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 301–400 of 2,854
Longitudinal 18F-MK-6240 tau tangles accumulation follows Braak stages
Pascoal, T. A., Benedet, A. L., Tudorascu, D., Therriault, J., Mathotaarachchi, S. S., Savard, M., Lussier, F. Z., Tissot, C., Chamoun, M., Kang, M. S., et al. (2021) · Brain · doi:10.1093/brain/awab248 · Cited by 122
Tan, R. H., Kril, J. J., Fatima, M., McGeachie, A. B., McCann, H., Shepherd, C. E., Forrest, S. L., Affleck, A. J., Kwok, J. B., Hodges, J. R., et al. (2015) · Brain · doi:10.1093/brain/awv220 · Cited by 113
Pryor, N. E., Moss, M. A., & Hestekin, C. N. (2012) · International Journal of Molecular Sciences · doi:10.3390/ijms13033038 · Cited by 113
“Although larger aggregates, including fibrils, remain important for clinical determination [1,2], small oligomeric aggregates are of interest due to their potentially toxic nature and hypothesized role in disease progression.”
BackgroundCathepsin A–related arteriopathy with strokes and leukoencephalopathy (CARASAL)
Bugiani, M., Kevelam, S. H., Bakels, H. S., Waisfisz, Q., Ceuterick-de Groote, C., Niessen, H. W. M., Abbink, T. E. M., Lesnik Oberstein, S. A. M. J., & van der Knaap, M. S. (2016) · Neurology · doi:10.1212/wnl.0000000000003251 · Cited by 111
DNA methylation signature of human hippocampus in Alzheimer’s disease is linked to neurogenesis
Altuna, M., Urdánoz‐Casado, A., de Gordoa, J. S., Zelaya, M. V., Labarga, A., Lepesant, J. M. J., Roldán, M., Blanco‐Luquin, I., Perdones-Montero, Á., Larumbe, R., et al. (2019) · Clinical Epigenetics · doi:10.1186/s13148-019-0672-7 · Cited by 107
Agujetas, V. R., Barbero‐Camps, E., de Dios, C., Podlesniy, P., Abadin, X., Morales, A., Marı́, M., Trullás, R., & Colell, A. (2021) · Molecular Neurodegeneration · doi:10.1186/s13024-021-00435-6 · Cited by 113
Staging of Alzheimer’s disease: past, present, and future perspectives
Therriault, J., Zimmer, E. R., Benedet, A. L., Pascoal, T. A., Gauthier, S. G., & Rosa‐Neto, P. (2022) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2022.05.008 · Cited by 123
Cerebrovascular insulin receptors are defective in Alzheimer’s disease
Leclerc, M., Bourassa, P., Tremblay, C., Caron, V., Sugère, C., Émond, V., Bennett, D. A., & Calon, F. (2022) · Brain · doi:10.1093/brain/awac309 · Cited by 113
“logical diagnosis is based on the ABC scoring method found in the revised National Institute of Aging–Alzheimer’s Association (NIA-AA) guidelines for the neuropathological diagnosis of Alzheimer’s disease.(62) Four levels of Alzheimer’s disease neuro-”
MethodTau biology, tauopathy, traumatic brain injury, and diagnostic challenges
Castellani, R. J., & Perry, G. (2019) · Journal of Alzheimer’s Disease · doi:10.3233/jad-180721 · Cited by 110
“unless the pathology is end-stage [119].”
Nucleic acid oxidation: an early feature of Alzheimer's disease
Bradley‐Whitman, M. A., Timmons, M. D., Beckett, T. L., Murphy, M. P., Lynn, B. C., & Lovell, M. A. (2014) · Journal of Neurochemistry · doi:10.1111/jnc.12444 · Cited by 112
Pathophysiology of Hypoperfusion of the Precuneus in Early A lzheimer's Disease
Miners, J. S., Palmer, J. C., & Love, S. (2015) · Brain Pathology · doi:10.1111/bpa.12331 · Cited by 109
“All of the brains had been subjected to detailed neuropathological assessment, and according to the NIAAA guidelines (38) AD pathology was a sufficient explanation for the dementia in these cases.”
MethodOutcomes after diagnosis of mild cognitive impairment in a large autopsy series
Abner, E. L., Kryscio, R. J., Schmitt, F. A., Fardo, D. W., Moga, D. C., Ighodaro, E. T., Jicha, G. A., Yu, L., Dodge, H. H., Xiong, C., et al. (2017) · Annals of Neurology · doi:10.1002/ana.24903 · Cited by 111
Self-citationHondius, D., Eigenhuis, K. N., Morrema, T. H. J., van der Schors, R. C., van Nierop, P., Bugiani, M., Li, K. W., Hoozemans, J. J. M., Smit, A. B., & Rozemüller, A. J. M. (2018) · Acta Neuropathologica Communications · doi:10.1186/s40478-018-0540-2 · Cited by 111
“Alzheimer’s disease pathology present as Aβ deposits, neurofibrillary tangles and neuritic plaques is staged [12–14] and indicated conform the ABC criteria [15].”
