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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Pathobiological Subtypes of Alzheimer Disease
Jellinger, K. A. (2020) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000508625 · Cited by 69
Chai, Y. L., Chong, J. R., Weng, J., Howlett, D., Halsey, A., Lee, J. H., Attems, J., Aarsland, D., Francis, P. T., Chen, C. P., et al. (2019) · Brain Pathology · doi:10.1111/bpa.12631 · Cited by 73
Dallaire‐Théroux, C., Callahan, B. L., Potvin, O., Saïkali, S., & Duchesne, S. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-161028 · Cited by 71
Swanson, M. E. V., Murray, H. C., Ryan, B., Faull, R. L. M., Dragunow, M., & Curtis, M. A. (2020) · Scientific Reports · doi:10.1038/s41598-020-68086-z · Cited by 65
d’Abramo, C., D'adamio, L., & Giliberto, L. (2020) · Journal of Personalized Medicine · doi:10.3390/jpm10030116 · Cited by 71
GAD65, GAD67, and GABAT Immunostaining in Human Brain and Apparent GAD65 Loss in Alzheimer's Disease
Schwab, C., Yu, S. Y., Wong, W., McGeer, E. G., & McGeer, P. L. (2013) · Journal of Alzheimer s Disease · doi:10.3233/jad-2012-121330 · Cited by 71
“, 2012 [35]: (A) amyloid- score, (B) neurofibrillary tangle score, (C) neuritic plaque score, (n) no, (l) low, (i) intermediate and (h) high”
Cognitive trajectories and spectrum of neuropathology in S uper A gers: The first 10 cases
Rogalski, E. J., Gefen, T. D., Mao, Q., Connelly, M., Weıntraub, S., Geula, C., Bigio, E. H., & Mesulam, M. M. (2018) · Hippocampus · doi:10.1002/hipo.22828 · Cited by 69
“463 multiple sections) to 111 (frequent) based on a modified version of a published scale (Mirra, Hart, & Terry, 1993; Montine et al., 2012).”
BackgroundSelf-citationKatsumata, Y., Fardo, D. W., Kukull, W. A., & Nelson, P. T. (2018) · Acta Neuropathologica Communications · doi:10.1186/s40478-018-0641-y · Cited by 72
Self-citationWhen Alzheimer's is LATE : Why Does it Matter?
Nelson, P. T., Schneider, J. A., Jicha, G. A., Duong, M. T., & Wolk, D. A. (2023) · Annals of Neurology · doi:10.1002/ana.26711 · Cited by 68
Self-citationJaisa-aad, M., Muñoz‐Castro, C., Healey, M. A., Hyman, B. T., & Serrano‐Pozo, A. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02712-2 · Cited by 76
“We classified donors in three groups corresponding to their ADNC burden [32].”
Self-citationZelaya, M. V., Pérez‐Valderrama, E., de Morentin, X. M., Tuñón, T., Ferrer, I., Luquín, M. R., Fernández‐Irigoyen, J., & Santamaría, E. (2015) · Oncotarget · doi:10.18632/oncotarget.6254 · Cited by 68
Microinfarcts are common and strongly related to dementia in the oldest‐old: The 90+ study
Corrada, M. M., Sonnen, J. A., Kim, R. C., & Kawas, C. H. (2016) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2016.04.006 · Cited by 71
“The presence of microinfarcts was assessed as suggested by the NIA-AA guidelines [8] using one Hematoxylin & Eosin–stained brain tissue section for each of six predefined regions: middle frontal, inferior parietal, superior temporal, occipital, basal ganglia, and thalamus.”
BackgroundMethodClinical Significance of TDP-43 Neuropathology in Amyotrophic Lateral Sclerosis
Cykowski, M. D., Powell, S. Z.-E., Peterson, L. E., Appel, J. E., Rivera, A. L., Takei, H., Chang, E., & Appel, S. H. (2017) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlx025 · Cited by 67
Michael, R., Lenferink, A. T. M., Vrensen, G. F. J. M., Gelpí, E., Barraquer, R. I., & Otto, C. (2017) · Scientific Reports · doi:10.1038/s41598-017-16002-3 · Cited by 68
The need to unify neuropathological assessments of vascular alterations in the ageing brain
Alafuzoff, I., Gelpi, E., Al-Sarraj, S., Arzberger, T., Attems, J., Bodi, I., Bogdanovic, N., Budka, H., Bugiani, O., Englund, E., et al. (2012) · Experimental Gerontology · doi:10.1016/j.exger.2012.06.001 · Cited by 65
“Recent National Institute on Aging—Alzheimer's Association (NIAAA) guidelines for neuropathologic assessment of Alzheimer's Disease (AD) incorporate not only an assessment of AD related pathology but also other pathologies commonly seen in the brains of aged subjects (Hyman et al., 2012; Montine et al., 2012).”
