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.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
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.
- 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
“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
Self-citation
Cited by
Sorted by citations
Items 201–300 of 2,854
The basis of cellular and regional vulnerability in Alzheimer’s disease
Mrdjen, D., Fox, E. J., Bukhari, S. A., Montine, K. S., Bendall, S. C., & Montine, T. J. (2019) · Acta Neuropathologica · doi:10.1007/s00401-019-02054-4 · Cited by 162
Self-citationMatchett, B. J., Grinberg, L. T., Theofilas, P., & Murray, M. E. (2021) · Acta Neuropathologica · doi:10.1007/s00401-020-02248-1 · Cited by 168
Robinson, J. L., Molina-Porcel, L., Corrada, M. M., Raible, K., Lee, E. B., Lee, V. M.-Y., Kawas, C. H., & Trojanowski, J. Q. (2014) · Brain · doi:10.1093/brain/awu190 · Cited by 157
Self-citation“New Old Pathologies”: AD, PART, and Cerebral Age-Related TDP-43 With Sclerosis (CARTS)
Nelson, P. T., Trojanowski, J. Q., Abner, E. L., Al-Janabi, O. M., Jicha, G. A., Schmitt, F. A., Smith, C. D., Fardo, D. W., Wang, W.-X., Kryscio, R. J., et al. (2016) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlw033 · Cited by 158
“A basic assumption is that AD is defined by 2 pathologic hallmarks: Ab amyloid plaques and tau neurofibrillary tangles (NFTs) (2).”
BackgroundMethodInfluentialSelf-citationIwata, A., Nagata, K., Hatsuta, H., Takuma, H., Bundo, M., Iwamoto, K., Tamaoka, A., Murayama, S., Saido, T. C., & Tsuji, S. (2013) · Human Molecular Genetics · doi:10.1093/hmg/ddt451 · Cited by 158
Walker, L., Stefanis, L., & Attems, J. (2019) · Journal of Neurochemistry · doi:10.1111/jnc.14698 · Cited by 169
“Of note, a recent study conducted by Irwin and colleagues reported 18% of neuropathologically confirmed DLB cases did not develop a motor disorder as part of their disease course, but the majority exhibited intermediate/high AD-related neuropathologic change, as assessed by National Institute on Ageing – Alzheimer’s A…”
Reed, M. J., Damodarasamy, M., & Banks, W. A. (2019) · Tissue Barriers · doi:10.1080/21688370.2019.1651157 · Cited by 158
“Changes with AD are likely similar to that of aging, with a general increase in BM thickening, but accurate assessment is again complicated by the regional changes that are a foundation of AD progression and classification.(92) AD patients with cerebral amyloid angiopathy (CAA) provide additional difficulty in the stu…”
BackgroundLee, E. B., Kinch, K., Johnson, V. E., Trojanowski, J. Q., Smith, D. H., & Stewart, W. (2019) · Acta Neuropathologica · doi:10.1007/s00401-019-02030-y · Cited by 157
Self-citationYounes, K., Borghesani, V., Montembeault, M., Spina, S., Mandelli, M. L., Welch, A. E., Weis, E., Callahan, P., Elahi, F. M., Hua, A. Y., et al. (2022) · Brain · doi:10.1093/brain/awac217 · Cited by 152
α‐Synuclein RT‐QuIC assay in cerebrospinal fluid of patients with dementia with Lewy bodies
Bongianni, M., Ladogana, A., Capaldi, S., Klotz, S., Baiardi, S., Cagnin, A., Perra, D., Fiorini, M., Poleggi, A., Legname, G., et al. (2019) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.50897 · Cited by 153
Challenges of multimorbidity of the aging brain: a critical update
Jellinger, K. A., & Attems, J. (2015) · Journal of Neural Transmission · doi:10.1007/s00702-014-1288-x · Cited by 154
“For VCI/VaD, recently determined vascular cognitive disease (VCD), despite several proposals (Kalaria et al. 2004; Montine et al. 2012), due to the high variability of morphological findings and multifactorial pathogenesis, no generally accepted mor- phological scheme for quantitating CVLs and no…”
BackgroundMethodInfluentialCSF biomarkers of neuroinflammation in distinct forms and subtypes of neurodegenerative dementia
Abu‐Rumeileh, S., Steinacker, P., Polischi, B., Mammana, A., Bartoletti‐Stella, A., Oeckl, P., Baiardi, S., Zenesini, C., Huss, A. M., Cortelli, P., et al. (2019) · Alzheimer s Research & Therapy · doi:10.1186/s13195-019-0562-4 · Cited by 157
Retinal pathological features and proteome signatures of Alzheimer’s disease
Koronyo, Y., Rentsendorj, A., Mirzaei, N., Regis, G. C., Sheyn, J., Shi, H., Barrón, E., Cook‐Wiens, G., Rodriguez, A., Medeiros, R., et al. (2023) · Acta Neuropathologica · doi:10.1007/s00401-023-02548-2 · Cited by 162
“1 3 scale for Aβ/neuritic plaques was determined by 4G8- and/or Thioflavin-S-positive and/or Gallyas silver-positive plaques measured per 1 mm2 brain area (0 = none; 1 = sparse [≤ 5 plaques]; 3 = moderate [6–20 plaques]; 5 = abundant/frequent [21–30 plaques or greater]; or N/A = not applicable), as previously describe…”