Lewy body pathology and chronic traumatic encephalopathy associated with contact sports
Adams, J. W., Alvarez, V. E., Mez, J., Huber, B. R., Tripodis, Y., Xia, W., Meng, G., Kubilus, C. A., Cormier, K., Kiernan, P. T., et al. (2018) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nly065 · Cited by 109
TREM2 brain transcript-specific studies in AD and TREM2 mutation carriers
Del‐Aguila, J. L., Benítez, B. A., Li, Z., Dube, U., Mihindukulasuriya, K. A., Budde, J., Farias, F., Fernández, M. V., Ibáñez, L., Jiang, S., et al. (2019) · Molecular Neurodegeneration · doi:10.1186/s13024-019-0319-3 · Cited by 106
“Briefly, the Knight-ADRC cohort included 15 participants with late-onset AD (NIA-AA criteria: intermediate or high) [37] with known risk variants in TREM2 gene (Table 2), 12 non-demented controls and 39 sporadic late-onset AD cases.”
MethodSelf-citationMcAleese, K. E., Colloby, S. J., Thomas, A. J., Al‐Sarraj, S., Ansorge, O., Neal, J., Roncaroli, F., Love, S., Francis, P. T., & Attems, J. (2021) · Alzheimer s & Dementia · doi:10.1002/alz.12291 · Cited by 110
Role of the Extracellular Matrix in Alzheimer’s Disease
Sun, Y., Xu, S., Jiang, M., Liu, X., Yang, L., Bai, Z., & Yang, Q. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.707466 · Cited by 119
“Abnormal expression of HA will demyelinate neurons, impair the transmission of nerve signals, limit remyelination, and cause white matter lesions (Figure 1; Montine et al., 2012).”
BackgroundSerrano‐Pozo, A., Qian, J., Monsell, S. E., Frosch, M. P., Betensky, R. A., & Hyman, B. T. (2013) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0000000000000016 · Cited by 106
“The new pathologic diagnostic criteria revise the historical view that the definite diagnosis of AD should reflect the presence of both the typical pathologic changes and a documented history of clinical dementia (3, 4).”
BackgroundMethodInfluentialSelf-citationKaur, U., Banerjee, P., Bir, A., Sinha, M. S., Biswas, A., & Chakrabarti, S. (2015) · Current Topics in Medicinal Chemistry · doi:10.2174/1568026615666150114160543 · Cited by 109
Seibyl, J. P., Catafau, A. M., Barthel, H., Ishii, K., Rowe, C. C., Leverenz, J. B., Ghetti, B. F., Ironside, J. W., Takao, M., Akatsu, H., et al. (2016) · Journal of Nuclear Medicine · doi:10.2967/jnumed.115.161927 · Cited by 108
“Indeed, BSS1 immunohistochemistry is recommended in current neuropathologic guidelines for the assessment of AD pathology (10,11).”
BackgroundBesser, L. M., Teylan, M., & Nelson, P. T. (2019) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlz126 · Cited by 109
“Braak staging for neurofibrillary degeneration (19) (Stages 0–VI) and CERAD semiquantitative scores for neuritic plaque density (17, 20) (none, sparse, moderate, frequent) are available for the vast majority of participants who have NACC Neuropathology Form data.”
BackgroundMethodInfluentialSelf-citationCCL2 is associated with microglia and macrophage recruitment in chronic traumatic encephalopathy
Cherry, J. D., Meng, G., Daley, S. A., Xia, W., Svirsky, S. E., Alvarez, V. E., Nicks, R., Pothast, M. J., Kelley, H. J., Huber, B. R., et al. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-02036-4 · Cited by 112
CryoET of β-amyloid and tau within postmortem Alzheimer’s disease brain
Gilbert, M. A. G., Fatima, N., Jenkins, J., O’Sullivan, T. J., Schertel, A., Halfon, Y., Wilkinson, M., Morrema, T. H. J., Geibel, M., Read, R. J., et al. (2024) · Nature · doi:10.1038/s41586-024-07680-x · Cited by 123
“Brain dissection and neuropathological diagnosis were performed according to international guidelines of Brain Net Europe II (BNE) consortium (http:// www.brainnet-europe.org) and NIA-AA 54 .”
Proposed research criteria for prodromal behavioural variant frontotemporal dementia
Barker, M. S., Gottesman, R. T., Manoochehri, M., Chapman, S., Appleby, B. S., Brushaber, D. E., Devick, K. L., Dickerson, B. C., Domoto‐Reilly, K., Fields, J. A., et al. (2021) · Brain · doi:10.1093/brain/awab365 · Cited by 110
Brain pathologies in extreme old age
Neltner, J. H., Abner, E. L., Jicha, G. A., Schmitt, F. A., Patel, E., Poon, L. W., Marla, G., Green, R. C., Davey, A., Johnson, M. A., et al. (2015) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2015.10.009 · Cited by 106
“Specifically, contrary to recent consensus recommendations for AD neuropathologic diagnosis (Montine, et al., 2012b), there was no Thal staging (Thal, et al., 2006) of A β immunohistochemistry available for most of the cases, so this was left out of the study and represents a study limitation.”