BackgroundMethodInfluentialSelf-citationBrainNet Europe’s Code of Conduct for brain banking
Klioueva, N. M., Rademaker, M. C., Dexter, D. T., Al‐Sarraj, S., Seilhean, D., Streichenberger, N., Schmitz, P., Bell, J. E., Ironside, J. W., Arzberger, T., et al. (2015) · Journal of Neural Transmission · doi:10.1007/s00702-014-1353-5 · Cited by 68
Mitochondrial targeting sequence variants of the CHCHD2 gene are a risk for Lewy body disorders
Ogaki, K., Koga, S., Heckman, M. G., Fiesel, F. C., Ando, M., Labbé, C., Lorenzo‐Betancor, O., Moussaud-Lamodière, E. L., Soto‐Ortolaza, A. I., Walton, R. L., et al. (2015) · Neurology · doi:10.1212/wnl.0000000000002170 · Cited by 67
“based upon thioflavin S fluorescent microscopy.(19) Immunohistochemistry for a-synuclein (non-Ab component precursor; 1:3,000; Mayo Clinic, Jacksonville, FL)(20) was used to establish neuropathologic diagnosis of LBD,(10,21) with deparaffinized and rehydrated sections pretreated with 95% formic acid for 30 minutes and…”
MethodSelf-citationNeuropathology and cognitive performance in self-reported cognitively healthy centenarians
Ganz, A. B., Beker, N., Hulsman, M., Sikkes, S. A. M., NBB, Scheltens, P., Smit, A. B., Rozemüller, A. J. M., Hoozemans, J. J. M., & Holstege, H. H. (2018) · Acta Neuropathologica Communications · doi:10.1186/s40478-018-0558-5 · Cited by 69
Islam, T., Hill, E., Abrahamson, E. E., Servaes, S., Smirnov, D. S., Zeng, X., Sehrawat, A., Chen, Y., Kac, P. R., Kvartsberg, H., et al. (2025) · Nature Medicine · doi:10.1038/s41591-024-03400-0 · Cited by 76
“For more recent cases, pathological diagnosis of AD was made using the National Institute on Aging (NIA)-Alzheimer's Association (AA) consensus criteria 50,92 .”
Mandler, M., Walker, L., Santic, R., Hanson, P. S., Upadhaya, A. R., Colloby, S. J., Morris, C. M., Thal, D. R., Thomas, A. J., Schneeberger, A., et al. (2014) · Acta Neuropathologica · doi:10.1007/s00401-014-1296-9 · Cited by 65
“5 Paired helical filament tau (HP-τ), pyroglutamylated Aβ (pE(3)-Aβ) and non-pe(3)-Aβ loads in different stages of AD pathology [18].”
BackgroundMethodInfluentialSelf-citationMoreno, F., Rabinovici, G. D., Karydas, A., Miller, Z., Hsu, S. C., Legati, A., Fong, J. C., Schonhaut, D. R., Esselmann, H., Watson, C., et al. (2015) · Acta Neuropathologica Communications · doi:10.1186/s40478-015-0190-6 · Cited by 69
Quantitative protein profiling of hippocampus during human aging
Xu, B., Gao, Y., Zhan, S., Xiong, F., Qiu, W., Qian, X., Wang, T., Wang, N., Zhang, D., Yang, Q., et al. (2015) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2015.11.029 · Cited by 67
“The fixed hemi-brain tissue blocks were systematically sampled, paraffin-embedded, and processed for standard histologic and immunohistologic stains as recommended (Montine et al., 2012).”
InfluentialPathogenesis of Alzheimer’s Disease
Castellani, R. J., & Perry, G. L. (2014) · Springer eBooks · doi:10.1007/978-1-4614-5836-4_162 · Cited by 67
Han, J.-Y., Besser, L. M., Xiong, C., Kukull, W. A., & Morris, J. C. (2019) · Alzheimer Disease & Associated Disorders · doi:10.1097/wad.0000000000000291 · Cited by 70
Cognitive Resilience to Alzheimer’s Disease Pathology in the Human Brain
Bowles, E. J. A., Crane, P. K., Walker, R. L., Chubak, J., LaCroix, A. Z., Anderson, M. L., Rosenberg, D. E., Keene, C. D., & Larson, E. B. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-180942 · Cited by 70
Protection of MCC950 against Alzheimer's disease via inhibiting neuronal pyroptosis in SAMP8 mice
Li, J., Zhuang, L., Luo, X., Liang, J., Sun, E., & He, Y. (2020) · Experimental Brain Research · doi:10.1007/s00221-020-05916-6 · Cited by 68
Martini, A. C., Helman, A. M., McCarty, K. L., Lott, I. T., Doran, E., Schmitt, F. A., & Head, E. (2020) · Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring · doi:10.1002/dad2.12113 · Cited by 66
Seo, S. W., Ayakta, N., Grinberg, L. T., Villeneuve, S., Lehmann, M., Reed, B., DeCarli, C., Miller, B. L., Rosen, H. J., Boxer, A. L., et al. (2017) · NeuroImage: Clinical · doi:10.1016/j.nicl.2016.11.008 · Cited by 63
“(Montine et al., 2012)”
Abu‐Rumeileh, S., Mometto, N., Bartoletti‐Stella, A., Polischi, B., Oppi, F., Poda, R., Maserati, M. S., Cortelli, P., Liguori, R., Capellari, S., et al. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180409 · Cited by 69
“Moreover, in 2 autopsied cases, the neuropathological assessment revealed an intermediate or high degree of AD pathology [30].”
