The DOI matches its Crossref record; 66 of the 66 references it cites were found in a registry or an index; 27 of the 65 sources its claims cite were checked for support.
National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach
Open accessAbstract
We present a practical guide for the implementation of recently revised National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease (AD). Major revisions from previous consensus criteria are: (1) recognition that AD neuropathologic changes may occur in the apparent absence of cognitive impairment, (2) an "ABC" score for AD neuropathologic change that incorporates histopathologic assessments of amyloid β deposits (A), staging of neurofibrillary tangles (B), and scoring of neuritic plaques (C), and (3) more detailed approaches for assessing commonly co-morbid conditions such as Lewy body disease, vascular brain injury, hippocampal sclerosis, and TAR DNA binding protein (TDP)-43 immunoreactive inclusions. Recommendations also are made for the minimum sampling of brain, preferred staining methods with acceptable alternatives, reporting of results, and clinico-pathologic correlations.
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11 No full text of the sources · 9 Partly supported · 4 Supported · 3 Supported so far · 1 Own interpretation · accuracy not yet measured
Every source the paper cites for this claim was checked and supports it.
In the paper
“recognition that AD neuropathologic changes may occur in the apparent absence of cognitive impairment”
- Also stated in: § CLINICO-PATHOLOGIC CORRELATION · plain
“Similar neuropathologic changes, albeit usually at lower levels, also occur in individuals who did not show cognitive or behavioral impairments during life [54].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > Abstract
What the sources say
- Supportedcites [54] Sperling RA, Aisen PS, Beckett LA et al (2011) Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement 7:280–292 source
Section 6 reports that AD-related biomarker abnormalities can be detected before overt clinical symptoms and that Aβ accumulation occurs in clinically normal older adults. Section 2 also notes that some people have diagnostic AD neuropathological features at autopsy without having developed dementia during life. No page numbers are available in our copy. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § CLINICO-PATHOLOGIC CORRELATION · plain
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“LBs may be detected in neurons of medulla, pons and midbrain with hematoxylin and eosin (H&E)-stained sections; however, greater sensitivity can be achieved with immunohistochemistry for α-synuclein and this approach is strongly preferred [3,4,13].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE > Method
What the sources say
- Partly supportedcites [3] Alafuzoff I, Parkkinen L, Al-Sarraj S et al (2008) Assessment of alpha-synuclein pathology: a study of the BrainNet Europe Consortium. J Neuropathol Exp Neurol 67:125–143 sourceExperimental — accuracy not yet measured
The Introduction (p. 125) says consensus guidelines recommend α-synuclein immunohistochemistry for synucleinopathies, supporting the preference for that approach. The paper’s staining results and Discussion assess variation among immunohistochemical methods, but do not establish that immunohistochemistry detects Lewy bodies more sensitively than H&E; searches for H&E and hematoxylin–eosin found no such comparison. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [4] Alafuzoff I, Pikkarainen M, Al-Sarraj S et al (2006) Interlaboratory comparison of assessments of Alzheimer disease-related lesions: a study of the BrainNet Europe Consortium. J Neuropathol Exp Neurol 65:740–757 source
- Partly supportedcites [13] Beach TG, White CL, Hamilton RL et al (2008) Evaluation of alpha-synuclein immunohistochemical methods used by invited experts. Acta Neuropathol 116:277–288 sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) calls α-synuclein immunohistochemistry the method of choice for diagnosing Lewy body disorders, supporting its preferred use. The paper compares immunohistochemical methods with one another, however, and does not establish that they detect Lewy bodies more sensitively than H&E staining. (LLM, conf=0.84)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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- Partly supported
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In the paper
“one MVL identified in standard sections of brain (Table 1 regions shaded green) is of unclear relationship to cognitive function, while multiple MVLs in these regions are associated with increased likelihood of cognitive impairment or dementia [24,52,62].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > CEREBROVASCULAR DISEASE and VASCULAR BRAIN INJURY > Reporting
What the sources say
- Partly supportedcites [24] Gorelick PB, Scuteri A, Black SE et al (2011) Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 42:2672–2713 sourceExperimental — accuracy not yet measured
Section 3.2 (page not available in our copy) reports that some studies associate multiple microscopic infarcts with dementia, even after accounting for macroscopic infarcts. It does not establish the claim for MVLs generally or specify that the lesions were identified in standard brain sections. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites [52] Sonnen JA, Larson EB, Crane PK et al (2007) Pathological correlates of dementia in a longitudinal, population-based sample of aging. Ann Neurol 62:406–413 source
- Not checked — no full text of the sourcecites [62] White L (2009) Brain lesions at autopsy in older Japanese-American men as related to cognitive impairment and dementia in the final years of life: a summary report from the Honolulu-Asia aging study. J Alzheimers Dis 18:713–725 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Clinico-pathologic correlations for individuals without cognitive impairment should indicate that it is possible for AD neuropathologic change to predate onset of symptoms by years [54].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > AD NEUROPATHOLOGIC CHANGE > Reporting
What the sources say
- Supportedcites [54] Sperling RA, Aisen PS, Beckett LA et al (2011) Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement 7:280–292 source
Section 2, “Redefining the earliest stages of AD,” says the pathological cascade may begin a decade or more before clinically evident impairment. Section 6 also describes AD-related abnormalities in cognitively normal individuals, supporting the claim that neuropathologic change can predate symptoms by years. (LLM, conf=0.94)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“one MVL identified in standard sections of brain (Table 1 regions shaded green) is of unclear relationship to cognitive function, while multiple MVLs in these regions are associated with increased likelihood of cognitive impairment or dementia [24,52,62].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > CEREBROVASCULAR DISEASE and VASCULAR BRAIN INJURY > Reporting