Self-citationSerrano‐Pozo, A., Qian, J., Muzikansky, A., Monsell, S. E., Montine, T. J., Frosch, M. P., Betensky, R. A., & Hyman, B. T. (2016) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlw026 · Cited by 110
Self-citationFerman, T. J., Aoki, N., Crook, J. E., Murray, M. E., Graff‐Radford, N. R., van Gerpen, J. A., Uitti, R. J., Wszołek, Z. K., Graff‐Radford, J., Pedraza, O., et al. (2017) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2017.09.014 · Cited by 105
“The Braak NFT stage [25] and Thal amyloid phase [26]were assigned based on the distribution ofNFTs and senile plaques, respectively, using previously published methods [27,28].”
MethodSelf-citationDementia with Lewy bodies: Impact of co‐pathologies and implications for clinical trial design
Toledo, J. B., Ruiz, C. A., Weil, R. S., Ferreira, D., Rodriguez‐Porcel, F. E., Pilotto, A., Wyman‐Chick, K. A., Grothe, M. J., Kane, J. P. M., Taylor, A., et al. (2022) · Alzheimer s & Dementia · doi:10.1002/alz.12814 · Cited by 112
Toledo, J. B., Korff, A., Shaw, L. M. J., Trojanowski, J. Q., & Zhang, J. (2013) · Acta Neuropathologica · doi:10.1007/s00401-013-1148-z · Cited by 106
“Pathologically, AD is defined by the presence of amyloid-β (Aβ) plaques and neurofibrillary tangles in the brain [35], but the accuracy of the clinical diagnosis of AD verified at autopsy is ~90 %, even in specialized centers [2, 57].”
Self-citationOverlapping but distinct TDP‐43 and tau pathologic patterns in aged hippocampi
Smith, V. D., Bachstetter, A. D., Ighodaro, E. T., Roberts, K. N., Abner, E. L., Fardo, D. W., & Nelson, P. T. (2017) · Brain Pathology · doi:10.1111/bpa.12505 · Cited by 105
“Since dentate granule neurons harbor NFTs without comorbid AD, one could argue that CARTS may be categorized as a tauopathy, but one where the spread of tau NFTs differs from classic AD or primary age-related tauopathy which are graded according to the Braak NFT staging (14, 53).”
Self-citationβ-Amyloid PET and neuropathology in dementia with Lewy bodies
Kantarci, K., Lowe, V. J., Chen, Q., Przybelski, S. A., Lesnick, T. G., Schwarz, C. G., Senjem, M. L., Gunter, J. L., Jack, C. R., Graff‐Radford, J., et al. (2019) · Neurology · doi:10.1212/wnl.0000000000008818 · Cited by 107
“We applied the label of AD only to cases who met the intermediate or high AD designations in the NIA-AA criteria.(28,29)”
MethodSelf-citationCykowski, M. D., Takei, H., Schulz, P. E., Appel, S. H., & Powell, S. Z.-E. (2014) · Acta Neuropathologica Communications · doi:10.1186/s40478-014-0171-1 · Cited by 110
“) utilized established criteria to assess Alzheimer disease (AD) neuropathologic changes, including neurofibrillary changes [20,21] and parenchymal amyloid [22,23], Lewy body pathology [16], ALS pathology [24], cerebral amyloid angiopathy (CAA), and vascular brain injury (VBI).”
MethodA critical review of chronic traumatic encephalopathy
Iverson, G. L., Gardner, A. J., McCrory, P., Zafonte, R., & Castellani, R. J. (2015) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2015.05.008 · Cited by 103
Cheng, H., Wang, M., Li, J., Cairns, N. J., & Han, X. (2013) · Journal of Neurochemistry · doi:10.1111/jnc.12368 · Cited by 103
Self-citationValidity of the 2014 traumatic encephalopathy syndrome criteria for CTE pathology
Mez, J., Alosco, M. L., Daneshvar, D. H., Saltiel, N. A., Baucom, Z., Abdolmohammadi, B., Uretsky, M., Nicks, R., Martin, B. M., Palmisano, J. N., et al. (2021) · Alzheimer s & Dementia · doi:10.1002/alz.12338 · Cited by 107
Devanand, D. P., Lee, S., Huey, E. D., & Goldberg, T. E. (2022) · JAMA Psychiatry · doi:10.1001/jamapsychiatry.2021.4363 · Cited by 105
Pathogenesis and Disease-modifying Therapy in Alzheimer's Disease: The Flat Line of Progress
Castellani, R. J., & Perry, G. L. (2012) · Archives of Medical Research · doi:10.1016/j.arcmed.2012.09.009 · Cited by 104
Bettcher, B. M., Johnson, S. C., Fitch, R., Casaletto, K. B., Heffernan, K. S., Asthana, S., Zetterberg, H., Blennow, K., Carlsson, C. M., Neuhaus, J. M., et al. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-170602 · Cited by 105
Silverberg, N. B., Elliott, C. L., Ryan, L. M., Masliah, E., & Hodes, R. J. (2018) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2018.03.004 · Cited by 112
“The 2012 Committee concluded that criteria should be based primarily on neuropathologic rather than clinical information, and that the criteria needed to include comorbidities and reflect molecular mechanisms of disease [21,22].”