Nuclear alpha-synuclein is present in the human brain and is modified in dementia with Lewy bodies
Koss, D. J., Erskine, D., Porter, A., Palmoski, P., Menon, H., Todd, O., Leite, M., Attems, J., & Outeiro, T. F. (2022) · Acta Neuropathologica Communications · doi:10.1186/s40478-022-01403-x · Cited by 65
“Disease conformation for each case was established by a review of clinical history following death and neuropathological assessment according to Lewy Body Braak staging [8], McKeith Criteria [42, 43] and the National institute of ageing—Alzheimer’s Association (NIA-AA) criteria [47], including neurofibrillary tangle B…”
MethodAccumulation of TMEM106B C-terminal fragments in neurodegenerative disease and aging
Perneel, J., Neumann, M., Heeman, B., Cheung, S., den Broeck, M. V., Wynants, S., Baker, M. C., Vicente, C. T., Faura, J., Rademakers, R., et al. (2022) · Acta Neuropathologica · doi:10.1007/s00401-022-02531-3 · Cited by 65
Hyperphosphorylated Tau is Elevated in Alzheimer's Disease with Psychosis
Murray, P. S., Kirkwood, C. M., Gray, M. C., Fish, K. N., Ikonomović, M. D., Hamilton, R. L., Kofler, J., Klunk, W. E., López, O. L., & Sweet, R. A. (2014) · Journal of Alzheimer s Disease · doi:10.3233/jad-131166 · Cited by 67
“Although neuropathologic diagnostic criteria emphasize combining these two stages [59, 60], for more subtle clinical pathologic correlations they are probably best analyzed separately.”
Brain Region-Specific Monoaminergic Correlates of Neuropsychiatric Symptoms in Alzheimer's Disease
Vermeiren, Y., Dam, D. V., Aerts, T., Engelborghs, S., & Deyn, P. P. D. (2014) · Journal of Alzheimer s Disease · doi:10.3233/jad-140309 · Cited by 68
CSF proteins and resting-state functional connectivity in Parkinson disease
Campbell, M. C., Koller, J. M., Snyder, A. Z., Buddhala, C., Kotzbauer, P. T., & Perlmutter, J. S. (2015) · Neurology · doi:10.1212/wnl.0000000000001681 · Cited by 65
Dam, D. V., Vermeiren, Y., Dekker, A. D., Naudé, P. J. W., & Deyn, P. P. D. (2016) · Current Alzheimer Research · doi:10.2174/1567205013666160502123607 · Cited by 68
Variation in TMEM106B in chronic traumatic encephalopathy
Cherry, J. D., Mez, J., Crary, J. F., Tripodis, Y., Alvarez, V. E., Mahar, I., Huber, B. R., Alosco, M. L., Nicks, R., Abdolmohammadi, B., et al. (2018) · Acta Neuropathologica Communications · doi:10.1186/s40478-018-0619-9 · Cited by 67
Evolution of neuronal and glial tau isoforms in chronic traumatic encephalopathy
Cherry, J. D., Kim, S. H., Stein, T. D., Pothast, M. J., Nicks, R., Meng, G., Huber, B. R., Mez, J., Alosco, M. L., Tripodis, Y., et al. (2020) · Brain Pathology · doi:10.1111/bpa.12867 · Cited by 68
“Cases were also assessed for other neurodegenerative diseases using well-established criteria for Alzheimer’s disease (AD) (24,42), Lewy body disease (LBD) (38),”
MethodTau PET imaging with 18F-PI-2620 in aging and neurodegenerative diseases
Mormino, E. C., Toueg, T. N., Azevedo, E. C., Castillo, J. B., Guo, W., Nadiadwala, A., Corso, N. K., Hall, J. N., Fan, A. P., Trelle, A. N., et al. (2020) · European Journal of Nuclear Medicine and Molecular Imaging · doi:10.1007/s00259-020-04923-7 · Cited by 67
“Aggregations of beta-amyloid (Aβ) into extracellular plaques and hyperphosphorylated tau into intracellular neurofibrillary tangles are the hallmark pathological features of Alzheimer’s disease (AD) [1].”
BackgroundDesmarais, P., Gao, A. F., Lanctôt, K. L., Rogaeva, E. A., Ramirez, J., Herrmann, N., Stuss, D. T., Black, S. E., Keith, J. L., & Masellis, M. (2021) · Alzheimer s Research & Therapy · doi:10.1186/s13195-021-00869-6 · Cited by 63
Cognitive Impairment in Older Adults and Therapeutic Strategies
Montine, T. J., Bukhari, S. A., & White, L. R. (2020) · Pharmacological Reviews · doi:10.1124/pharmrev.120.000031 · Cited by 67
Self-citationSemi-Automated Digital Image Analysis of Pick’s Disease and TDP-43 Proteinopathy
Irwin, D. J., Byrne, M. D., McMillan, C. T., Cooper, F. I., Arnold, S. E., Lee, E. B., Deerlin, V. M. V., Xie, S. X., Lee, V. M. ‐., Grossman, M., et al. (2015) · Journal of Histochemistry & Cytochemistry · doi:10.1369/0022155415614303 · Cited by 63
“We chose this size because it maximized the number of tiles for random sampling (i.e. majority of tissue samples had >50 tiles) and the upper limit of inclusion counts per tile to prevent manual count fatigue (Neltner et al. 2012).”