What the sources say
- Partly supportedcites [24] Gorelick PB, Scuteri A, Black SE et al (2011) Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 42:2672–2713 sourceExperimental — accuracy not yet measured
Section 3.2 (page unavailable) says the number of infarcts needed for cognitive impairment is difficult to determine and reports that multiple microscopic infarcts may be related to dementia. It does not specifically assess the cognitive significance of one MVL identified in standard brain sections. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites [52] Sonnen JA, Larson EB, Crane PK et al (2007) Pathological correlates of dementia in a longitudinal, population-based sample of aging. Ann Neurol 62:406–413 source
- Not checked — no full text of the sourcecites [62] White L (2009) Brain lesions at autopsy in older Japanese-American men as related to cognitive impairment and dementia in the final years of life: a summary report from the Honolulu-Asia aging study. J Alzheimers Dis 18:713–725 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“this may represent pre-clinical LBD [12,22,31].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE > Reporting
What the sources say
- Supportedcites [12] Beach TG, Adler CH, Sue LI et al (2008) Reduced striatal tyrosine hydroxylase in incidental Lewy body disease. Acta Neuropathol 115:445–451 source
The Introduction defines incidental Lewy body disease as Lewy bodies without clinically documented parkinsonism or dementia. The Results and discussion report reduced striatal tyrosine hydroxylase in these individuals and say this suggests ILBD is likely a precursor to Parkinson’s disease and/or dementia with Lewy bodies, supporting the citing sentence’s qualified “may represent” claim. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites [22] Dickson DW, Fujishiro H, DelleDonne A et al (2008) Evidence that incidental Lewy body disease is pre-symptomatic Parkinson’s disease. Acta Neuropathol 115:437–444 source
- Supportedcites [31] Jicha GA, Schmitt FA, Abner E et al (2010) Prodromal clinical manifestations of neuropathologically confirmed Lewy body disease. Neurobiol Aging 31:1805–1813 source
The Introduction (page unavailable) says Lewy body pathology has been found in autopsied people described as normal and suggests that DLB pathology may predate clinical diagnosis. The Discussion (page unavailable) also says the study’s subjects were cognitively and neurologically normal at enrollment. Together, these support the qualified suggestion that LBD without apparent cognitive or motor deficits may be pre-clinical. (LLM, conf=0.91)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“LBs are frequent in the setting of moderate-to-severe levels of AD neuropathologic change [27,59], including some early-onset familial AD cases [32,33].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE
What the sources say
- Supportedcites [32] Leverenz JB, Fishel MA, Peskind ER et al (2006) Lewy body pathology in familial Alzheimer disease: evidence for disease- and mutation-specific pathologic phenotype. Arch Neurol 63:370–376 source
The Results report Lewy body pathology in the amygdala of 24 of 25 familial AD cases with PSEN1 mutations. The section on PSEN1-associated AD reports a mean age at onset of about 43 years in the groups it compares, supporting the early-onset qualifier. The indexed copy provides section labels but no page numbers. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites [33] Lippa CF, Duda JE, Grossman M et al (2007) DLB and PDD boundary issues: diagnosis, treatment, molecular pathology, and biomarkers. Neurology 68:812–819 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Accumulation of Aβ plaques and NFTs follows distinct regional progressions across brain regions as AD advances.”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > AD NEUROPATHOLOGIC CHANGE
What the sources say
- Partly supportedcites [14] Braak H, Alafuzoff I, Arzberger T et al (2006) Staging of Alzheimer disease-associated neurofibrillary pathology using paraffin sections and immunocytochemistry. Acta Neuropathol 112:389–404 sourceExperimental — accuracy not yet measured
The staging-system section describes a predictable regional progression of neurofibrillary pathology, from transentorhinal and entorhinal regions to limbic and then neocortical areas. It does not describe a separate regional progression of Aβ plaques or compare that progression with NFTs. Its references to neuritic plaques occur in the context of tau-immunoreactive pathology, not an Aβ-plaque staging scheme. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [15] Braak H, Braak E (1991) Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol 82:239–259 source
- Not checked — no full text of the sourcecites [57] Thal DR, Rub U, Orantes M, Braak H (2002) Phases of A beta-deposition in the human brain and its relevance for the development of AD. Neurology 58:1791–1800 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“CVD and vascular brain injury (VBI) [50] commonly are encountered in the brains with AD neuropathologic change [25].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > CEREBROVASCULAR DISEASE and VASCULAR BRAIN INJURY
What the sources say
- Partly supportedcites [25] Grinberg LT, Thal DR (2010) Vascular pathology in the aged human brain. Acta Neuropathol 119:277–290 sourceExperimental — accuracy not yet measured
The ‘Cerebral amyloid angiopathy’ section (page unavailable) reports that around 80–100% of AD patients have CAA, supporting the claim that cerebrovascular disease commonly accompanies AD pathology. It identifies infarction and hemorrhage as possible complications of CAA, but does not establish that vascular brain injury itself is commonly found in AD brains. (LLM, conf=0.82)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“LBs are frequent in the setting of moderate-to-severe levels of AD neuropathologic change [27,59], including some early-onset familial AD cases [32,33].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE
What the sources say
- Not checked — no full text of the sourcecites [27] Hamilton RL (2000) Lewy bodies in Alzheimer’s disease: a neuropathological review of 145 cases using alpha-synuclein immunohistochemistry. Brain Pathol 10:378–384 source
- Supportedcites [59] Uchikado H, Lin WL, DeLucia MW, Dickson DW (2006) Alzheimer disease with amygdala Lewy bodies: a distinct form of alpha-synucleinopathy. J Neuropathol Exp Neurol 65:685–697 source