BackgroundSelf-citationManne, S., Kondru, N. C., Hepker, M., Jin, H., Anantharam, V., Lewis, M. M., Huang, X., Kanthasamy, A., & Kanthasamy, A. G. (2019) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-019-09835-4 · Cited by 101
“All tissues had been examined histologically for accurate diagnoses using accepted criteria (Montine 2012) prior to testing in the RT-QuIC assay.”
MethodContribution of mixed pathology to medial temporal lobe atrophy in Alzheimer's disease
de Florès, R., Wisse, L. E. M., Das, S. R., Xie, L., McMillan, C. T., Trojanowski, J. Q., Robinson, J. L., Grossman, M., Lee, E. B., Irwin, D. J., et al. (2020) · Alzheimer s & Dementia · doi:10.1002/alz.12079 · Cited by 103
Self-citationDysregulation of Systemic Immunity in Aging and Dementia
Lutshumba, J., Nikolajczyk, B. S., & Bachstetter, A. D. (2021) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2021.652111 · Cited by 104
“By the age of 55 years old, it is estimated that only 5% of naïve T cells are produced in the thymus (Murray et al., 2003), and overall thymic output is decreased by more than 95% in 60-yearold people compared to 25-year-old people as measured by Frontiers in Cellular Neuroscience |…”
BackgroundMitra, S., Anjum, J., Muni, M., Das, R. C., Rauf, A., Islam, F., Emran, T. B., Semwal, P., Hemeg, H. A., Alhumaydhi, F. A., et al. (2022) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2022.112877 · Cited by 106
Sun, M., Bell, W., LaClair, K. D., Ling, J. P., Han, H., Kageyama, Y., Pletniková, O., Troncoso, J. C., Wong, P. C., & Chen, L. L. (2017) · Acta Neuropathologica · doi:10.1007/s00401-017-1701-2 · Cited by 106
“Neuropathological examinations were performed according to National Institute on Aging-Alzheimer’s Association (NIA-AA) guidelines [9, 20].”
MethodLatimer, C. S., Shively, C. A., Keene, C. D., Jorgensen, M. J., Andrews, R. N., Register, T. C., Montine, T. J., Wilson, A. M., Neth, B. J., Mintz, A., et al. (2019) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2018.06.3057 · Cited by 98
“This work was supported by the Wake Forest Alzheimer’s Disease Core Center (P30- AG049638), the Vervet Research Colony (P40-OD010965), and the Roena B. Kulynych Center for Memory and Cognition Research.”
BackgroundMethodInfluentialSelf-citationSubtypes of dementia with Lewy bodies are associated with α-synuclein and tau distribution
Ferman, T. J., Aoki, N., Boeve, B. F., Aakre, J. A., Kantarci, K., Graff‐Radford, J., Parisi, J. E., van Gerpen, J. A., Graff‐Radford, N. R., Uitti, R. J., et al. (2020) · Neurology · doi:10.1212/wnl.0000000000009763 · Cited by 100
“All AD cases were high likelihood AD using National Institute on Aging–Alzheimer’s Association criteria.(20) Individuals with brainstem-only or amygdala-only Lewy body disease were excluded.”
