neuronal loss severity, and gliosis (both visually assessed) (Irwin et al., 2016; Montine et al., 2012).”
Self-citationKoga, S., Kouri, N., Walton, R. L., Ebbert, M., Josephs, K. A., Litvan, I., Graff‐Radford, N. R., Ahlskog, J. E., Uitti, R. J., van Gerpen, J. A., et al. (2018) · Acta Neuropathologica · doi:10.1007/s00401-018-1878-z · Cited by 82
“Braak neurofibrillary tangle (NFT) stage and Thal amyloid phase were assigned based upon lesion density and distribution with thioflavin S fluorescent microscopy according to published criteria [6, 45, 46, 55].”
MethodSelf-citationden Haan, J., Morrema, T. H. J., Rozemüller, A. J. M., Bouwman, F. H., & Hoozemans, J. J. M. (2018) · Acta Neuropathologica Communications · doi:10.1186/s40478-018-0577-2 · Cited by 76
“Neuropathological diagnosis of AD was made following the NIA-AA criteria including Thal-staging for Aβ stage, Braak-andBraak-staging for NFTs and CERAD-staging for neuritic plaques [1, 38, 48].”
Uncovering pathophysiological changes in frontotemporal dementia using serum lipids
Phan, K., He, Y., Pickford, R., Bhatia, S., Katzeff, J. S., Hodges, J. R., Piguet, O., Halliday, G. M., & Kim, W. S. (2020) · Scientific Reports · doi:10.1038/s41598-020-60457-w · Cited by 72
Fan, Y., Nirujogi, R. S., Garrido, A., Ruiz‐Martínez, J., Bergareche‐Yarza, A., Rezola, E. M., Vinagre‐Aragón, A., Croitoru, I. M., Pagola, A. G., Markinez, L. P., et al. (2021) · Acta Neuropathologica · doi:10.1007/s00401-021-02325-z · Cited by 73
Ghosh, S., Sachdeva, B., Sachdeva, P., Chaudhary, V., Rani, G. M., & Sinha, J. K. (2022) · Carbon letters · doi:10.1007/s42823-022-00397-9 · Cited by 74
Hou, S. S., Yang, J. L., Lee, J. H., Kwon, Y., Calvo-Rodríguez, M., Bao, K., Ahn, S., Kashiwagi, S., Kumar, A. T. N., Bacskai, B. J., et al. (2023) · Nature Biomedical Engineering · doi:10.1038/s41551-023-01003-7 · Cited by 74
Effects of intermittent fasting on cognitive health and Alzheimer’s disease
Elias, A., Padinjakara, N., & Lautenschlager, N. T. (2023) · Nutrition Reviews · doi:10.1093/nutrit/nuad021 · Cited by 85
“Extracellular b -amyloid plaques and intracellular tangles are the characteristic neurological lesions in AD.”
InfluentialRabinovici, G. D., Knopman, D. S., Arbizu, J., Benzinger, T. L. S., Donohoe, K. J., Hansson, O., Herscovitch, P., Kuo, P. H., Lingler, J. H., Minoshima, S., et al. (2025) · Journal of Nuclear Medicine · doi:10.2967/jnumed.124.268756 · Cited by 87
“In contrast to that for amyloid PET, autopsy and PET studies have shown that the level of cortical tau correlates with cognitive status and symptomatic disease stage ( 1,2,191 ).”
Yang, Z., Slavin, M. J., & Sachdev, P. S. (2013) · Nature Reviews Neurology · doi:10.1038/nrneurol.2013.105 · Cited by 74
Iacono, D., Resnick, S. M., O’Brien, R., Zonderman, A. B., An, Y., Pletnikova, O., Rudow, G., Crain, B., & Troncoso, J. C. (2014) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0000000000000052 · Cited by 73
“Table 2 shows the ‘‘ABC’’ scores and levels of AD neuropathologic changes for each subject as proposed by the National Institute on Aging-Alzheimer’s Association recommendations for pathologic criteria (14).”
Selective Vulnerability of Brainstem Nuclei in Distinct Tauopathies: A Postmortem Study
Eser, R. A., Ehrenberg, A. J., Petersen, C., Dunlop, S. R., Mejia, M. B., Suemoto, C. K., Walsh, C. M., Rajana, H., Oh, J. Y., Theofilas, P., et al. (2018) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlx113 · Cited by 71
Grothe, M. J., Moscoso, A., Silva‐Rodríguez, J., Lange, C., Nho, K. T., Saykin, A. J., Nelson, P. T., Schöll, M., Buchert, R., Teipel, S. J., et al. (2022) · Alzheimer s & Dementia · doi:10.1002/alz.12763 · Cited by 70
Self-citationKivisäkk, P., Sweeney, T., Carlyle, B. C., Trombetta, B. A., LaCasse, K., El‐Mufti, L. H., Tuncali, I., Chibnik, L. B., Das, S., Scherzer, C. R., et al. (2023) · Frontiers in Neurology · doi:10.3389/fneur.2023.1069411 · Cited by 76
Self-citationCerebellar ataxia in progressive supranuclear palsy: An autopsy study of PSP‐C
Koga, S., Josephs, K. A., Ogaki, K., Labbé, C., Uitti, R. J., Graff‐Radford, N. R., van Gerpen, J. A., Cheshire, W. P., Aoki, N., Rademakers, R., et al. (2016) · Movement Disorders · doi:10.1002/mds.26499 · Cited by 76
“The neuropathologic protocol includes the assessment of Alzheimertype pathology,(19) including the assignment of Braak neurofibrillary tangle (NFT) stage(20) and Thal amyloid phase(21) with thioflavin S fluorescent microscopy.(22) Immunohistochemistry for tau (CP13, 1:1000, Dr.”