The Materials and Methods section (page unavailable) says all 347 cases met pathologic criteria for AD and had Braak NFT stage IV or greater, indicating advanced AD in almost all cases. The “Frequency of α-Synuclein Pathology in Alzheimer Disease” section (page unavailable) reports Lewy-body pathology in 62 AD/ALB and 149 AD/LBD cases, supporting that Lewy bodies are frequent in this setting. (LLM, conf=0.90)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 2
- Probably not a substantial claim. 1
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Relatively isolated HS may occur in very old individuals, and in this context it is associated with TDP-43-immunoreactive inclusions and with cognitive impairment [45,47].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > HIPPOCAMPAL SCLEROSIS and TAR DNA BINDING PROTEIN (TDP)-43 INCLUSIONS > Reporting
What the sources say
- Partly supportedcites [45] Nelson PT, Abner EL, Schmitt FA et al (2010) Modeling the association between 43 different clinical and pathological variables and the severity of cognitive impairment in a large autopsy cohort of elderly persons. Brain Pathol 20:66–79 sourceExperimental — accuracy not yet measured
The Discussion reports that hippocampal sclerosis (HS) was associated with lower MMSE scores and states that HS is associated with TDP-43 proteinopathy. The Results describe TDP-43-positive inclusions. Neither passage establishes these associations specifically for relatively isolated HS in very old individuals. (LLM, conf=0.86)
- Supportedcites [47] Nelson PT, Schmitt FA, Lin Y et al (2011) Hippocampal sclerosis in advanced age: clinical and pathological features. Brain 134:1506–1518 source
The Introduction describes hippocampal sclerosis in older individuals as unrelated to Alzheimer’s pathology and associated with significant cognitive dysfunction. The Discussion reports aberrant TDP-43 staining in approximately 90% of patients with hippocampal sclerosis, and Table 7 describes HS-Ageing as most prevalent in the oldest-old and associated with dementia. The association is not universal, but the citing sentence does not claim that it is. (LLM, conf=0.92)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
In the paper
“Although not part of this classification scheme, it is important to realize that LBD also occurs frequently in the olfactory bulb in older adults and should be sampled when possible [20].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > LEWY BODY DISEASE > Method
What the sources say
- Not checked — no full text of the sourcecites [20] Del Tredici K, Rub U, De Vos RA et al (2002) Where does Parkinson disease pathology begin in the brain? J Neuropathol Exp Neurol 61:413–426 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“A subset of senile plaques called neuritic plaques appear closely associated with neuronal injury and are characterized by the occurrence of dystrophic neurites that frequently have phospho-tau immunoreactivity [19,36,37,55].”
§ National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach > AD NEUROPATHOLOGIC CHANGE
What the sources say
- Not checked — no full text of the sourcecites [19] DeKosky ST, Scheff SW (1990) Synapse loss in frontal cortex biopsies in Alzheimer’s disease: correlation with cognitive severity. Ann Neurol 27:457–464 source
- Not checked — no full text of the sourcecites [36] Masliah E, Mallory M, Deerinck T et al (1993) Re-evaluation of the structural organization of neuritic plaques in Alzheimer’s disease. J Neuropathol Exp Neurol 52:619–632 source
- Not checked — no full text of the sourcecites [37] Masliah E, Terry RD, Mallory M et al (1990) Diffuse plaques do not accentuate synapse loss in Alzheimer’s disease. Am J Pathol 137:1293–1297
- Not checked — no full text of the sourcecites [55] Terry RD, Masliah E, Salmon DP et al (1991) Physical basis of cognitive alterations in Alzheimer’s disease: synapse loss is the major correlate of cognitive impairment. Ann Neurol 30:572–580 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
Many other neurodegenerative disorders can cause dementia and may be co-morbid with AD neuropathologic change, especially in the elderly.
“There are many other neurodegenerative disorders that can cause dementia in addition to those discussed here, and any may be co-morbid with AD neuropathologic change, especially in the elderly.”
The paper relies on this without support.
Multiple diseases in the cerebrum can conspire to worsen cognitive symptoms.
“Multiple diseases in cerebrum can conspire to worsen cognitive symptoms; however, it often is difficult to judge the extent to which each disease observed at autopsy may have contributed to a given patient’s cognitive state.”
The paper relies on this without support.
Abnormal neuropil and neuronal cytoplasmic α-synuclein immunoreactivity are usually present with Lewy bodies but will not be apparent by H&E; in some instances, these changes occur in the absence of Lewy bodies.
“Abnormal neuropil and neuronal cytoplasmic α-synuclein immunoreactivity are usually present with LBs but will not be apparent by H&E; in some instances, these changes occur in the absence of LBs.”
The paper relies on this without support.
Diffuse white matter injury is a form of VBI but it is more difficult to judge objectively and is not specific to VBI.
“Diffuse white matter injury is a form of VBI but it is more difficult to judge objectively and is not specific to VBI.”
The paper relies on this without support.
Hippocampal sclerosis can be observed in the context of AD neuropathologic change, FTLD, and VBI, likely reflecting a heterogeneous etiology.
“HS can be observed in the context of AD neuropathologic change, frontotemporal lobar degeneration (FTLD), and VBI, likely reflecting a heterogeneous etiology.”
The paper relies on this without support.
Hippocampal sclerosis can be focal, so its absence in the recommended screening section does not rule out the possibility of HS elsewhere in the hippocampal formation.
“HS can be focal, thus its absence in the recommended screening section does not rule out the possibility of HS elsewhere in the hippocampal formation.”
The paper relies on this without support.
Hippocampal sclerosis can occur in several different diseases and has varying clinical implications in different settings.
“Clinico-pathological correlations need to recognize that HS can occur in several different diseases and has varying clinical implications in different settings.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The new NIA criteria use the same combination of NPs and Braak stage as the minimum lesion density necessary for attributing the cause of dementia to AD (39, 40).”
From Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer Disease Centers, 2005–2010 (2012) · cites this paper as [40]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The definitive diagnosis of AD requires microscopic examination of multiple brain regions employing staining methods that can detect Alzheimer type neuropathologic change [24], with diagnosis based upon the morphology and density of lesions and their topographic distribution.”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [24]
The cited source says what the claim attributes to it.
In the citing paper
“This finding is highlighted by the fact that nearly one third of patients with pathological findings of high likelihood Alzheimer’s disease [24] were thought to other disorders, and 3% were considered clinically normal at the time of their last clinical exam (Table 2).”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [24]
The cited source says what the claim attributes to it.
In the citing paper
“However, both Aβ and paired helical filament (PHF) tau deposits are required to fulfill neuropathologic criteria for AD [105,106]”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [105]
The cited source says what the claim attributes to it.
In the citing paper
“Autopsy analyses classified the level of ADNC from “none” to “high” using an established scoring system when available.”
From Automatic classification of AD pathology in FTD phenotypes using natural speech (2024) · cites this paper as [30]
The cited source says what the claim attributes to it.
In the citing paper
“Participants in the Confirmed-AD group (n ¼ 1854) were diagnosed with primary or contributing ADdementia at their last UDS visit before death and met our criteria for ADNC: moderate to frequent neuritic plaques and Braak stages III through VI, which loosely aligns with NIA-AA criteria for intermediate or high ADNC (13).”
From Concordance of Clinical Alzheimer Diagnosis and Neuropathological Features at Autopsy (2020) · cites this paper as [13]
The cited source says what the claim attributes to it.
In the citing paper
“The shortcomings of the NIA-Reagan criteria have been recognized and a revised set of criteria are currently in press (39, 40).”
From Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer Disease Centers, 2005–2010 (2012) · cites this paper as [40]
The cited source says what the claim attributes to it.
In the citing paper
“In the revision of the 1997 criteria, combinations of plaque and tangle pathologies considered sufficient to cause dementia and qualify for the neuropathological diagnosis of AD are explicitly stated (40, 41).”
From Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer Disease Centers, 2005–2010 (2012) · cites this paper as [40]
The cited source says what the claim attributes to it.
In the citing paper
“Neuropathologic diagnosis of AD was in accordance with current NIA-AA guidelines (Hyman et al., 2012; Montine et al., 2012).”
From Cholesterol and matrisome pathways dysregulated in astrocytes and microglia (2022) · cites this paper as Montine et al., 2012
In the citing paper
“Neuropathological assessment was performed by 2 authors (T.G.B. and T.J.M.) blinded to clinical and imaging results and using NIA–AA diagnostic scoring guidelines.5,40”
From Positron Emission Tomography Imaging With [ 18 F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [40]
In the citing paper
“Additional changes that may also occur in the brains of AD patients include amyloid angiopathy, age-related brain atrophy, synaptic pathology, white matter rarefaction, granulovacuolar degeneration, neuron loss, TDP-43 proteinopathy, and neuroinflammation (20-26), which may contribute to cognitive impairment; however, these are not considered pathognomonic features of AD (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“In contrast, dense and extensive neocortical NFTs are very consistently associated with dementia and thus, according to new diagnostic criteria, these are required to constitute high burden of AD neuropathologic change (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“The current revision of the National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of AD stipulate that subjects with moderately dense neuritic AβPs may be regarded as having an intermediate level of AD neuropathologic change and that other potential contributors to cognitive impairment and dementia should be sought (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“There is no universally applied rubric for CVD pathologic diagnosis, although the recent National Institute on Aging–Alzheimer’s Association criteria attempted to systematize neuropathologic assessment of this complex form of brain injury (3).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [3]
In the citing paper
“Alzheimer's disease cases met criteria for a high likelihood of AD (Montine et al., 2012).”
From Alzheimer's amyloid‐β and tau protein accumulation is associated with decreased expression of the LDL receptor‐associated protein in human brain tissue (2020) · cites this paper as Montine et al., 2012
Citations
Cites
McKhann, G. M., Knopman, D. S., Chertkow, H., Hyman, B. T., Jack, C. R., Kawas, C. H., Klunk, W. E., Koroshetz, W. J., Manly, J. J., Mayeux, R., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.005 · Cited by 18,657 · cited 1×
“‘‘Alzheimer’s disease’’ refers to a constellation of cognitive and behavioral changes that are typical for patients who have substantial amounts of its hallmark lesions [6, 39].”
Self-citationNeuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123 · cited 8×
“‘‘Intermediate’’ or ‘‘High’’ AD neuropathologic change (italicized) is considered sufficient explanation for dementia a NFT stage should be determined by the method of Braak [14, 15] b Ab/amyloid plaque score should be determined by the method of Thal et al.”
InfluentialStaging of brain pathology related to sporadic Parkinson’s disease
Braak, H., Tredici, K. D., Rüb, U., de Vos, R. A. I., Jansen Steur, E. N. H., & Braak, E. (2003) · Neurobiology of Aging · doi:10.1016/s0197-4580(02)00065-9 · Cited by 10,777 · cited 2×
“Given our focus on cognitive impairment and dementia rather than movement disorders [16], we recommend a modification of Fig.”
Albert, M. S., DeKosky, S. T., Dickson, D., Dubois, B., Feldman, H. H., Fox, N. C., Gamst, A., Holtzman, D. M., Jagust, W. J., Petersen, R. C., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.008 · Cited by 10,152 · cited 1×
“‘‘Alzheimer’s disease’’ refers to a constellation of cognitive and behavioral changes that are typical for patients who have substantial amounts of its hallmark lesions [6, 39].”
Self-citationSperling, R. A., Aisen, P. S., Beckett, L. A., Bennett, D. A., Craft, S., Fagan, A. M., Iwatsubo, T., Jack, C. R., Kaye, J., Montine, T. J., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.003 · Cited by 7,155 · cited 2×
“Similar neuropathologic changes, albeit usually at lower levels, also occur in individuals who did not show cognitive or behavioral impairments during life [54].”