MethodInterleukin-17A: The Key Cytokine in Neurodegenerative Diseases
Chen, J., Liu, X., & Zhong, Y. (2020) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2020.566922 · Cited by 157
Cortical tau load is associated with white matter hyperintensities
McAleese, K. E., Firbank, M., Dey, M., Colloby, S. J., Walker, L., Johnson, M., Beverley, J. R., Taylor, J. P., Thomas, A. J., O’Brien, J. T., et al. (2015) · Acta Neuropathologica Communications · doi:10.1186/s40478-015-0240-0 · Cited by 161
Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease
Illán-Gala, I., Lleo, A., Karydas, A., Staffaroni, A. M., Zetterberg, H., Sivasankaran, R., Grinberg, L. T., Spina, S., Kramer, J. H., Ramos, E. M., et al. (2021) · Neurology · doi:10.1212/wnl.0000000000011226 · Cited by 150
“AD pathology was classified according to the National Institute on Aging–Alzheimer’s Association guidelines for the likelihood of ADpathology as low, intermediate, or high.(33) For secondary analyses, we considered that participants with either a positive amyloid PET or at least comorbid AD (as defined by at least int…”
MethodClinical marker for Alzheimer disease pathology in logopenic primary progressive aphasia
Giannini, L. A. A., Irwin, D. J., McMillan, C. T., Ash, S., Rascovsky, K., Wolk, D. A., Van Deerlin, V. M., Lee, E. B., Trojanowski, J. Q., & Grossman, M. (2017) · Neurology · doi:10.1212/wnl.0000000000004034 · Cited by 144
Self-citationHomotypic fibrillization of TMEM106B across diverse neurodegenerative diseases
Chang, A., Xiang, X., Wang, J., Lee, C., Arakhamia, T., Simjanoska, M., Wang, C., Carlomagno, Y., Zhang, G., Dhingra, S., et al. (2022) · Cell · doi:10.1016/j.cell.2022.02.026 · Cited by 150
Self-citationLazar, A. N., Mourtas, S., Youssef, I., Parizot, C., Dauphin, A., Delatour, B., Antimisiaris, S. G., & Duyckaerts, C. (2013) · Nanomedicine Nanotechnology Biology and Medicine · doi:10.1016/j.nano.2012.11.004 · Cited by 149
Self-citationThe Role of Telomerase Protein TERT in Alzheimer's Disease and in Tau-Related Pathology In Vitro
Spilsbury, A., Miwa, S., Attems, J., & Saretzki, G. (2015) · The Journal of Neuroscience · doi:10.1523/jneurosci.2925-14.2015 · Cited by 140
Recent update on the heterogeneity of the Alzheimer’s disease spectrum
Jellinger, K. A. (2021) · Journal of Neural Transmission · doi:10.1007/s00702-021-02449-2 · Cited by 155
Dahl, M. J., Mather, M., Werkle‐Bergner, M., Kennedy, B. L., Guzman, S. J., Hurth, K. M., Miller, C. A., Qiao, Y., Shi, Y., Chui, H. C., et al. (2021) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2021.11.006 · Cited by 149
Suemoto, C. K., Ferretti‐Rebustini, R. E. D. L., Rodriguez, R. D., Leite, R. E. P., Soterio, L., Brucki, S. M. D., Spera, R. R., Cippiciani, T. M., Farfel, J. M., Filho, A. D. P. C., et al. (2017) · PLoS Medicine · doi:10.1371/journal.pmed.1002267 · Cited by 152
“The new National Institutes of Health-Alzheimer Association criteria [43] were adopted by the BBBABSG in 2013.”
MethodCognitive and Pathological Influences of Tau Pathology in Lewy Body Disorders
Coughlin, D. G., Xie, S. X., Liang, M., Williams, A., Peterson, C. S., Weintraub, D. A., McMillan, C. T., Wolk, D. A., Akhtar, R. S., Hurtig, H. I., et al. (2018) · Annals of Neurology · doi:10.1002/ana.25392 · Cited by 150
“Final neuropathology diagnosis for each case was rendered using standard semiquantitative assessments for each pathology in each brain region.(21) Based on modern neuropathological criteria using Aβ amyloid Thal phase, Braak tau stage, and CERAD plaque score (ie, ABC scoring),(21) we categorized LBD patients into thos…”
MethodSelf-citationProfound degeneration of wake‐promoting neurons in Alzheimer's disease
Oh, J. Y., Eser, R. A., Ehrenberg, A. J., Morales, D. O., Petersen, C., Kudlacek, J., Dunlop, S. R., Theofilas, P., Resende, E. D. P. F., Cosme, C. G., et al. (2019) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2019.06.3916 · Cited by 156
“Subjects with PSP, CBD, and NC scored as A 1B 1C0 according to the National Institute on Aging and Alzheimer’s Association guidelines for the neuropathological assessment of AD [19].”
MethodBoada, M., López, O. L., Olazarán, J., Núñez, L., Pfeffer, M., Paricio, M., Lorites, J., Piñol‐Ripoll, G., Gámez, J. E., Anaya, F., et al. (2020) · Alzheimer's & Dementia · doi:10.1002/alz.12137 · Cited by 143
“Patients received one of three treatments: (1) infusion of”
MethodDing, R., Hase, Y., Ameen‐Ali, K. E., Ndung'u, M., Stevenson, W., Barsby, J., Gourlay, R., Akinyemi, T. O., Akinyemi, R., Uemura, M. T., et al. (2020) · Brain Pathology · doi:10.1111/bpa.12888 · Cited by 145
“Mixed AD and VaD case was classified when there was sufficient degree of AD pathology (45) and significant vascular pathology (Table 1).”