MethodSelf-citationBasal forebrain cholinergic system in the dementias: Vulnerability, resilience, and resistance
Geula, C., Dunlop, S. R., Ayala, I., Kawles, A. S., Flanagan, M. E., Gefen, T., & Mesulam, M. (2021) · Journal of Neurochemistry · doi:10.1111/jnc.15471 · Cited by 102
Plaque-associated local toxicity increases over the clinical course of Alzheimer disease
Serrano-Pozo, A., Betensky, R. A., Frosch, M. P., & Hyman, B. T. (2016) · The American Journal of Pathology · doi:10.1016/j.ajpath.2015.10.010 · Cited by 100
Self-citationLachén‐Montes, M., González-Morales, A., Zelaya, M. V., Pérez‐Valderrama, E., Ausín, K., Ferrer, I., Fernández‐Irigoyen, J., & Santamaría, E. (2017) · Scientific Reports · doi:10.1038/s41598-017-09481-x · Cited by 97
Bentivenga, G. M., Mammana, A., Baiardi, S., Rossi, M., Ticca, A., Magliocchetti, F., Mastrangelo, A., Poleggi, A., Ladogana, A., Capellari, S., et al. (2024) · Acta Neuropathologica · doi:10.1007/s00401-023-02663-0 · Cited by 106
Braak, H., & Tredici, K. D. (2014) · Acta Neuropathologica · doi:10.1007/s00401-014-1356-1 · Cited by 105
“Nevertheless, application of the criteria required to confirm neuropathologically that the diagnosis of clinically manifest AD [15] does not warrant the disqualification of tau-only cases because the statement that “a diagnosis of AD neuropathologic changes requires at least a minimum threshold level of Aβ deposition”…”
Background[18F]AV‐1451 clustering of entorhinal and cortical uptake in Alzheimer's disease
Whitwell, J. L., Graff‐Radford, J., Tosakulwong, N., Weigand, S. D., Machulda, M. M., Senjem, M. L., Schwarz, C. G., Spychalla, A. J., Jones, D. T., Drubach, D. A., et al. (2018) · Annals of Neurology · doi:10.1002/ana.25142 · Cited by 95
A brief history of “Alzheimer disease”
Knopman, D. S., Petersen, R. C., & Jack, C. R. (2019) · Neurology · doi:10.1212/wnl.0000000000007583 · Cited by 104
“Persons who were considered cognitively normal who had abnormal Alzheimer biomarkers were labeled as “asymptomatic at risk for AD.””
MethodInfluentialMcAleese, K. E., Miah, M., Graham, S., Hadfield, G. M., Walker, L., Johnson, M. A., Colloby, S. J., Thomas, A. J., DeCarli, C. S., Koss, D. J., et al. (2021) · Acta Neuropathologica · doi:10.1007/s00401-021-02376-2 · Cited by 95
Current Concepts of Mixed Pathologies in Neurodegenerative Diseases
Forrest, S. L., & Kovács, G. G. (2022) · Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques · doi:10.1017/cjn.2022.34 · Cited by 104
Kobayashi, E., Nakano, M., Kubota, K., Himuro, N., Mizoguchi, S., Chikenji, T., Otani, M., Mizue, Y., Nagaishi, K., & Fujimiya, M. (2018) · Scientific Reports · doi:10.1038/s41598-018-19442-7 · Cited by 98
Baker, S., Polanco, J. C., & Götz, J. (2016) · Journal of Alzheimer's Disease · doi:10.3233/jad-160371 · Cited by 98
“: +61 7 3346 6329; Fax: +61 733466301; E-mail: j.goetz@uq.edu.au. mortem and in vivo , with the Braak staging, based on phosphorylation at the AT8 phospho-epitope of tau, becoming an integral diagnostic tool [1–3].”
Association of Apolipoprotein E ε4 With Transactive Response DNA-Binding Protein 43
Wennberg, A. M. V., Tosakulwong, N., Lesnick, T. G., Murray, M. E., Whitwell, J. L., Liesinger, A. M., Petrucelli, L., Boeve, B. F., Parisi, J. E., Knopman, D. S., et al. (2018) · JAMA Neurology · doi:10.1001/jamaneurol.2018.3139 · Cited by 96
Self-citationLatimer, C. S., Burke, B. T., Liachko, N. F., Currey, H. N., Kilgore, M. D., Gibbons, L. E., Henriksen, J. C., Darvas, M., Domoto‐Reilly, K., Jayadev, S., et al. (2019) · Acta Neuropathologica Communications · doi:10.1186/s40478-019-0743-1 · Cited by 102
“For microvascular brain injury, samples of bilateral middle frontal gyrus, inferior parietal lobule, super/middle temporal gyrus, and medial occipital lobe including calcarine cortex, as well as bilateral neostriatum (at the level of the anterior commissure) and thalamus, were sampled for histologic analysis using hem…”
Iverson, G. L., Gardner, A. J., Shultz, S. R., Solomon, G. S., McCrory, P. R., ZAFONTE, R. D., Perry, G. L., Hazrati, L., Keene, C. D., & Castellani, R. J. (2019) · Brain · doi:10.1093/brain/awz286 · Cited by 105
Ruffmann, C., Calboli, F. C. F., Bravi, I., Gveric, D. O., Curry, L. K., de Smith, A. J., Pavlou, S., Buxton, J. L., Blakemore, A. I. F., Takousis, P., et al. (2015) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12294 · Cited by 100
Antonell, A., Lladó, A., Altirriba, J., Botta‐Orfila, T., Balasa, M., Fernández, M., Ferrer, I., Sánchez‐Valle, R., & Molinuevo, J. L. (2013) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2012.12.026 · Cited by 101
“Disease evaluation and classification was performed according to international consensus criteria (Hyman et al., 2012; Montine et al., 2012).”
MethodStructure and Mechanism of Action of Tau Aggregation Inhibitors
Cisek, K. K., Cooper, G., Huseby, C. J., & Kuret, J. (2014) · Current Alzheimer Research · doi:10.2174/1567205011666141107150331 · Cited by 98
“Neurofibrillary lesions composed of tau protein are a defining pathology of AD [1, 2].”