BackgroundMethodResultInfluentialSelf-citationDols‐Icardo, O., García‐Redondo, A., Rojas‐García, R., Borrego‐Hernández, D., Illán‐Gala, I., Muñoz-Blanco, J. L., Rábano, A., Cervera‐Carles, L., Juárez-Rufián, A., Spataro, N., et al. (2017) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp-2017-316820 · Cited by 64
Barupal, D. K., Fan, S., Wancewicz, B., Cajka, T., Sa, M., Showalter, M. R., Baillie, R., Tenenbaum, J. D., Louie, G., Initiative, A. D. N., et al. (2018) · Scientific Data · doi:10.1038/sdata.2018.263 · Cited by 65
Iverson, G. L., Luoto, T. M., Karhunen, P. J., & Castellani, R. J. (2019) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlz045 · Cited by 63
“Slides from selected blocks were immunostained for amyloid-b and stained with Bielschowsky silver impregnation in order to approximate Thal amyloid phase (29), CERAD plaque score (30), and to apply the National Institute on Aging-Alzheimer’s Association (NIA-AA) 2012 approach for documenting AD neuropathologic changes…”
BackgroundMethodKing, A., Bódi, I., & Troakes, C. (2020) · Brain Sciences · doi:10.3390/brainsci10080479 · Cited by 69
“In order to develop a system that combined all these above pathological features, the National Institute on Aging/Alzheimer’s Association (NIA-AA) established scores comprising the extent of Aβ pathology, (A), Braak or modified Braak score, (B) and CERAD plaque score (C) (Table 1) and, from this combination, gave a li…”
BackgroundAmini, M., Pedram, M. M., Moradi, A., & Ouchani, M. (2021) · Computational and Mathematical Methods in Medicine · doi:10.1155/2021/5511922 · Cited by 64
“In some instances, AD is also associated with other diseases that cause dementia as brain vascular injury, Lewy body disease, and Parkinson ’ s disease [15].”
BackgroundElevated Plasma Phosphorylated Tau 181 in Amyotrophic Lateral Sclerosis
Cousins, K. A. Q., Shaw, L. M. J., Shellikeri, S., Dratch, L., Rosario, L., Elman, L. B., Quinn, C. C., Amado, D. A., Wolk, D. A., Tropea, T. F., et al. (2022) · Annals of Neurology · doi:10.1002/ana.26462 · Cited by 66
Self-citationAccumulation of Ambient Black Carbon Particles Within Key Memory-Related Brain Regions
Vanbrabant, K., Dam, D. V., Bongaerts, E., Vermeiren, Y., Bové, H., Hellings, N., Ameloot, M. M., Plusquin, M., Deyn, P. P. D., & Nawrot, T. S. (2024) · JAMA Network Open · doi:10.1001/jamanetworkopen.2024.5678 · Cited by 64
Graham, S. F., Nasaruddin, M. L., Carey, M. P., Hölscher, C., McGuinness, B., Kehoe, P. G., Love, S., Passmore, P., Elliott, C. T., Meharg, A. A., et al. (2014) · Journal of Alzheimer s Disease · doi:10.3233/jad-140684 · Cited by 63
“The neuropathological diagnoses were made using widely accepted criteria [9, 10], uniformly applied according to a standardized protocol by members of the BDR Neuropathology Group.”
MethodEllison, E. M., Abner, E. L., & Lovell, M. A. (2016) · Journal of Neurochemistry · doi:10.1111/jnc.13912 · Cited by 64
Hunt, A. P., Minett, G. M., Gibson, O. R., Kerr, G., & Stewart, I. B. (2020) · Frontiers in Physiology · doi:10.3389/fphys.2019.01556 · Cited by 68
“The pathophysiology of Alzheimer’s is evidenced by intracellular and extracellular amyloid-β plaques as well as neurofibrillary tangles of hyperphosphorylated tau (Montine et al., 2012; Ciechanover and Kwon, 2017).”
BackgroundRegional correlation of biochemical measures of amyloid and tau phosphorylation in the brain
Horie, K., Barthélemy, N. R., Mallipeddi, N., Li, Y., Franklin, E. E., Perrin, R. J., Bateman, R. J., & Sato, C. (2020) · Acta Neuropathologica Communications · doi:10.1186/s40478-020-01019-z · Cited by 62
Nag, S., & Schneider, J. A. (2023) · Nature Reviews Neurology · doi:10.1038/s41582-023-00846-7 · Cited by 69
Self-citationTopographic staging of tau positron emission tomography images
Schwarz, A. J., Shcherbinin, S., Slieker, L. J., Risacher, S. L., Charil, A., Irizarry, M. C., Fleisher, A., Southekal, S. S., Joshi, A. D., Devous, M. D., et al. (2018) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1016/j.dadm.2018.01.006 · Cited by 63
Takeuchi, R., Tada, M., Shiga, A., Toyoshima, Y., Konno, T., Sato, T., Nozaki, H., Kato, T., Horie, M., Shimizu, H., et al. (2016) · Acta Neuropathologica Communications · doi:10.1186/s40478-016-0335-2 · Cited by 66
CRISPR-Cas9: A Promising Genome Editing Therapeutic Tool for Alzheimer’s Disease—A Narrative Review
Barman, N. C., Khan, M. N. M., Islam, M., Nain, Z., Roy, R. K., Haque, A., & BARMAN, S. K. (2020) · Neurology and Therapy · doi:10.1007/s40120-020-00218-z · Cited by 65
“with language, mood, movement, and physiological dysfunction [5, 6].”