BackgroundMethodResultBraak, H., Zetterberg, H., Tredici, K. D., & Blennow, K. (2013) · Acta Neuropathologica · doi:10.1007/s00401-013-1139-0 · Cited by 148
Davidson, Y. S., Robinson, A., Prasher, V. P., & Mann, D. M. A. (2018) · Acta Neuropathologica Communications · doi:10.1186/s40478-018-0559-4 · Cited by 146
“Alzheimer’s disease (AD) is characterised pathologically by the abundant presence of deposits of amyloid β protein (Aβ) in the brain parenchyma in the form of amyloid plaques, and in blood vessel walls as cerebral amyloid angiopathy (CAA), and neurofibrillary tangles (NFT) composed of hyperphosphorylated tau proteins…”
Whitfield, D., Vallortigara, J., Alghamdi, A., Howlett, D. R., Hortobágyi, T., Johnson, M., Attems, J., Newhouse, S., Ballard, C. G., Thomas, A. J., et al. (2014) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2014.06.015 · Cited by 144
The Amygdala as a Locus of Pathologic Misfolding in Neurodegenerative Diseases
Nelson, P. T., Abner, E. L., Patel, E., Anderson, S., Wilcock, D. M., Kryscio, R. J., Eldik, L. J. V., Jicha, G. A., Gal, Z. T., Nelson, R. S., et al. (2017) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlx099 · Cited by 141
Self-citationKnopman, D. S., Haeberlein, S. B., Carrillo, M. C., Hendrix, J. A., Kerchner, G., Margolin, R. A., Maruff, P. T., Miller, D. S., Tong, G., Tome, M. B., et al. (2018) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2018.03.002 · Cited by 144
“[10] Montine TJ, Phelps CH, Beach TG, Bigio EH, Cairns NJ, Dickson DW, et al.”
BackgroundInfluentialSelf-citationQuadri, M., Mandemakers, W., Grochowska, M. M., Masius, R., Geut, H., Fabrizio, E., Breedveld, G. J., Kuipers, D., Minneboo, M., Vergouw, L. J. M., et al. (2018) · The Lancet Neurology · doi:10.1016/s1474-4422(18)30179-0 · Cited by 143
Gender Differences in Alzheimer Disease: Brain Atrophy, Histopathology Burden, and Cognition
Filon, J. R., Intorcia, A. J., Sue, L. I., Vazquez Arreola, E., Wilson, J., Davis, K. J., Sabbagh, M. N., Belden, C. M., Caselli, R. J., Adler, C. H., et al. (2016) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlw047 · Cited by 143
Self-citationMez, J., Solomon, T. M., Daneshvar, D. H., Murphy, L., Kiernan, P. T., Montenigro, P. H., Kriegel, J., Abdolmohammadi, B., Fry, B. T., Babcock, K. J., et al. (2015) · Alzheimer s Research & Therapy · doi:10.1186/s13195-015-0148-8 · Cited by 153
“Well-established pathological criteria are used for diagnosis of all comorbid diseases, including ALS [30, 31], AD [32–37], Parkinson’s disease and Lewy body disease [38–40], FTLD (including progressive supranuclear palsy, corticobasal degeneration, and Pick’s disease) [41–45], and multiple system atrophy [43].”
BackgroundOverview of Transgenic Mouse Models for Alzheimer's Disease
Myers, A., & McGonigle, P. (2019) · Current Protocols in Neuroscience · doi:10.1002/cpns.81 · Cited by 148
Rabinovici, G. D., Knopman, D. S., Arbizu, J., Benzinger, T. L. S., Donohoe, K. J., Hansson, O., Herscovitch, P., Kuo, P. H., Lingler, J. H., Minoshima, S., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.14338 · Cited by 163
X-linked ubiquitin-specific peptidase 11 increases tauopathy vulnerability in women
Yan, Y., Wang, X., Chaput, D., Shin, M.-K., Koh, Y., Gan, L., Pieper, A. A., Woo, J.-A. A., & Kang, D. E. (2022) · Cell · doi:10.1016/j.cell.2022.09.002 · Cited by 144
Lazar, A. N., Bich, C., Panchal, M., Desbenoît, N., Petit, V. W., Touboul, D., Dauphinot, L., Marquer, C., Laprévôte, O., Brunelle, A., et al. (2012) · Acta Neuropathologica · doi:10.1007/s00401-012-1041-1 · Cited by 141
“The diagnosis was made according to the latest guidelines for the neuropathologic assessment of Alzheimer’s disease [24].”
BackgroundMethodSelf-citationPost-mortem assessment in vascular dementia: advances and aspirations
McAleese, K. E., Alafuzoff, I. I., Charidimou, A., Reuck, J. D., Grinberg, L. T., Hainsworth, A. H., Hortobágyi, T., Ince, P. G., Jellinger, K. A., Gao, J., et al. (2016) · BMC Medicine · doi:10.1186/s12916-016-0676-5 · Cited by 144
“Widely used consensus criteria for the pathological diagnosis of common neurodegenerative disease, such as AD and Lewy body disease, have been available for some time [19–21, 30–33].”