BackgroundSwirski, M., Miners, J. S., de Silva, R., Lashley, T., Ling, H., Holton, J. L., Révész, T., & Love, S. (2014) · Alzheimer s Research & Therapy · doi:10.1186/s13195-014-0077-y · Cited by 98
Lesions without symptoms: understanding resilience to Alzheimer disease neuropathological changes
Gómez-Isla, T., & Frosch, M. P. (2022) · Nature Reviews Neurology · doi:10.1038/s41582-022-00642-9 · Cited by 96
Self-citationRodriguez, R. D., Suemoto, C. K., Molina, M., Nascimento, C. F., Leite, R. E. P., Ferretti‐Rebustini, R. E. D. L., Farfel, J. M., Heinsen, H., Nitríni, R., Uéda, K., et al. (2016) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlw034 · Cited by 95
“A neuropathological diagnosis of AD was granted to individuals showing, at least, intermediate AD neuropathologic changes (52).”
MethodABCC9 gene polymorphism is associated with hippocampal sclerosis of aging pathology
Nelson, P. T., Estus, S., Abner, E. L., Parikh, I. J., Malik, M., Neltner, J. H., Ighodaro, E. T., Wang, W., Wilfred, B. R., Wang, L., et al. (2014) · Acta Neuropathologica · doi:10.1007/s00401-014-1282-2 · Cited by 92
“HS-Aging is defined by pathological manifestations: neuron loss, gliosis, and atrophy in the hippocampal formation, not deemed attributable to Alzheimer disease (AD)-type plaques and tangles [1, 44, 51].”
BackgroundMethodSelf-citationCerebrovascular disease promotes tau pathology in Alzheimer’s disease
Laing, K. K., Simoes, S., Baena-Caldas, G. P., Lao, P. J., Kothiya, M., Igwe, K. C., Chesebro, A. G., Houck, A. L., Pedraza, L., Hernandez, A. I., et al. (2020) · Brain Communications · doi:10.1093/braincomms/fcaa132 · Cited by 94
The coarse-grained plaque: a divergent Aβ plaque-type in early-onset Alzheimer’s disease
Boon, B. D. C., Bulk, M., Jonker, A. J., Morrema, T. H. J., van den Berg, E., Popovic, M. M., Walter, J., Kumar, S., van der Lee, S. J., Holstege, H. H., et al. (2020) · Acta Neuropathologica · doi:10.1007/s00401-020-02198-8 · Cited by 99
Grothe, M. J., Moscoso, A., Ashton, N. J., Karikari, T. K., Lantero‐Rodriguez, J., Snellman, A., Zetterberg, H., Blennow, K., Schöll, M., & Initiative, A. D. N. (2021) · Neurology · doi:10.1212/wnl.0000000000012513 · Cited by 99
Kvartsberg, H., Lashley, T., Murray, C. E., Brinkmalm, G., Cullen, N. C., Höglund, K., Zetterberg, H., Blennow, K., & Portelius, E. (2018) · Acta Neuropathologica · doi:10.1007/s00401-018-1910-3 · Cited by 96
Bird, T. D. (2015) · Cited by 92
Neuroimaging correlates with neuropathologic schemes in neurodegenerative disease
Lowe, V. J., Lundt, E. S., Albertson, S. M., Przybelski, S. A., Senjem, M. L., Parisi, J. E., Kantarci, K., Boeve, B., Jones, D. T., Knopman, D., et al. (2019) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2019.03.016 · Cited by 90
“Thal amyloid phase has been incorporated into recent neuropathologic assessment guidelines, along with Braak tangle stage and CERAD neuritic plaque score [17,18].”
MethodSelf-citationPijnenburg, Y. A. L., Verwey, N. A., van der Flier, W. M., Scheltens, P., & Teunissen, C. E. (2015) · Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring · doi:10.1016/j.dadm.2015.11.001 · Cited by 91
“Eleven AD cases had been neuropathologically confirmed [17,18], whereas the 19 cases with a clinical diagnosis of AD according to the criteria of McKhann et al.”
MethodBoros, B. D., Greathouse, K. M., Gearing, M., & Herskowitz, J. H. (2019) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2018.09.003 · Cited by 90
“The Amyloid Braak CERAD (ABC) score was used as a global measure of AD pathology (Montine et al., 2012).”
MethodCopathology in Progressive Supranuclear Palsy: Does It Matter?
Ječmenica‐Lukić, M., Kurz, C., Respondek, G., Grau‐Rivera, O., Compta, Y., Gelpí, E., Troakes, C., Barcelona Brain Bank collaborative group, T. M. P. S. G., Swieten, J. C. V., Giese, A., et al. (2020) · Movement Disorders · doi:10.1002/mds.28011 · Cited by 93
Development of Phenothiazine Hybrids with Potential Medicinal Interest: A Review
Posso, M. C., Domingues, F., Ferreira, S. M. P., & Silvestre, S. (2022) · Molecules · doi:10.3390/molecules27010276 · Cited by 92
“In addition, there are two types of neuropathological changes in this disorder: extracellular β-amyloid plaques (Aβ) and intracellular neurofibrillary tangles [55].”