BackgroundTowards clinical application of tau PET tracers for diagnosing dementia due to Alzheimer's disease
Ossenkoppele, R., & Hansson, O. (2021) · Alzheimer's & Dementia · doi:10.1002/alz.12356 · Cited by 62
“63 We discuss in this section how tauPET relates to (1) AβPET/CSF, (2) CSFphosphorylated tau, and (3) neurodegenerative markers.”
BackgroundUemura, M. T., Robinson, J. L., Cousins, K. A. Q., Tropea, T. F., Kargilis, D., McBride, J. D., Suh, E. R., Xie, S. X., Xu, Y., Porta, S., et al. (2021) · Acta Neuropathologica · doi:10.1007/s00401-021-02383-3 · Cited by 59
“After their exclusion, 1,061 cases were grouped into four cohorts by LBD subtype and ADNC according to 3rd and 4th McKeith criteria [23, 24] and National Institute on Aging and the Alzheimer’s Association (NIA-AA) guidelines [27, 28]: (1) LBD cohort, with cases that had more severe LBD than ADNC; (2) AD cohort, with c…”
MethodSelf-citationNilsson, J., Cousins, K. A. Q., Gobom, J., Portelius, E., Chen‐Plotkin, A. S., Shaw, L. M. J., Grossman, M., Irwin, D. J., Trojanowski, J. Q., Zetterberg, H., et al. (2022) · Alzheimer s & Dementia · doi:10.1002/alz.12809 · Cited by 62
Self-citationCell type-specific changes identified by single-cell transcriptomics in Alzheimer’s disease
Luquez, T., Gaur, P., Kosater, I. M., Lam, M., Lee, D. I., Mares, J. A., Paryani, F., Yadav, A., & Menon, V. (2022) · Genome Medicine · doi:10.1186/s13073-022-01136-5 · Cited by 64
Nanomedicine in the Management of Alzheimer’s Disease: State-of-the-Art
Ullah, S. N. M. N., Afzal, O., Altamimi, A. S. A., Ather, H., Sultana, S., Almalki, W. H., Bharti, P., Sahoo, A., Dwivedi, K., Khan, G., et al. (2023) · Biomedicines · doi:10.3390/biomedicines11061752 · Cited by 68
Cryo-EM structure of Alzheimer’s disease tau filaments with PET ligand MK-6240
Kunach, P., Vaquer‐Alicea, J., Smith, M. S., Monistrol, J., Hopewell, R., Moquin, L., Therriault, J., Tissot, C., Rahmouni, N., Massarweh, G., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-52265-x · Cited by 64
“The authors find a primary binding pocket similar to other tau PET ligands, identify key amino acid interactions, and the binding orientation.”
A practical overview of the use of amyloid-PET Centiloid values in clinical trials and research
Iaccarino, L., Burnham, S. C., Tunali, I., Wang, J., Navitsky, M. A., Arora, A., & Pontecorvo, M. J. (2025) · NeuroImage Clinical · doi:10.1016/j.nicl.2025.103765 · Cited by 68
Protective properties of lysozyme on β-amyloid pathology: implications for Alzheimer disease
Helmfors, L., Boman, A., Civitelli, L., Nath, S., Sandin, L., Janefjord, C., McCann, H., Zetterberg, H., Blennow, K., Halliday, G. M., et al. (2015) · Neurobiology of Disease · doi:10.1016/j.nbd.2015.08.024 · Cited by 62
“Cases were selected based on their characterization with Alzheimer disease according to established neuropathological criteria (Montine et al., 2012).”
The Neuroanatomy of the Reticular Nucleus Locus Coeruleus in Alzheimer’s Disease
Giorgi, F. S., Ryskalin, L., Ruffoli, R., Biagioni, F., Limanaqi, F., Ferrucci, M., Busceti, C. L., Bonuccelli, U., & Fornai, F. (2017) · Frontiers in Neuroanatomy · doi:10.3389/fnana.2017.00080 · Cited by 63
“Cortical pathology consists of: (i) argyrophilic structures formed by abnormal intracellular aggregates of phospho-Tau (P-Tau) fibrils, known as neurofibrillary tangles (NFT); and (ii) extracellular aggregates of Aβ known as amyloid plaques (Hyman et al., 2012; Montine et al., 2012).”