Self-citationAlzheimer's disease cerebrospinal fluid biomarker in cognitively normal subjects
Toledo, J. B., Zetterberg, H., van Harten, A. C., Glodzik, L., Martinez-Lage, P., Bocchio-Chiavetto, L., Rami, L., Hansson, O., Sperling, R., Engelborghs, S., et al. (2015) · Brain · doi:10.1093/brain/awv199 · Cited by 136
“…Alzheimer’s disease biomarkers findings has led to a deeper understanding of the long preclinical stages of Alzheimer’s disease (Jack et al. , 2013 a ) and this is corroborated by the finding of Alzheimer’s disease pathology in autopsies of elderly cognitively normal subjects (Montine et al. , 2012).”
Self-citationCeccom, J., Loukh, N., Lauwers‐Cancès, V., Touriol, C., Nicaise, Y., Gentil, C., Uro‐Coste, E., Pitson, S. M., Maurage, C., Duyckaerts, C. J., et al. (2014) · Acta Neuropathologica Communications · doi:10.1186/2051-5960-2-12 · Cited by 140
Self-citationThe amyloid plaque proteome in early onset Alzheimer’s disease and Down syndrome
Drummond, E., Kavanagh, T., Pires, G., Marta-Ariza, M., Kanshin, E., Nayak, S., Faustin, A., Berdah, V., Ueberheide, B., & Wisniewski, T. (2022) · Acta Neuropathologica Communications · doi:10.1186/s40478-022-01356-1 · Cited by 137
New landscape of the diagnosis of Alzheimer’s disease
Frisoni, G. B., Hansson, O., Nichols, E., Garibotto, V., Schindler, S. E., van der Flier, W. M., Jessen, F., Villain, N., Arenaza-Urquijo, E. M., Crivelli, L., et al. (2025) · The Lancet · doi:10.1016/s0140-6736(25)01294-2 · Cited by 143
Plasma amyloid beta measurements - a desired but elusive Alzheimer's disease biomarker
Toledo, J. B., Shaw, L. M. J., & Trojanowski, J. Q. (2013) · Alzheimer s Research & Therapy · doi:10.1186/alzrt162 · Cited by 139
Self-citationTheofilas, P., Ehrenberg, A. J., Nguy, A. K., Thackrey, J. M., Dunlop, S. R., Mejia, M. B., Alho, A. T. D. L., Leite, R. E. P., Rodriguez, R. D., Suemoto, C. K., et al. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.09.007 · Cited by 134
“AD pathology was staged according to the new NIA-AA guidelines (Montine et al., 2012).”
Akyol, S., Ugur, Z., Yılmaz, A., Ustun, I., Gorti, S. K. K., Oh, K., McGuinness, B., Passmore, P., Kehoe, P. G., Maddens, M. E., et al. (2021) · Cells · doi:10.3390/cells10102591 · Cited by 138
Mattsson, N., Grinberg, L. T., Boxer, A. L., Ossenkoppele, R., Jonsson, M., Seeley, W., Ehrenberg, A. J., Spina, S., Janelidze, S., Rojas-Martinex, J., et al. (2022) · Neurology · doi:10.1212/wnl.0000000000200040 · Cited by 141
“Neuropathology Comprehensive neuropathologic assessments were performed by investigators at the UCSF Neurodegenerative Disease Brain Bank who were blinded to CSF results, following previously described procedures.(32) Classifications of AD,(33) FTLD-TDP, and FTLD-tau (including PSP and corticobasal degeneration [CBD])…”
MethodKostylev, M. A., Kaufman, A. C., Nygaard, H. B., Patel, P., Haas, L. T., Gunther, E. C., Vortmeyer, A., & Strittmatter, S. M. (2015) · Journal of Biological Chemistry · doi:10.1074/jbc.m115.643577 · Cited by 133
“Many of the brains were collected and classified prior to 2012 (49, 50), so diagnosis was made using the National Institutes of Health, NIA, consensus method for the neuropathological diagnosis of AD at the time of autopsy (47, 51, 52).”
MethodChakrabarti, S., Kumar Khemka, V., Banerjee, A., Chatterjee, G., Ganguly, A., & Biswas, A. (2015) · Aging and disease · doi:10.14336/ad.2014.002 · Cited by 134
“There are other accompaying features of AD pathology like neuronal loss, degeneration of synapses, dendrites and axons, gliosis, white matter rarefaction, ganulovacuolar degeneration and cerebral amyloid angiopathy [20, 22].”
BackgroundInfluentialNeuropathological and transcriptomic characteristics of the aged brain
Miller, J. A., Guillozet-Bongaarts, A., Gibbons, L. E., Postupna, N., Renz, A., Beller, A. E., Sunkin, S. M., Ng, L., Rose, S. E., Smith, K. A., et al. (2017) · eLife · doi:10.7554/elife.31126 · Cited by 134
“…of AD and Lewy body disease (LBD; hippocampus and temporal and parietal cortex) (Braak and Braak, 1991; McKeith et al., 1996; Hyman et al., 2012; Montine et al., 2012), hippocampal sclerosis and phospho (p) TDP-43 pathology (hippocampus and temporal cortex) (Nelson et al., 2016), chronic…”
BackgroundSelf-citationAged chimpanzees exhibit pathologic hallmarks of Alzheimer's disease
Edler, M. K., Sherwood, C. C., Meindl, R. S., Hopkins, W. D., Ely, J. J., ERWIN, J. M., Mufson, E. J., Hof, P. R., & Raghanti, M. A. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.07.006 · Cited by 138
“…scoring system based on 86 clinical staging parameters for Aβ and NFT deposition in humans (see Pathology Identification and Scoring) 87 (Attems et al., 2007; Braak et al., 2006; Braak and Braak, 1991; Mirra et al., 1991; Montine et al., 2012; Thal 88 et al., 2002; Vonsattel et al., 1991).”