BackgroundChronic Traumatic Encephalopathy in the Brains of Military Personnel
Priemer, D. S., Iacono, D., Rhodes, C. H., Olsen, C. H., & Perl, D. P. (2022) · New England Journal of Medicine · doi:10.1056/nejmoa2203199 · Cited by 103
Fatima, M., Tan, R. H., Halliday, G. M., & Kril, J. J. (2015) · Acta Neuropathologica Communications · doi:10.1186/s40478-015-0226-y · Cited by 91
“Exclusion criteria were strong family history of a neurological condition, presence of co-existing dementia or neuropathology sufficient to reach criteria for another neurodegenerative disease [18, 19].”
BackgroundLeshchyns’ka, I., Liew, H. T., Shepherd, C. E., Halliday, G. M., Stevens, C. H., Ke, Y. D., Ittner, L. M., & Sytnyk, V. (2015) · Nature Communications · doi:10.1038/ncomms9836 · Cited by 94
Neuronal injury biomarkers and prognosis in ADNI subjects with normal cognition
Toledo, J. B., Weiner, M. W., Wolk, D. A., Da, X., Chen, K., Arnold, S. E., Jagust, W., Jack, C., Reiman, E. M., Davatzikos, C., et al. (2014) · Acta Neuropathologica Communications · doi:10.1186/2051-5960-2-26 · Cited by 89
“Alzheimer’s disease (AD) is the most common neurodegenerative disease (ND), characterized and diagnosed by the presence of tau neurofibrillary tangles and amyloid plaques in the central nervous system [1].”
Self-citationAdler, C. H., Beach, T. G., Zhang, N., Shill, H. A., Driver‐Dunckley, E. D., Caviness, J. N., Mehta, S. H., Sabbagh, M. N., Serrano, G. E., Sue, L. I., et al. (2019) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlz080 · Cited by 93
“annotation for both AD and DLB, due to reportedly poor interobserver agreement on ordinal semiquantitative density scoring, others, including a group sponsored by the NIA-AA in the setting of AD lesions, have found interobserver histopathological density score agreement to be reliable and useful (9).”
BackgroundSelf-citationCSF tau and β-amyloid predict cerebral synucleinopathy in autopsied Lewy body disorders
Irwin, D. J., Xie, S. X., Coughlin, D. G., Nevler, N., Akhtar, R. S., McMillan, C. T., Lee, E. B., Wolk, D. A., Weintraub, D. A., Chen‐Plotkin, A. S., et al. (2018) · Neurology · doi:10.1212/wnl.0000000000005166 · Cited by 94
Self-citationThe complexities of the pathology–pathogenesis relationship in Alzheimer disease
Castellani, R. J., & Perry, G. L. (2014) · Biochemical Pharmacology · doi:10.1016/j.bcp.2014.01.009 · Cited by 91
“A more recent piece of evidence that AD pathology is a response rather than etiology, may be found in the 2012 NIA-Alzheimer Association consensus guidelines [30].”
BackgroundManousopoulou, A., Gatherer, M., Smith, C., Nicoll, J. A. R., Woelk, C. H., Johnson, M., Kalaria, R. N., Attems, J., Garbis, S. D., & Carare, R. O. (2016) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12342 · Cited by 90
Lee, M. Y., Lee, J.-H., Hyeon, S. J., Cho, H., Hwang, Y. J., Shin, J., McKee, A. C., Kowall, N. W., Kim, J., Stein, T. D., et al. (2020) · Aging Cell · doi:10.1111/acel.13153 · Cited by 87
Crist, A. M., Hinkle, K. M., Wang, X., Moloney, C. M., Matchett, B. J., Labuzan, S. A., Frankenhauser, I., Azu, N. O., Liesinger, A. M., Lesser, E. R., et al. (2021) · Nature Communications · doi:10.1038/s41467-021-22399-3 · Cited by 93
“Tangle maturity levels were identified based on the following set of rules: (1) pretangles exhibit diffuse/granular staining, stain less intensely than mature tangles, and contain a nucleus; (2) mature tangles exhibit intense immunostaining (generally throughout the entire neuron) and contain a nucleus; (3) ghost tang…”
BackgroundMethodSelf-citationSánchez‐Juan, P., Valeriano-Lorenzo, E., Ruiz-González, A., Pastor, A. B., Lara, H. R., López-González, F., Zea‐Sevilla, M. A., Valentí, M., Payo, B. F., Ruiz, P., et al. (2024) · Brain · doi:10.1093/brain/awae035 · Cited by 96
“25 Lewy body pathology was assessed through Braak α -synuclein staging (0–6) 26 and Lewy body Pathology Consensus (LPC) classification (0–5).”