Self-citationDiagnosis and management of dementia with Lewy bodies: Third report of the DLB consortium
McKeith, I. G., Dickson, D. W., Lowe, J., Emre, M., O'Brien, J. T., Feldman, H., Cummings, J., Duda, J. E., Lippa, C., Perry, E. K., et al. (2005) · Neurology · doi:10.1212/01.wnl.0000187889.17253.b1 · Cited by 5,069
Self-citationMirra, S. S., Heyman, A., McKeel, D., Sumi, S. M., Crain, B. J., Brownlee, L. M., Vogel, F. S., Hughes, J. P., Belle, G. V., Berg, L., et al. (1991) · Neurology · doi:10.1212/wnl.41.4.479 · Cited by 4,961 · cited 11×
“Region Stain for A /amyloid plaques [57] Stain for NFTs [14,15] Stain for NPs [41] Stain for LBs H&E”
InfluentialSelf-citationDeJesus-Hernandez, M., Mackenzie, I. R., Boeve, B. F., Boxer, A. L., Baker, M., Rutherford, N. J., Nicholson, A. M., Finch, N. A., Flynn, H., Adamson, J., et al. (2011) · Neuron · doi:10.1016/j.neuron.2011.09.011 · Cited by 4,936 · cited 1×
“With the exception of individuals with mutations in TARDBP, GRN, VCP or c9ORF72 [10, 18], it is not clear whether TDP-43 proteinopathy in these other neurodegenerative diseases is”
Self-citationTerry, R. D., Masliah, E., Salmon, D. P., Butters, N., DeTeresa, R., Hill, R., Hansen, L. A., & Katzman, R. (1991) · Annals of Neurology · doi:10.1002/ana.410300410 · Cited by 4,397 · cited 1×
“frequently have phospho-tau immunoreactivity [19, 36, 37, 55].”
Self-citationGorelick, P. B., Scuteri, A., Black, S. E., DeCarli, C., Greenberg, S. M., Iadecola, C., Launer, L. J., Laurent, S., Lopez, O. L., Nyenhuis, D., et al. (2011) · Stroke · doi:10.1161/str.0b013e3182299496 · Cited by 3,811
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Items 601–700 of 2,854
Neurobiology of cognitive impairment in Parkinson’s disease
Jellinger, K. A. (2012) · Expert Review of Neurotherapeutics · doi:10.1586/ern.12.131 · Cited by 59
Cholerton, B., Larson, E. B., Quinn, J. F., Zabetian, C. P., Mata, I. F., Keene, C. D., Flanagan, M. E., Crane, P. K., Grabowski, T. J., Montine, K. S., et al. (2015) · American Journal Of Pathology · doi:10.1016/j.ajpath.2015.12.001 · Cited by 61
“DLB most commonly is associated with a combination of the pathological features of AD and LBD, and less commonly with widespread LBD in the absence of AD neuropathologic changes.(17,18) Although recognized as a disorder of motor control and characterized by brainstem Lewy bodies (LBs), PD also is accompanied by cognit…”
BackgroundSelf-citationAshby, E. L., Miners, J. S., Kehoe, P. G., & Love, S. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-150831 · Cited by 60
“All cases had been subjected to detailed neuropathological assessment and diagnosis had been made following standard protocols [37, 38].”
The phosphatase calcineurin regulates pathological TDP-43 phosphorylation
Liachko, N. F., Saxton, A. D., McMillan, P. J., Strovas, T. J., Currey, H. N., Taylor, L. M., Wheeler, J. M., Oblak, A. L., Ghetti, B. F., Montine, T. J., et al. (2016) · Acta Neuropathologica · doi:10.1007/s00401-016-1600-y · Cited by 66
“Neither cases nor controls showed neuropathologic changes of Lewy body accumulation, ischemic injury, or hemorrhage in consensus screening sections [20, 41].”
BackgroundSelf-citationAlzheimer’s disease, apolipoprotein E and hormone replacement therapy
Depypere, H. T., Vierin, A., Weyers, S., & Sieben, A. (2016) · Maturitas · doi:10.1016/j.maturitas.2016.09.009 · Cited by 60
Neuropathological correlates of parkinsonian disorders in a large Dutch autopsy series
Geut, H., Hepp, D. H., Foncke, E. M. J., Berendse, H. W., Rozemüller, A. J. M., Huitinga, I., & van de Berg, W. D. J. (2020) · Acta Neuropathologica Communications · doi:10.1186/s40478-020-00914-9 · Cited by 57
Fink, H. A., Linskens, E. J., Silverman, P. C., McCarten, J. R., Hemmy, L. S., Ouellette, J. M., Greer, N. L., Wilt, T. J., & Butler, M. (2020) · Annals of Internal Medicine · doi:10.7326/m19-3888 · Cited by 57
“gov/ct2/show/NCT03901092), CSF, and blood biomarkers with autopsy-confirmed AD pathology on the basis of the most current consensus definitions (16, 20).”