BackgroundMethodInfluentialThe vascular factor in Alzheimer's disease: A study in Golgi technique and electron microscopy
Baloyannis, S. J., & Baloyannis, I. S. (2012) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2012.07.010 · Cited by 150
Microglial mechanisms drive amyloid-β clearance in immunized patients with Alzheimer’s disease
van Olst, L., Simonton, B., Edwards, A. J., Forsyth, A. V., Boles, J. S., Jamshidi, P., Watson, T. H., Shepard, N., Krainc, T., Argue, B. M., et al. (2025) · Nature Medicine · doi:10.1038/s41591-025-03574-1 · Cited by 164
“According to NIA-AA 2012 consensus guidelines 52 , the AD neuropathologic changes would be categorized as ‘high’.”
The role of extracellular Tau in the spreading of neurofibrillary pathology
Medina, M., & Avila, J. (2014) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2014.00113 · Cited by 161
“As a matter of fact, recent NIA-AA guidelines recommend the assessment of Braak and Braak staging of neurofibrillary degeneration as part of the so called “ABC score” for the neuropathological diagnosis of AD (Montine et al., 2012).”
MethodArteriolosclerosis that affects multiple brain regions is linked to hippocampal sclerosis of ageing
Neltner, J. H., Abner, E. L., Baker, S., Schmitt, F. A., Kryscio, R. J., Jicha, G. A., Smith, C. D., Hammack, E., Kukull, W. A., Brenowitz, W. D., et al. (2013) · Brain · doi:10.1093/brain/awt318 · Cited by 130
“…HS-Ageing is char- acterized by cell loss, gliosis and atrophy in the hippocampal for- mation that is out of proportion with Alzheimer’s disease pathology in the same structures (Jellinger, 1994; Amador-Ortiz and Dickson, 2008; Nelson et al., 2011; Montine et al., 2012; Zarow et al., 2012).”
BackgroundSelf-citationPET staging of amyloidosis using striatum
Hanseeuw, B. J., Betensky, R. A., Mormino, E. C., Schultz, A. P., Sepulcre, J., Becker, J. A., Jacobs, H. I. L., Buckley, R. F., LaPoint, M. R., Vannini, P., et al. (2018) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2018.04.011 · Cited by 134
Distinct Patterns of Sirtuin Expression During Progression of Alzheimer’s Disease
Lutz, M. I., Milenković, I., Regelsberger, G., & Kovács, G. G. (2014) · NeuroMolecular Medicine · doi:10.1007/s12017-014-8288-8 · Cited by 134
Alosco, M. L., Cherry, J. D., Huber, B. R., Tripodis, Y., Baucom, Z., Kowall, N. W., Saltiel, N. A., Goldstein, L. E., Katz, D. I., Dwyer, B. C., et al. (2020) · Acta Neuropathologica · doi:10.1007/s00401-020-02197-9 · Cited by 135
Adamowicz, D. H., Roy, S., Salmon, D. P., Galasko, D. R., Hansen, L. A., Masliah, E., & Gage, F. H. (2016) · Journal of Neuroscience · doi:10.1523/jneurosci.3047-16.2016 · Cited by 133
“Pathological diagnoses of AD and DLB are made using National Institute on Aging-Alzheimer’s Association (NIA-AA) guidelines (Montine et al., 2012) and guidelines proposed by the DLB Consortium (McKeith et al., 2005).”
MethodSelf-citationRoemer, S. F., Grinberg, L. T., Crary, J. F., Seeley, W. W., McKee, A. C., Kovács, G. G., Beach, T. G., Duyckaerts, C. J., Ferrer, I., Gelpí, E., et al. (2022) · Acta Neuropathologica · doi:10.1007/s00401-022-02479-4 · Cited by 130
“Particular emphasis was given to selecting brain regions that would overlap as much as possible with the widely used NIA-AA sampling scheme [38] (Table 4).”
BackgroundMethodInfluentialSelf-citationCerebral amyloid PET imaging in Alzheimer’s disease
Jack, C. R., Barrio, J. R., & Kepe, V. (2013) · Acta Neuropathologica · doi:10.1007/s00401-013-1185-7 · Cited by 137
“3) [9, 75, 76, 106, 107] demonstrate that in Thal Aβ phase 2, Aβ deposition in these”
BackgroundMethodSynaptic phosphorylated α-synuclein in dementia with Lewy bodies
Colom‐Cadena, M., Pegueroles, J., Herrmann, A. G., Henstridge, C. M., Muñoz, L., Querol‐Vilaseca, M., Martín-Paniello, C. S., Luque-Cabecerans, J., Clarimón, J., Belbin, O., et al. (2017) · Brain · doi:10.1093/brain/awx275 · Cited by 130
“In cases with concomitant Alzheimer’s disease pathology, current National Institute of Ageing/Alzheimer Association guidelines were applied (Montine et al., 2012).”