MethodToledo, J. B., Bjerke, M., Da, X., Landau, S. M., Foster, N. L., Jagust, W., Jack, C., Weiner, M., Davatzikos, C., Shaw, L. M., et al. (2015) · JAMA Neurology · doi:10.1001/jamaneurol.2014.4829 · Cited by 88
“There are several non– mutually exclusive explanations for this finding: (1) the changes are small and might not be detected owing to the inherent variability of the measurements, (2) a longer follow-up is needed to see larger changes, and (3) the different dynamic ranges of these 2 biomarkers could lead to different…”
Self-citationJack, C. R. (2014) · Acta Neuropathologica · doi:10.1007/s00401-014-1362-3 · Cited by 93
“Three of the four had low probability AD and the fourth was not AD by NIA–AA pathological criteria [12, 26].”
RETRACTED AND REPLACED: Nerve growth factor metabolic dysfunction in Down’s syndrome brains
Iulita, M. F., Carmo, S. D., Ower, A. K., Fortress, A. M., Aguilar, L. F., Hanna, M., Wısnıewskı, T., Granholm, A., Buhusi, M. C., Busciglio, J. A., et al. (2014) · Brain · doi:10.1093/brain/awt372 · Cited by 94
“…examination using DSM-IV (Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, American Psychiatric Association) and ABC criteria (Montine et al., 2012) as well as considering medical and behavioural history obtained through a knowledgeable informant such as a parent/caregiver.”
RetractedXu, J., Begley, P., Church, S. J., Patassini, S., McHarg, S., Kureishy, N., Hollywood, K. A., Waldvogel, H. J., Liu, H., Zhang, S., et al. (2016) · Scientific Reports · doi:10.1038/srep27524 · Cited by 85
Oligomers, fact or artefact? SDS-PAGE induces dimerization of β-amyloid in human brain samples
Watt, A. D., Perez, K. A., Rembach, A., Sherratt, N. A., Hung, L. W., Johanssen, T., McLean, C., Kok, W. M., Hutton, C. A., Fodero‐Tavoletti, M. T., et al. (2013) · Acta Neuropathologica · doi:10.1007/s00401-013-1083-z · Cited by 88
“Pathological diagnosis of AD was made in accordance with the standard criteria set out by the National Institute on Aging, and Reagan Institute Working Group on Diagnostic Criteria for the Neuropathological Assessment of Alzheimer‟s Disease [6,28] and pathological diagnosis of frontotemporal lobar degeneration (FTLD)…”
Approach to atypical Alzheimer’s disease and case studies of the major subtypes
Dickerson, B. C., McGinnis, S. M., Xia, C., Price, B. H., Atri, A., Murray, M. E., Mendez, M. F., & Wolk, D. A. (2017) · CNS Spectrums · doi:10.1017/s109285291600047x · Cited by 86
CCL11 is increased in the CNS in chronic traumatic encephalopathy but not in Alzheimer’s disease
Cherry, J. D., Stein, T. D., Tripodis, Y., Alvarez, V. E., Huber, B. R., Au, R., Kiernan, P. T., Daneshvar, D. H., Mez, J., Solomon, T. M., et al. (2017) · PLoS ONE · doi:10.1371/journal.pone.0185541 · Cited by 87
Tayler, H. M., Miners, J. S., Güzel, Ö., MacLachlan, R. A., & Love, S. (2021) · Brain Pathology · doi:10.1111/bpa.12935 · Cited by 90
“Neuropathological changes, according to National Institute on AgeingAlzheimer's Association (NIA-AA) guidelines (29) were a sufficient explanation for Alzheimer’s disease.”
MethodCairns, N. J., Perrin, R. J., Franklin, E. E., Carter, D., Vincent, B., Xie, M., Bateman, R. J., Benzinger, T., Friedrichsen, K., Brooks, W. S., et al. (2015) · Neuropathology · doi:10.1111/neup.12205 · Cited by 86
Self-citationPop, V., Sorensen, D. W., Kamper, J. E., Ajao, D. O., Murphy, M. P., Head, E., Hartman, R. E., & Badaut, J. (2012) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1038/jcbfm.2012.154 · Cited by 89
Amyloid-β Positron Emission Tomography Imaging Probes: A Critical Review
Kepe, V., Moghbel, M. C., Långström, B., Zaidi, H., Vinters, H. V., Huang, S., Satyamurthy, N., Doudet, D. J., Mishani, E., Cohen, R. M., et al. (2013) · Journal of Alzheimer s Disease · doi:10.3233/jad-130485 · Cited by 87
Self-citationDecreased IL-8 levels in CSF and serum of AD patients and negative correlation of MMSE and IL-1β
Hesse, R., Wahler, A., Gummert, P., Kirschmer, S., Otto, M., Tumani, H., Lewerenz, J., Schnack, C., & von Arnim, C. A. F. (2016) · BMC Neurology · doi:10.1186/s12883-016-0707-z · Cited by 81
“Currently, AD can be definitively diagnosed only after death by post-mortem examination of the brain [25, 26].”
Background
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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