BackgroundMartínez, D. B., Soldevilla, M. A. G., Santiago, A. P., & Martínez, J. T. (2019) · Medicine - Programa de Formación Médica Continuada Acreditado · doi:10.1016/j.med.2019.03.012 · Cited by 65
Lumsden, A. L., Rogers, J. T., Majd, S., Newman, M., Sutherland, G. T., Verdile, G., & Lardelli, M. T. (2018) · Frontiers in Neuroscience · doi:10.3389/fnins.2018.00533 · Cited by 60
Chin, K. S., Yassi, N., Churilov, L. P., Masters, C. L., & Watson, R. (2020) · Parkinsonism & Related Disorders · doi:10.1016/j.parkreldis.2020.09.030 · Cited by 60
Lochocki, B., Boon, B. D. C., Verheul, S. R., Zada, L., Hoozemans, J. J. M., Ariese, F., & de Boer, J. F. (2021) · Communications Biology · doi:10.1038/s42003-021-01981-x · Cited by 61
Ferrer, I., Andrés‐Benito, P., Ausín, K., Pamplona, R., del Río, J. A., Fernández‐Irigoyen, J., & Santamaría, E. (2021) · Brain Pathology · doi:10.1111/bpa.12996 · Cited by 61
Stathas, S., Alvarez, V. E., Xia, W., Nicks, R., Meng, G., Daley, S. A., Pothast, M. J., Shah, A., Kelley, H. J., Esnault, C. D., et al. (2021) · Alzheimer s & Dementia · doi:10.1002/alz.12502 · Cited by 62
Arnold, S. E., Toledo, J. B., Appleby, D. H., Xie, S. X., Wang, W., Baek, Y., Wolk, D. A., Lee, E. B., Miller, B. L., Lee, V. M. ‐., et al. (2013) · The Journal of Comparative Neurology · doi:10.1002/cne.23430 · Cited by 66
“…topical to this study according to established criteria and standards of practice (Schmidt et al., 1988; Neumann et al., 2006; Uryu et al., 2008; Montine et al., 2012) as well as to recognize other neuropathological conditions (e.g., neoplasms, infections, Creutzfeldt-Jakob) that were not…”
BackgroundMethodSelf-citationLachén‐Montes, M., González-Morales, A., de Morentin, X. M., Pérez‐Valderrama, E., Ausín, K., Zelaya, M. V., Serna, A., Aso, E., Ferrer, I., Fernández‐Irigoyen, J., et al. (2016) · Journal of Proteomics · doi:10.1016/j.jprot.2016.07.032 · Cited by 61
Dekens, D. W., Naudé, P. J. W., Engelborghs, S., Vermeiren, Y., Dam, D. V., Voshaar, R. C. O., Eisel, U. L. M., & Deyn, P. P. D. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160330 · Cited by 61
Serrano‐Pozo, A., Aldridge, G. M., & Zhang, Q. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-170184 · Cited by 59
Edlow, B. L., Keene, C. D., Perl, D. P., Iacono, D., Folkerth, R. D., Stewart, W. B., Jr., Donald, C. L. M., Augustinack, J. C., Diaz-Arrastia, R. R., Estrada, C., et al. (2018) · Journal of Neurotrauma · doi:10.1089/neu.2017.5457 · Cited by 59
Thomas, A. J., Mahin-Babaei, F., Saidi, M., Lett, D. J., Taylor, J., Walker, L., & Attems, J. (2018) · Alzheimer s Research & Therapy · doi:10.1186/s13195-018-0356-0 · Cited by 64
Receptors for pro‐resolving mediators are increased in Alzheimer's disease brain
Emre, C., Hjorth, E., Bharani, K., Carroll, S., Granholm, A., & Schultzberg, M. (2020) · Brain Pathology · doi:10.1111/bpa.12812 · Cited by 60
“After characterizing neuropathological changes with standardized grading systems, scoring was adapted to a 4-point scale (0–3) with three parameters including: Braak stage 0-VI, Thal phases including both neuritic and diffuse plaques, and CERAD (neuritic plaques only, A–C) (Table 2) according to NIA—Alzheimer's Associ…”
MethodRegional and hemispheric susceptibility of the temporal lobe to FTLD-TDP type C pathology
Borghesani, V., Battistella, G., Mandelli, M. L., Welch, A. E., Weis, E., Younes, K., Neuhaus, J. M., Grinberg, L. T., Seeley, W., Spina, S., et al. (2020) · NeuroImage Clinical · doi:10.1016/j.nicl.2020.102369 · Cited by 61
“Primary and secondary pathological changes were established by the pathologist based on consensus criteria (Kovacs et al., 2016; Mackenzie et al., 2011; McKeith et al., 1996; Montine et al., 2012).”
Singh, A., Allen, D., Fracassi, A., Tumurbaatar, B., Natarajan, C., Scaduto, P., Woltjer, R., Kayed, R., Limon, A., Krishnan, B., et al. (2020) · Journal of Alzheimer's Disease · doi:10.3233/jad-200716 · Cited by 56
Ghirelli, A., Tosakulwong, N., Weigand, S. D., Clark, H. M., Ali, F., Botha, H., Duffy, J. R., Utianski, R. L., Buciuc, M., Murray, M. E., et al. (2020) · Annals of Neurology · doi:10.1002/ana.25893 · Cited by 59
“No cases in this study met criteria for high ADNC.32,44 Other series have similarly shown that concomitant plaques and NFTs are relatively 1018 Volume 88, No. 5 ANNALS of Neurology common in FTLD,13–18 with frequencies of NFTs ranging from 38% to 80%13,14,17 and plaques ranging from 22% to 63%.14–17 Coexistence of hig…”
ResultInfluentialSelf-citationClinicopathologic subtype of Alzheimer's disease presenting as corticobasal syndrome
Sakae, N., Josephs, K. A., Litvan, I., Murray, M. E., Duara, R., Uitti, R. J., Wszołek, Z. K., van Gerpen, J. A., Graff‐Radford, N. R., & Dickson, D. W. (2019) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2019.04.011 · Cited by 66
“5%), all meeting criteria for intermediate- to high-likelihood AD using National Institute on Aging–Alzheimer Association criteria [27].”