BackgroundMethodSelf-citationNeurons selectively targeted in frontotemporal dementia reveal early stage TDP-43 pathobiology
Nana, A. L., Sidhu, M., Gaus, S. E., Hwang, J., Li, L., Park, Y., Kim, E. J., Pasquini, L., Allen, I. E., Rankin, K. P., et al. (2018) · Acta Neuropathologica · doi:10.1007/s00401-018-1942-8 · Cited by 123
Shireby, G. L., Dempster, E. L., Policicchio, S. S. S., Smith, R. G., Pishva, E., Chioza, B. A., Davies, J. P., Burrage, J., Lunnon, K., Vellame, D. S., et al. (2022) · Nature Communications · doi:10.1038/s41467-022-33394-7 · Cited by 127
NMNAT2:HSP90 Complex Mediates Proteostasis in Proteinopathies
Ali, Y., Allen, H. M., Yu, L., Li‐Kroeger, D., Bakhshizadehmahmoudi, D., Hatcher, A., Aubin, C., Xu, J., Bjorklund, N. L., Taglialatela, G., et al. (2016) · PLoS Biology · doi:10.1371/journal.pbio.1002472 · Cited by 131
“NDAN group had normal cognitive function but possessed the same levels of plaque and tangle burden as AD patients (Braak stage of IV through VI and CERAD rating of moderate to frequent; please see S3 Table for individual subjects) [107,108], suggesting that NDAN subjects are resistant to or have extraordinarily delaye…”
BackgroundPathology and hippocampal atrophy in Alzheimer's disease
Halliday, G. M. (2017) · The Lancet Neurology · doi:10.1016/s1474-4422(17)30343-5 · Cited by 129
Acetylated Tau Neuropathology in Sporadic and Hereditary Tauopathies
Irwin, D. J., Cohen, T. J., Grossman, M., Arnold, S. E., McCarty-Wood, E., Van Deerlin, V. M., Lee, V. M.-Y., & Trojanowski, J. Q. (2013) · The American Journal of Pathology · doi:10.1016/j.ajpath.2013.04.025 · Cited by 125
Self-citationMicroglia in Aging and Alzheimer’s Disease: A Comparative Species Review
Edler, M. K., Mhatre-Winters, I., & Richardson, J. R. (2021) · Cells · doi:10.3390/cells10051138 · Cited by 126
Distinct cytokine profiles in human brains resilient to Alzheimer's pathology
Barroeta-Espar, I., Weinstock, L. D., Perez-Nievas, B. G., Meltzer, A. C., Siao Tick Chong, M., Amaral, A. C., Murray, M. E., Moulder, K. L., Morris, J. C., Cairns, N. J., et al. (2019) · Neurobiology of Disease · doi:10.1016/j.nbd.2018.10.009 · Cited by 133
Self-citationPsychosis in neurodegenerative disease: differential patterns of hallucination and delusion symptoms
Naasan, G., Shdo, S. M., Morenas‐Rodríguez, E., Spina, S., Grinberg, L. T., López, L., Karydas, A., Seeley, W. W., Miller, B. L., & Rankin, K. P. (2020) · Brain · doi:10.1093/brain/awaa413 · Cited by 124
“We classified patients into major categories according to four primary pathologies: (i) Alzheimer’s disease without Lewy body disease (LBD) defined as a primary pathology of Alzheimer’s disease meeting the ADNC criteria (Montine et al., 2012) without concomitant LBD or with LBD showing a Parkinson’s disease Braak stag…”
Epigenomics of Alzheimer's disease
Bennett, D. A., Yu, L., Yang, J., Srivastava, G. P., Aubin, C., & Jager, P. L. D. (2014) · Translational research · doi:10.1016/j.trsl.2014.05.006 · Cited by 126
Neuropathology of dementia in a large cohort of patients with Parkinson's disease
Horvath, J. E., Herrmann, F. R., Burkhard, P. R., Bouras, C., & Kövari, E. (2013) · Parkinsonism & Related Disorders · doi:10.1016/j.parkreldis.2013.05.010 · Cited by 124
“Using the neuropathologic criteria of the National Institute on Aging-Alzheimer’s Association guidelines [23], combining both Ab plaques and NFT scores for the diagnosis of AD, 31 patients (20.”
MethodMicroRNA-146a suppresses ROCK1 allowing hyperphosphorylation of tau in Alzheimer’s disease
Wang, G., Huang, Y. M., Wang, L., Zhang, Y., Xu, J., Zhou, Y., Lourenco, G. F., Zhang, B., Wang, Y., Ren, R., et al. (2016) · Scientific Reports · doi:10.1038/srep26697 · Cited by 126
Pathological Influences on Clinical Heterogeneity in Lewy Body Diseases
Coughlin, D. G., Hurtig, H. I., & Irwin, D. J. (2019) · Movement Disorders · doi:10.1002/mds.27867 · Cited by 132
“The studies listed above have relied on traditional neuropathological assessments which use semiquantitative, subjective ordinal measurements and severity scales that tend to emphasize topography rather than density of pathology.(12,108) Digital histological measurements, using image analysis techniques, offer a poten…”
BackgroundCOVID‐19‐related neuropathology and microglial activation in elderly with and without dementia
Poloni, T. E., Medici, V., Moretti, M., Visoná, S. D., Cirrincione, A., Carlos, A. F., Davin, A., Gagliardi, S., Pansarasa, O., Cereda, C., et al. (2021) · Brain Pathology · doi:10.1111/bpa.12997 · Cited by 124
“Successively, the severity of AD neuropathology was defined according to Montine's scheme (low- intermediate- high AD pathology) (33).”