BackgroundLau, H. H. C., Ingelsson, M., & Watts, J. C. (2020) · Acta Neuropathologica · doi:10.1007/s00401-020-02201-2 · Cited by 57
Advances in Deep Neuropathological Phenotyping of Alzheimer Disease: Past, Present, and Future
Shakir, M., & Dugger, B. N. (2022) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlab122 · Cited by 58
Alzheimer disease neuropathology in a patient previously treated with aducanumab
Plowey, E. D., Bussière, T., Rajagovindan, R., Sebalusky, J., Hamann, S., von Hehn, C., Castrillo‐Viguera, C., Sandrock, A. W., Haeberlein, S. B., van Dyck, C. H., et al. (2022) · Acta Neuropathologica · doi:10.1007/s00401-022-02433-4 · Cited by 60
“According to NIA/AA consensus guidelines [18], tissue sections confirmed the presence of Alzheimer disease neuropathologic changes: Aβ plaques were observed in neocortex and hippocampus but not in the striatum (Thal Phase 2); NFTs were observed in sections of association neocortex (Braak stage V); and sparse neocortic…”
MethodInfluentialHypothesis review: Alzheimer's overture guidelines
Ferrer, I. (2022) · Brain Pathology · doi:10.1111/bpa.13122 · Cited by 55
Ossenkoppele, R., Coomans, E. M., Apostolova, L. G., Baker, S. L., Barthel, H., Beach, T. G., Benzinger, T. L. S., Betthauser, T. J., Bischof, G. N., Bottlaender, M., et al. (2025) · Nature Neuroscience · doi:10.1038/s41593-025-02000-6 · Cited by 60
“…established AD-specific region of interest (ROI), covering medial and lateral parts of the temporal cortex 4,19 , or the presence of Braak stage V–VI for neurofibrillary tangle pathology on neuropathological examination (that is, ‘B3’ according to the AD neuro-pathological scoring system 23 ).”
Self-citationComparison of symptomatic and asymptomatic persons with Alzheimer disease neuropathology
Monsell, S. E., Mock, C., Roe, C. M., Ghoshal, N., Morris, J. C., Cairns, N. J., & Kukull, W. A. (2013) · Neurology · doi:10.1212/wnl.0b013e318295d7a1 · Cited by 57
“staging scheme compresses 7 Braak stages into 4 “B” stages (0–3), which improves interrater reliability.(7) The majority of symptomatic participants were at the high end of B and C scores, with B score of 3 (Braak stage V–VI) and frequent CERAD neuritic plaques.”
BackgroundMethodInfluentialSelf-citationTDP-43 pathology and cognition in ALS
Prudlo, J., König, J., Schuster, C., Kasper, E., Büttner, A., Teipel, S. J., & Neumann, M. (2016) · Neurology · doi:10.1212/wnl.0000000000003062 · Cited by 55
The Identification of Aluminum in Human Brain Tissue Using Lumogallion and Fluorescence Microscopy
Mirza, A., King, A., Troakes, C., & Exley, C. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160648 · Cited by 60
Neuron loss and degeneration in the progression of TDP-43 in frontotemporal lobar degeneration
Yousef, A., Robinson, J. L., Irwin, D. J., Byrne, M. D., Kwong, L. K., Lee, E. B., Xu, Y., Xie, S. X., Rennert, L., Suh, E. R., et al. (2017) · Acta Neuropathologica Communications · doi:10.1186/s40478-017-0471-3 · Cited by 55
“Manuela Neumann and Elisabeth Kremmer), α-synuclein (monoclonal antibody Syn303; generated in CNDR), as well as amyloid-β (monoclonal antibody NAB228; generated in CNDR), as described previously [3, 18, 32, 38, 39, 52].”
BackgroundSelf-citationMimuro, M., Yoshida, M., Kuzuhara, S., & Kokubo, Y. (2017) · Neuropathology · doi:10.1111/neup.12434 · Cited by 56
“Lewy body pathology was assessed by the modified guidelines of previous consensus guidelines.(14,15) TDP-43 pathology in ALS was assessed by staging of Brettschneider.”
MethodNeuropathologic features associated with basal forebrain atrophy in Alzheimer disease
Teipel, S. J., Fritz, H.-C., Grothe, M. J., & Initiative, A. D. N. (2020) · Neurology · doi:10.1212/wnl.0000000000010192 · Cited by 56
P‐tau235: a novel biomarker for staging preclinical Alzheimer’s disease
Lantero‐Rodriguez, J., Snellman, A., Benedet, A. L., Milà‐Alomà, M., Camporesi, E., Montoliu‐Gaya, L., Ashton, N. J., Vrillon, A., Karikari, T. K., Gispert, J. D., et al. (2021) · EMBO Molecular Medicine · doi:10.15252/emmm.202115098 · Cited by 59
Distinct populations of highly potent TAU seed conformers in rapidly progressing Alzheimer’s disease
Kim, C., Haldiman, T., Kang, S.-G., Hromadkova, L., Han, Z. Z., Chen, W., Lissemore, F., Lerner, A., de Silva, R., Cohen, M. L., et al. (2022) · Science Translational Medicine · doi:10.1126/scitranslmed.abg0253 · Cited by 55
Cognition at Each Stage of Lewy Body Disease with Co-occurring Alzheimer’s Disease Pathology
Ryman, S. G., Yutsis, M. V., Tian, L., Henderson, V. W., Montine, T. J., Salmon, D. P., Galasko, D. R., & Poston, K. L. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-201187 · Cited by 60
“The presence and stage of ADNC [23, 24] and LBD [25] were used to characterize the extent of neuropathology and assign participants to one of the following eight groups (detailed in Fig.”
MethodSelf-citationMolecular Mechanism of Nuclear Tau Accumulation and its Role in Protein Synthesis
Portillo, M., Eremenko, E., Kaluski, S., García-Venzor, A., Onn, L., Stein, D., Slobodnik, Z., Zaretsky, A., Ueberham, U., Einav, M., et al. (2020) · Cell Reports · doi:10.1016/j.celrep.2021.109035 · Cited by 61
Decoding perineuronal net glycan sulfation patterns in the Alzheimer's disease brain
Logsdon, A. F., Francis, K. L., Richardson, N. E., HU, S. J. W., Faber, C. L., Phan, B. A., Nguyen, V., Setthavongsack, N., Banks, W. A., Woltjer, R. L., et al. (2021) · Alzheimer s & Dementia · doi:10.1002/alz.12451 · Cited by 56
Murray, M. E., Moloney, C. M., Kouri, N., Syrjanen, J. A., Matchett, B. J., Rothberg, D. M., Tranovich, J. F., Sirmans, T. N. H., Wiste, H. J., Boon, B. D. C., et al. (2022) · Molecular Neurodegeneration · doi:10.1186/s13024-022-00578-0 · Cited by 58
“Neuropathologic grouping for graphical visualization was prioritized as follows: progressive supranuclear palsy (n = 2) [27], AD (n = 9) [22], argyrophilic grain disease (n = 3) [28], primary age-related tauopathy (n = 14) [29], and pathological aging (n = 7) [30, 31] (Fig.”