BackgroundSelf-citationGuennewig, B., Lim, J., Marshall, L. L., McCorkindale, A. N., Paasila, P. J., Patrick, E., Kril, J. J., Halliday, G. M., Cooper, A. A., & Sutherland, G. T. (2021) · Scientific Reports · doi:10.1038/s41598-021-83872-z · Cited by 59
Synapse Stability in the Precuneus Early in the Progression of Alzheimer's Disease
Scheff, S. W., PRICE, D. A., Schmitt, F. A., Roberts, K. N., Ikonomović, M. D., & Mufson, E. J. (2013) · Journal of Alzheimer s Disease · doi:10.3233/jad-122353 · Cited by 60
“The neuropathologic profile of individuals with AD includes increased levels of both diffuse plaques (DP) and neuritic amyloid plaques (NP) throughout neocortical association areas as well as an abundance of neurofibrillary tangles (NFT) primarily in the mesial temporal cortex [1, 2].”
Chronic Traumatic Encephalopathy Presenting as Alzheimer’s Disease in a Retired Soccer Player
Grinberg, L. T., Anghinah, R., Nascimento, C. F., Amaro, E., Leite, R. P., Martin, M. D. G. M., Naslavsky, M. S., Takada, L. T., Filho, W. J., Pasqualucci, C. A., et al. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160312 · Cited by 59
Contreras, J. A., Goñi, J., Risacher, S. L., Amico, E., Yoder, K. K., Džemidžić, M., West, J. D., McDonald, B. C., Farlow, M. R., Sporns, O., et al. (2016) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1016/j.dadm.2016.12.004 · Cited by 60
“This is an open access article under the CC BY-NC-ND commons.org/licenses/by-nc-nd/4.0/).”
BackgroundInfluentialComparison of symptomatic and asymptomatic persons with primary age-related tauopathy
Besser, L. M., Crary, J. F., Mock, C., & Kukull, W. A. (2017) · Neurology · doi:10.1212/wnl.0000000000004521 · Cited by 59
“PART definite overlaps with the “not AD neuropathologic change” and AS with the “low AD neuropathologic change” categories set forth by the National Institute on Aging (NIA)–Alzheimer’s Association guidelines for AD neuropathologic assessment.(19) PART-definite participants were less often symptomatic (58%) than AS pa…”
Methodde la Monte, S. M. (2019) · Advances in experimental medicine and biology · doi:10.1007/978-981-13-3540-2_4 · Cited by 59
Chronic traumatic encephalopathy pathology in multiple system atrophy
Koga, S., Dickson, D. W., & Bieniek, K. F. (2016) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlw073 · Cited by 58
Self-citationLiu, P., Yang, Q., Yu, N., Cao, Y., Wang, X., Wang, Z., Qiu, W.-Y., & Ma, C. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210461 · Cited by 59
Canine Cognitive Dysfunction (CCD) scores correlate with amyloid beta 42 levels in dog brain tissue
Urfer, S. R., Darvas, M., Czeibert, K., Sándor, S., Promislow, D., Creevy, K. E., Kubinyi, E., & Kaeberlein, M. R. (2021) · GeroScience · doi:10.1007/s11357-021-00422-1 · Cited by 63
Ruíz‐Barrio, I., Miki, Y., Jaunmuktane, Z., Warner, T. T., & Pablo‐Fernández, E. D. (2022) · Neurology · doi:10.1212/wnl.0000000000201659 · Cited by 58
“Alzheimer disease neuropathologic changes were assessed using the ABC scoring system proposed by the National Institute on Aging (absent, low, intermediate, and high).(32) Assessment of cerebrovascular pathology following the Vascular Cognitive Impairment Neuropathology Guidelines(33) including semiquantitative gradin…”
MethodVandeVrede, L. A., Cho, H., Sanderson‐Cimino, M. E., Wekselman, F., Cobigo, Y., Gorno‐Tempini, M. L., Heuer, H. W., Kramer, J. H., Lago, A. L., Leichter, D., et al. (2025) · JAMA Neurology · doi:10.1001/jamaneurol.2024.5017 · Cited by 68
A 2-process model for neuropathology of Alzheimer's disease
Mungas, D., Tractenberg, R., Schneider, J. A., Crane, P. K., & Bennett, D. A. (2014) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2013.08.007 · Cited by 58
“Alzheimer’s disease (AD) has been defined by neuropathological features of neuritic plaques and neurofibrillary tangles since it was first identified in 1906 and these two types of neuropathology continue to constitute the basis for the neuropathological diagnosis of AD (Hyman, 1997; Hyman et al., 2012; Montine et al.…”
Self-citationKoga, S., Lin, W. ‐., Walton, R. L., Ross, O. A., & Dickson, D. W. (2018) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12485 · Cited by 57