MethodPetersen, C., Nolan, A. L., de Paula França Resende, E., Miller, Z., Ehrenberg, A. J., Gorno-Tempini, M. L., Rosen, H. J., Kramer, J. H., Spina, S., Rabinovici, G. D., et al. (2019) · Acta Neuropathologica · doi:10.1007/s00401-019-02036-6 · Cited by 113
Magnetic Resonance Spectroscopy in Alzheimer’s Disease: Systematic Review and Meta-Analysis
Wang, H., Tan, L., Wang, H.-F., Liu, Y., Yin, R.-H., Wang, W.-Y., Chang, X.-L., Jiang, T., & Yu, J.-T. (2015) · Journal of Alzheimer’s Disease · doi:10.3233/jad-143225 · Cited by 123
“An ideal diagnostic marker for AD should meet at least three basic requirements: (i) reflect the core neurobiological changes subsequent to the disease process; (ii) be validated by postmortem studies, assuming that the neuropathological findings are the gold standards; and (iii) be measurable as early as possible in…”
BackgroundClinical value of neurofilament and phospho-tau/tau ratio in the frontotemporal dementia spectrum
Meeter, L. H. H., Vijverberg, E. G., Del Campo, M., Rozemuller, A. J. M., Donker Kaat, L., de Jong, F. J., van der Flier, W. M., Teunissen, C. E., van Swieten, J. C., & Pijnenburg, Y. A. L. (2018) · Neurology · doi:10.1212/wnl.0000000000005261 · Cited by 122
“) as low (n = 21, ABC score “not” or “low”) or high (n = 4, ABC score “intermediate” or “high”).(20) For 1 of 26 autopsied patients, insufficient information was available for this scoring.”
BackgroundSIRT1, miR-132 and miR-212 link human longevity to Alzheimer’s Disease
Hadar, A., Milanesi, E., Walczak, M., Puzianowska‐Kuźnicka, M., Kuźnicki, J., Squassina, A., Niola, P., Chillotti, C., Attems, J., Gozes, I., et al. (2018) · Scientific Reports · doi:10.1038/s41598-018-26547-6 · Cited by 123
Paasila, P. J., Davies, D., Kril, J. J., Goldsbury, C. S., & Sutherland, G. T. (2019) · Brain Pathology · doi:10.1111/bpa.12717 · Cited by 120
“04), had greater AD-type pathology according to the ABC scoring system (35) and Braak staging (7) and had lower brain pH (P = 0.”
BackgroundMethodMultisite assessment of NIA‐AA guidelines for the neuropathologic evaluation of Alzheimer's disease
Montine, T. J., Monsell, S. E., Beach, T. G., Bigio, E. H., Bu, Y., Cairns, N. J., Frosch, M., Henriksen, J., Kofler, J., Kukull, W. A., et al. (2016) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2015.07.492 · Cited by 113
“BrainNet has determined that immunohistochemical approaches are superior to histochemical approaches for some lesions, and these findings were incorporated already into the NIA-AA revised guidelines [1,2].”
BackgroundMethodInfluentialSelf-citationVerheijen, J., Van den Bossche, T., van der Zee, J., Engelborghs, S., Sanchez-Valle, R., Lladó, A., Graff, C., Thonberg, H., Pastor, P., Ortega-Cubero, S., et al. (2016) · Acta Neuropathologica · doi:10.1007/s00401-016-1566-9 · Cited by 112
“All three had high-level AD neuropathologic changes (A3B3C3) [34], confirming the clinical AD diagnosis.”
BackgroundIs synaptic loss a unique hallmark of Alzheimer’s disease?
Scheff, S. W., Neltner, J. H., & Nelson, P. T. (2014) · Biochemical Pharmacology · doi:10.1016/j.bcp.2013.12.028 · Cited by 118
“An important step forward for neuropathologists is the most recent (2012) revision of recommendations for the neuropathologic approach to AD diagnoses [30,31].”
BackgroundSelf-citationEvidence of amyloid-β cerebral amyloid angiopathy transmission through neurosurgery
Jaunmuktane, Z., Quaegebeur, A., Taipa, R. J. F., Baptista, M. V., Barbosa, R. P., Koriath, C., Sciot, R., Mead, S., & Brandner, S. (2018) · Acta Neuropathologica · doi:10.1007/s00401-018-1822-2 · Cited by 118
“There were also widespread parenchymal Aβ deposits corresponding to Thal phase 5 and CERAD score 1, whilst neurofibrillary tangle tau pathology did not exceed Braak and Braak stage II, in keeping with low level Alzheimer’s disease neuropathological change [21, 35].”
BackgroundProkop, S., Miller, K. R., Labra, S. R., Pitkin, R. M., Hoxha, K., Narasimhan, S., Changolkar, L., Rosenbloom, A., Lee, V. M.-Y., & Trojanowski, J. Q. (2019) · Acta Neuropathologica · doi:10.1007/s00401-019-02048-2 · Cited by 119
“Stages of AD pathology were defined according to the current diagnostic criteria for AD neuropathological changes [2] as no AD (12 cases), low AD (14 cases), intermediate AD (6 cases) and high AD (17 cases) pathology.”