MethodSelf-citationMann, D. M. A., Davidson, Y. S., Robinson, A. C., Allen, N., Hashimoto, T., Richardson, A., Jones, M., Snowden, J. S., Pendleton, N., Potier, M.-C., et al. (2018) · Acta Neuropathologica · doi:10.1007/s00401-018-1866-3 · Cited by 73
Arena, J. D., Smith, D. H., Lee, E. B., Gibbons, G. S., Irwin, D. J., Robinson, J. L., Lee, V. M. ‐., Trojanowski, J. Q., Stewart, W. B., Jr., & Johnson, V. E. (2020) · Brain · doi:10.1093/brain/awaa071 · Cited by 77
“addition, non-demented controls without history of TBI and with known aging-related tau pathologies were selected including; PART (n=1), ARTAG and PART (n=3) and ARTAG with low AD neuropathologic change (n=4) (Cairns et al., 2007; Montine et al., 2012; Crary et al., 2014; Kovacs et al., 2016; McKee et al., 2016) (Tabl…”
BackgroundMethodInfluentialSelf-citationEhrenberg, A. J., Kelberman, M. A., Liu, K. Y., Dahl, M. J., Weinshenker, D., Falgàs, N., Dutt, S., Mather, M., Ludwig, M., Betts, M. J., et al. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.12937 · Cited by 74
Kovács, G. G., Rozemüller, A. J. M., Swieten, J. C. V., Gelpí, E., Majtényi, K., Al‐Sarraj, S., Troakes, C., Bódi, I., King, A., Hortobágyi, T., et al. (2012) · Neuropathology and Applied Neurobiology · doi:10.1111/j.1365-2990.2012.01272.x · Cited by 79
Bernstein, A. I., Lin, Y., Street, R. C., Lin, L., Dai, Q., Yu, L., Bao, H., Gearing, M., Lah, J. J., Nelson, P. T., et al. (2016) · Human Molecular Genetics · doi:10.1093/hmg/ddw109 · Cited by 73
“AD diagnoses were made in accordance with established criteria (NIA-AA) (67).”
MethodSelf-citationFluorescence and autoradiographic evaluation of tau PET ligand PBB3 to α‐synuclein pathology
Koga, S., Ono, M., Sahara, N., Higuchi, M., & Dickson, D. W. (2017) · Movement Disorders · doi:10.1002/mds.27013 · Cited by 76
“Alzheimer’s disease (AD), the most common neurodegenerative disease of dementia, has 2 proteins as pathologic hallmarks: amyloid and tau.(8,9) Amyloid positron emission tomography (PET) imaging using [(11)C]Pittsburgh Compound B (PiB) has been sucsessfully used to detect cerebral amyloid deposition in individuals with…”
BackgroundSelf-citationShade, L. M. P., Katsumata, Y., Abner, E. L., Aung, K. Z., Claas, S. A., Qiao, Q., Heberle, B. A., Brandon, J. A., Page, M. L., Hohman, T. J., et al. (2024) · Nature Genetics · doi:10.1038/s41588-024-01939-9 · Cited by 72
“…including diffuse plaques and Braak NFT staging 28–30 ), non-AD neurodegenerative pro-teinopathies (LATE-NC and Lewy bodies 12,31 ), cerebrovascular pathologies (CAA, gross infarcts, microinfarcts, circle of Willis atherosclerosis and arteriolosclerosis 30,32 ) and hippocampal sclerosis 32 .”