BackgroundMethodSelf-citationBonora, E., Graziano, C., Minopoli, F., Bacchelli, E., Magini, P., Diquigiovanni, C., Lomartire, S., Bianco, F., Vargiolu, M., Parchi, P., et al. (2014) · EMBO Molecular Medicine · doi:10.1002/emmm.201303235 · Cited by 54
“Furthermore, large cohorts of trios of ID (Vissers et al, 2010) and ASD (Iossifov et al, 2012; Neale et al, 2012; O’Roak et al, 2012; Sanders et al, 2012) patients filtered for de novo variants (Veltman & Brunner, 2012) could be reassessed in order to verify whether additional maternally…”
BackgroundIkonomović, M. D., Buckley, C. J., Abrahamson, E. E., Kofler, J., Mathis, C. A., Klunk, W. E., & Farrar, G. (2020) · Acta Neuropathologica · doi:10.1007/s00401-020-02175-1 · Cited by 58
Vontell, R. T., de Rivero Vaccari, J. P., Sun, X., Gultekin, S. H., Bramlett, H. M., Dietrich, W. D., & Keane, R. W. (2023) · Brain Pathology · doi:10.1111/bpa.13142 · Cited by 57
“Pathologic change that incorporates histopathologic assessments of Aβ deposits and the staging of neurofibrillary tangles [38].”
BackgroundResultInfluentialKim, W. H., Adluru, N., Chung, M. K., Okonkwo, O. C., Johnson, S. C., Bendlin, B. B., & Singh, V. (2015) · NeuroImage · doi:10.1016/j.neuroimage.2015.05.050 · Cited by 54
“Post-mortem diagnosis of the disease is determined by regional density of beta-amyloid plaques, and neuro fi brillary tangles (Montine et al., 2012).”
BackgroundDrug delivery strategies with lipid-based nanoparticles for Alzheimer’s disease treatment
Jang, Y.-J., Kang, S.-J., Park, H. S., Lee, D., Kim, J. H., Kim, J.-E., Kim, D., Chung, C., Yoon, J., & Bhang, S. H. (2025) · Journal of Nanobiotechnology · doi:10.1186/s12951-025-03109-3 · Cited by 64
Neuropathologic correlates of cognition in a population-based sample
Cholerton, B., Larson, E., Baker, L., Craft, S., Crane, P., Millard, S., Sonnen, J., & Montine, T. (2013) · Journal of Alzheimer's Disease · doi:10.3233/jad-130281 · Cited by 55
Self-citationUnfolded protein response is activated in L ewy body dementias
Baek, J., Whitfield, D., Howlett, D. C., Francis, P. T., Bereczki, E., Ballard, C. G., Hortobágyi, T., Attems, J., & Aarsland, D. (2015) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12260 · Cited by 55
Abu‐Rumeileh, S., Lattanzio, F., Maserati, M. S., Rizzi, R., Capellari, S., & Parchi, P. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160740 · Cited by 53
“…the other hand, although AD typically presents with a slowly progressive and well defined profile of cognitive decline, there also are well recognized variants of the disease with a rapid clinical progression and/or focal neurological signs manifesting relatively early in the disease course [3–6].”
Backgroundvan Groen, T., Schemmert, S., Brener, O., Gremer, L., Ziehm, T., Tusche, M., Nagel‐Steger, L., Kadish, I., Schartmann, E., Elfgen, A., et al. (2017) · Scientific Reports · doi:10.1038/s41598-017-16565-1 · Cited by 53
Fathy, Y. Y., Jonker, A. J., Oudejans, E., de Jong, F. J. J., van Dam, A., Rozemüller, A. J. M., & van de Berg, W. D. J. (2018) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12501 · Cited by 54
Increased Hyaluronan and TSG-6 in Association with Neuropathologic Changes of Alzheimer’s Disease
Reed, M. J., Damodarasamy, M., Pathan, J. L., Chan, C. K., Spiekerman, C. F., Wight, T. N., Banks, W. A., Day, A. J., Vernon, R. B., & Keene, C. D. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180797 · Cited by 54
Divergent patterns of TDP‐43 and tau pathologies in primary progressive aphasia
Giannini, L. A. A., Xie, S. X., McMillan, C. T., Liang, M., Williams, A., Jester, C., Rascovsky, K., Wolk, D. A., Ash, S., Lee, E. B., et al. (2019) · Annals of Neurology · doi:10.1002/ana.25465 · Cited by 52
Self-citationAltered mechanisms of protein synthesis in frontal cortex in Alzheimer disease and a mouse model.
Garcia‐Esparcia, P., Sideris-Lampretsas, G., Hernández‐Ortega, K., Grau‐Rivera, O., Sklaviadis, T., Gelpí, E., & Ferrer, I. (2017) · Europe PMC (PubMed Central) · Cited by 53
Segundo‐Acosta, P. S., Montero‐Calle, A., Fuentes, M., Rábano, A., Villalba, M., & Barderas, R. (2019) · Journal of Proteome Research · doi:10.1021/acs.jproteome.9b00258 · Cited by 54
Ohm, D. T., Fought, A. J., Martersteck, A., Coventry, C., Sridhar, J., Gefen, T. D., Weıntraub, S., Bigio, E. H., Mesulam, M. M., Rogalski, E. J., et al. (2020) · Brain Pathology · doi:10.1111/bpa.12902 · Cited by 59
“As described previously (59, 60), the participants included five right-handed individuals who received clinical diagnoses of PPA (29, 51, 52) and pathologic diagnoses of “high” AD neuropathologic change based on published consensus criteria (35, 56).”