InfluentialSelf-citationCalderón‐Garcidueñas, A. L., & Duyckaerts, C. J. (2017) · Handbook of clinical neurology · doi:10.1016/b978-0-12-802395-2.00023-7 · Cited by 126
Self-citationCastle, M. J., Baltanás, F. C., Kovács, I., Nagahara, A. H., Barba, D., & Tuszynski, M. H. (2020) · Human Gene Therapy · doi:10.1089/hum.2019.367 · Cited by 117
The Alzheimer's Biomarker Consortium‐Down Syndrome: Rationale and methodology
Handen, B. L., Lott, I. T., Christian, B. T., Schupf, N., O’Bryant, S. E., Mapstone, M. E., Fagan, A. M., Lee, J. H., Tudorascu, D., Wang, M., et al. (2020) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.12065 · Cited by 116
Mormino, E. C., & Papp, K. V. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-179928 · Cited by 124
Profile of cognitive impairment and underlying pathology in multiple system atrophy
Koga, S., Parks, A. C., Uitti, R. J., van Gerpen, J. A., Cheshire, W. P., Wszołek, Z. K., & Dickson, D. W. (2016) · Movement Disorders · doi:10.1002/mds.26874 · Cited by 115
Self-citationYokoi, T., Watanabe, H., Yamaguchi, H., Bagarinao, E., Masuda, M., Imai, K., Ogura, A., Ohdake, R., Kawabata, K., Hara, K., et al. (2018) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2018.00304 · Cited by 116
Arnold, M. R., Coughlin, D. G., Brumbach, B. H., Smirnov, D. S., Concha‐Marambio, L., Farris, C. M., Ma, Y., Kim, Y., Wilson, E. N., Kaye, J. A., et al. (2022) · Annals of Neurology · doi:10.1002/ana.26453 · Cited by 120
“AD neuropathological change was assigned according to NACC guidelines after Braak tau stage, CERAD stage, and Thal phase was determined.(33,37) Distribution of Lewy-related pathology (LRP) was determined via α-synuclein immunohistochemistry staining (OADC: αSyn MJFR1, Abcam; UCSD-ADRC: pSer129 αSyn 81A, Biolegend Labo…”
MethodSlevin, M., Matou, S., Zeinolabediny, Y., Corpas, R., Weston, R., Liu, D., Boras, E., Di Napoli, M., Petcu, E., Sarroca, S., et al. (2015) · Scientific Reports · doi:10.1038/srep13281 · Cited by 115
Locus coeruleus at asymptomatic early and middle Braak stages of neurofibrillary tangle pathology
Andrés‐Benito, P., Fernández‐Dueñas, V., Carmona, M., Escobar, L. A., Torrejón-Escribano, B., Aso, E., Ciruela, F., & Ferrer, I. (2017) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12386 · Cited by 114
The CSF neurofilament light signature in rapidly progressive neurodegenerative dementias
Abu‐Rumeileh, S., Capellari, S., Maserati, M. S., Polischi, B., Martinelli, P., Caroppo, P., Ladogana, A., & Parchi, P. (2018) · Alzheimer s Research & Therapy · doi:10.1186/s13195-017-0331-1 · Cited by 119
“Moreover, in the five autopsied cases, neuropathological assessment revealed an intermediate or high degree of AD pathology [35], whereas in one clinical case, genetic screening showed a pathogenic mutation in PSEN1.”
Amylin as a potential link between type 2 diabetes and alzheimer disease
Martínez-Valbuena, I., Valenti‐Azcarate, R., Amat, I., Riverol, M., Marcilla, I., de Andrea, C. E., Sánchez-Arias, J. A., Carmona‐Abellán, M., Martí‐Andrés, G., Erro, M. E., et al. (2019) · Annals of Neurology · doi:10.1002/ana.25570 · Cited by 120
Polymicrobial Infections In Brain Tissue From Alzheimer’s Disease Patients
Pisa, D., Alonso, R., Fernández-Fernández, A. M., Rábano, A., & Carrasco, L. (2017) · Scientific Reports · doi:10.1038/s41598-017-05903-y · Cited by 114
Bulk, M., Abdelmoula, W. M., Nabuurs, R. J. A., van der Graaf, L. M., Mulders, C. W. H., Mulder, A. A., Jost, C. R., Koster, A. J., van Buchem, M. A., Natté, R., et al. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.10.017 · Cited by 118
Xia, Y., Prokop, S., Gorion, K.-M. M., Kim, J. D., Sorrentino, Z. A., Bell, B. M., Manaois, A. N., Chakrabarty, P., Davies, P., & Giasson, B. I. (2020) · Acta Neuropathologica Communications · doi:10.1186/s40478-020-00967-w · Cited by 118
“Endogenous Table 2 List of Tau Antibodies Antibody Specificity Peptide/Protein Used for Immunization AT8 Combinations of pSer202, pThr205, pSer208 PHF-tau from AD brain [8, 58] CP13 pSer202 PHF-tau from AD braina 7F2 pThr205 193DRSGYS-pS-PG-pS-PG-pT-PGSRSR211-Cys [73] 3G12 pSer208 Cys-202SPGTPG-pS-RSRTP213 2D1 Phospho…”
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.)
About these checks
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.
A language model drew the claims from the paper on 2026-10-18, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-18 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