Self-citationGoossens, J., Bjerke, M., Mossevelde, S. V., den Bossche, T. V., Goeman, J., Vil, B. B. D., Sieben, A., Martin, J., Cras, P. P., Deyn, P. P. D., et al. (2018) · Alzheimer s Research & Therapy · doi:10.1186/s13195-018-0364-0 · Cited by 59
Neuropathological fingerprints of survival, atrophy and language in primary progressive aphasia
Mesulam, M. M., Coventry, C., Bigio, E. H., Sridhar, J., Gill, N. P., Fought, A. J., Zhang, H., Thompson, C. K., Geula, C., Gefen, T. D., et al. (2021) · Brain · doi:10.1093/brain/awab410 · Cited by 63
Self-citationLevites, Y., Dammer, E. B., Ran, Y., Tsering, W., Duong, D. M., Abreha, M. H., Gadhavi, J. D., Lolo, K., Trejo‐Lopez, J. A., Phillips, J., et al. (2024) · Cell Reports Medicine · doi:10.1016/j.xcrm.2024.101669 · Cited by 60
Franklin, E. E., Perrin, R. J., Vincent, B. D., Baxter, M., Morris, J. C., Cairns, N. J., & Initiative, A. D. N. (2015) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2015.05.010 · Cited by 57
“This new data acquisition form reflects the new NACC guidelines for the standard neuropathologic assessment of AD at NIAfunded Alzheimer Disease Centers (ADCs) and incorporates the new neuropathologic diagnostic criteria for AD of the National Institute on Aging-Alzheimer’s Association (NIA-AA) [2], which underscore t…”
BackgroundMethodSelf-citationHippocampal Endosomal, Lysosomal, and Autophagic Dysregulation in Mild Cognitive Impairment
Perez, S. E., He, B., Nadeem, M., Wuu, J., Ginsberg, S. D., Ikonomović, M. D., & Mufson, E. J. (2015) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0000000000000179 · Cited by 57
“The TDP-43 inclusions are common pathologic hallmarks of amyotrophic lateral sclerosis and frontotemporal dementia (105) and have been associated with autophagy dysfunction in both disorders (106, 107).”
BackgroundInfluential
Metadata
- Authors
- Montine, T. J., Phelps, C. H., Beach, T. G., Bigio, E. H., Cairns, N. J., Dickson, D. W., Duyckaerts, C., Frosch, M. P., Masliah, E., Mirra, S. S., Nelson, P. T., Schneider, J. A., Thal, D. R., Trojanowski, J. Q., Vinters, H. V., & Hyman, B. T.
- Affiliations
- University of Washington (US)
- National Institutes of Health (US)
- Banner Sun Health Research Institute (US)
- Northwestern University (US)
- Washington University in St. Louis (US)
- Mayo Clinic (US)
- Pitié-Salpêtrière Hospital (FR)
- Harvard University (US)
- University of California San Diego (US)
- SUNY Downstate Health Sciences University (US)
- University of Kentucky (US)
- Rush University Medical Center (US)
- Universität Ulm (DE)
- University of Pennsylvania (US)
- University of California, Los Angeles (US)
- Corresponding author
- Montine, Thomas J.
- ORCID
- Venue
- Acta Neuropathologica
- Published
- 2011-11-20
- Volume
- 123
- Issue
- 1
- Pages
- 1-11
- ISSN
- 0001-6322 (ISSN-L)
- 1432-0533
- PMC
- PMC3268003
- OpenAlex
- W2128228199
- Cited by
- 2,894
- References
- 66
- Citations by year
- 2026: 254 · 2025: 290 · 2024: 329 · 2023: 251 · 2022: 284 · 2021: 257 · 2020: 244 · 2019: 183 · 2018: 164 · 2017: 148 · 2016: 144 · 2015: 136 · 2014: 92 · 2013: 69 · 2012: 46
- FWCI
- 39.19
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Acta Neuropathologica (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5u01ag024904-10)
- National Institute on Aging (U01-AG-024904, R01AG017917, AG18840, AG-15819, R01AG015866, P30AG028383, R01AG042210, R01AG018440, U01AG016976, P50AG005131, P50AG016570, P01AG003949, P30AG010124, R01AG015819, P30AG010161, AG24904, P50AG005681, P30AG019610, P01AG003991, P50AG005136, P50AG005134, P30AG013854, U19AG010483, RF1AG015819, P01AG012435, U19AG024904, P30AG062421)
- National Institute of Neurological Disorders and Stroke (P50NS062684)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, amyloid-beta deposition, neurofibrillary tangles, neuritic plaques, ABC score, Lewy body disease, vascular brain injury, hippocampal sclerosis, TDP-43 inclusions, staining techniques, clinicopathological correlation, preclinical Alzheimer's disease
- MeSH terms
- Alzheimer Disease, Brain, Cerebrovascular Disorders, DNA-Binding Proteins, Hippocampus, Humans, Sclerosis, United States, Cerebrovascular Trauma, Lewy Body Disease, National Institute on Aging (U.S.)
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