Self-citationNeuropsychological changes in asymptomatic persons with Alzheimer disease neuropathology
Monsell, S. E., Mock, C., Hassenstab, J., Roe, C. M., Cairns, N. J., Morris, J. C., & Kukull, W. (2014) · Neurology · doi:10.1212/wnl.0000000000000650 · Cited by 71
Self-citationThe proteome of granulovacuolar degeneration and neurofibrillary tangles in Alzheimer’s disease
Hondius, D., Koopmans, F., Leistner, C., Pita-Illobre, D., Peferoen-Baert, R. M. B., Marbus, F., Paliukhovich, I., Li, K. W., Rozemüller, A. J. M., Hoozemans, J. J. M., et al. (2021) · Acta Neuropathologica · doi:10.1007/s00401-020-02261-4 · Cited by 70
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Distribution of Pathology in Frontal Variant Alzheimer's Disease
Blennerhassett, R. C., Lillo, P., Halliday, G. M., Hodges, J. R., & Kril, J. J. (2014) · Journal of Alzheimer s Disease · doi:10.3233/jad-131241 · Cited by 74
Enrichment and Stratification for Predementia Alzheimer Disease Clinical Trials
Holland, D., McEvoy, L. K., Desikan, R. S., Dale, A. M., & Initiative, A. D. N. (2012) · PLoS ONE · doi:10.1371/journal.pone.0047739 · Cited by 71
“We examined the ROIs that are affected by neurofibrillary pathology early in the disease process [25]: the hippocampus (a proposed diagnostic biomarker [69] that has also been investigated as an outcome measure in clinical trials [70]), entorhinal cortex, parahippocampus, fusiform gyrus, amygdala, and the retrosplenia…”
BackgroundMethodAbsence of Alzheimer Disease Neuropathologic Changes in Eyes of Subjects With Alzheimer Disease
Williams, E. A., McGuone, D., Frosch, M. P., Hyman, B. T., Laver, N., & Stemmer-Rachamimov, A. O. (2017) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlx020 · Cited by 71
Self-citationChronic traumatic encephalopathy-like abnormalities in a routine neuropathology service
Noy, S., Krawitz, S., & Del Bigio, M. R. (2016) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlw092 · Cited by 70
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Self-citationEarly Selective Vulnerability of the CA2 Hippocampal Subfield in Primary Age-Related Tauopathy
Walker, J. M., Richardson, T. E., Farrell, K. W., Iida, M. A., Foong, C., Shang, P., Attems, J., Ayalon, G., Beach, T. G., Bigio, E. H., et al. (2020) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlaa153 · Cited by 69
“Furthermore, cases that qualified as intermediate or high ADNC based on the NIA-AA Reagan criteria (5) were defined as such.”
BackgroundMethodSelf-citationJosephs, K. A., Duffy, J. R., Clark, H. M., Utianski, R. L., Strand, E. A., Machulda, M. M., Botha, H., Martin, P. R., Pham, N. T. T., Stierwalt, J. A. G., et al. (2021) · Nature Communications · doi:10.1038/s41467-021-23687-8 · Cited by 77
Self-citationCharacterizing brain tau and cognitive decline along the amyloid timeline in Alzheimer’s disease
Cody, K. A., Langhough, R. E., Zammit, M. D., Clark, L. R., Chin, N. A., Christian, B. T., Betthauser, T. J., & Johnson, S. C. (2024) · Brain · doi:10.1093/brain/awae116 · Cited by 71
Nagao, S., Yokota, O., Ikeda, C., Takeda, N., Ishizu, H., Kuroda, S., Sudo, K., Terada, S., Murayama, S., & Uchitomi, Y. (2013) · European Archives of Psychiatry and Clinical Neuroscience · doi:10.1007/s00406-013-0472-6 · Cited by 73
Nelson, P. T., Wang, W., Partch, A. B., Monsell, S. E., Valladares, O., Ellingson, S. R., Wilfred, B. R., Naj, A. C., Wang, L.-S., Kukull, W. A., et al. (2014) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0000000000000151 · Cited by 69
“Hippocampal sclerosis of aging (HS-Aging) is diagnosed neuropathologically when neuron loss and astrocytosis are observed in the hippocampal formation, and are not considered attributable to Alzheimer disease (AD)-type plaques and tangles (1-3).”
Self-citationStem cell therapies in age-related neurodegenerative diseases and stroke
Wang, Y., Ji, X., Leak, R. K., Chen, F., & Cao, G. (2016) · Ageing Research Reviews · doi:10.1016/j.arr.2016.11.002 · Cited by 74
VEGFR1 and VEGFR2 in Alzheimer’s Disease
Harris, R., Miners, J. S., Allen, S. J., & Love, S. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-170745 · Cited by 70
Astrocytic Tau Deposition Is Frequent in Typical and Atypical Alzheimer Disease Presentations
Nolan, A., Resende, E. D. P. F., Petersen, C., Neylan, K. D., Spina, S., Huang, E. J., Seeley, W. W., Miller, Z., & Grinberg, L. T. (2019) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlz094 · Cited by 69
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“The neuropathological findings were consistent with AD Braak stage VI, by the NIA Consensus Criteria [1,2].”
BackgroundMethodGkanatsiou, E., Portelius, E., Toomey, C. E., Blennow, K., Zetterberg, H., Lashley, T., & Brinkmalm, G. (2019) · Neuroscience Letters · doi:10.1016/j.neulet.2019.02.033 · Cited by 68
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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