Self-citationMackmull, M., Nagel, L., Sesterhenn, F., Muntel, J., Großbach, J., Stalder, P., Bruderer, R., Reiter, L., van de Berg, W. D. J., de Souza, N., et al. (2022) · Nature Structural & Molecular Biology · doi:10.1038/s41594-022-00837-0 · Cited by 47
Insights into the use of biomarkers in clinical trials in Alzheimer's disease
Pascoal, T. A., Aguzzoli, C. S., Lussier, F. Z., Crivelli, L., Suemoto, C. K., Fortea, J., Rosa‐Neto, P., Zimmer, E. R., Ferreira, P. C. L., & Bellaver, B. (2024) · EBioMedicine · doi:10.1016/j.ebiom.2024.105322 · Cited by 60
“36 As previous studies have shown that changes in both soluble and insoluble tau species can occur in response to A β pathology and may represent different facets of the same process, 1 we postulate that in the presence of A+, evidence of tau abnormality measured using either fl uid or PET indicates…”
Systems biology of neurodegenerative diseases
Wood, L. B., Winslow, A. R., & Strasser, S. D. (2015) · Integrative Biology · doi:10.1039/c5ib00031a · Cited by 56
Clinico-Pathological Correlations of the Most Common Neurodegenerative Dementias
Taipa, R. J. F., Pinho, J., & Pires, M. M. (2012) · Frontiers in Neurology · doi:10.3389/fneur.2012.00068 · Cited by 54
“…was proposed by the National Institute on Aging-Alzheimer’s Association, in which there is emphasis on identification of amyloid deposits, staging of neurofibrillary tangles, scoring of neuritic plaques, and systematic search for other neurodegenerative dementia pathologies (Montine et al., 2012).”
BackgroundMatrix metalloproteinase 9–mediated intracerebral hemorrhage induced by cerebral amyloid angiopathy
Zhao, L., Arbel‐Ornath, M., Wang, X., Betensky, R. A., Greenberg, S. M., Frosch, M. P., & Bacskai, B. J. (2015) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2015.07.016 · Cited by 52
“The neuropathologies of each case were assessed according to the ABC scoring scheme (Montine et al., 2012) (Table 1).”
MethodSelf-citationZeng, J., Libien, J. M., Shaik, F., Wolk, J., & Hernandez, A. I. (2016) · Neural Plasticity · doi:10.1155/2016/8987928 · Cited by 54
“Of these, synaptic loss most closely correlates with cognitive decline [5], whereas beta-amyloid accumulation, the presence of neuritic plaques, and NFT are the pathological markers required to make a definitive diagnosis of AD [6].”
BackgroundGarcia‐Esparcia, P., López‐González, I., Grau‐Rivera, O., Garrido, M. G., Koneti, A., Llorens, F., Zafar, S., Carmona, M., del Río, J. A., Zerr, I., et al. (2017) · Frontiers in Neurology · doi:10.3389/fneur.2017.00089 · Cited by 54
Epidemiological Approaches to Understanding the Link Between Type 2 Diabetes and Dementia
Sutherland, G. T., Lim, J., Srikanth, V. K., & Bruce, D. G. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-161194 · Cited by 58
Degeneration of dopaminergic circuitry influences depressive symptoms in Lewy body disorders
Patterson, L., Rushton, S., Attems, J., Thomas, A. J., & Morris, C. M. (2018) · Brain Pathology · doi:10.1111/bpa.12697 · Cited by 53
“© 2018 The Authors Brain Pathology published by John Wiley & Sons Ltd on behalf of International Society of Neuropathology 546 change (66) and can therefore be classified as neuropathologically mixed AD/DLB with a LBD clinical phenotype (99).”
BackgroundAssessing circular RNAs in Alzheimer's disease and frontotemporal lobar degeneration
Cervera‐Carles, L., Dols‐Icardo, O., Molina‐Porcel, L., Alcolea, D. A., González, A. C., Muñoz, L., & Clarimón, J. (2020) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2020.03.017 · Cited by 53
The Pattern of AQP4 Expression in the Ageing Human Brain and in Cerebral Amyloid Angiopathy
Owasil, R., O’Neill, R., Keable, A., Nimmo, J., MacGregor Sharp, M., Kelly, L., Saito, S., Simpson, J. E., Weller, R. O., Smith, C., et al. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21041225 · Cited by 48
“Cases from Newcastle were diagnosed according to internationally used criteria including neuritic Braak stages [48], Thal amyloid phases [49], CERAD scores [50], NIA‐AA guidelines [51] and McKeith criteria for Lewy body disease [52]; these cases showed varying degrees of AD pathology with no Lewy Body pathology.”
Cerebrospinal Fluid P-Tau181P: Biomarker for Improved Differential Dementia Diagnosis
Struyfs, H., Niemantsverdriet, E., Goossens, J., Fransén, E., Martin, J., Deyn, P. P. D., & Engelborghs, S. (2015) · Frontiers in Neurology · doi:10.3389/fneur.2015.00138 · Cited by 53
Chen, A., Oakley, A. E., Monteiro, M. P. A. O., Tuomela, K., Allan, L. M., Mukaetova‐Ladinska, E. B., O'Brien, J. T., & Kalaria, R. N. (2015) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2015.10.021 · Cited by 53
“Pathological diagnosis of AD was consistent with the National Institute on AgingeAlzheimer’s Association guidelines for the neuropathological assessment of AD (Montine et al., 2012).”
MethodMAPT H1 haplotype is associated with enhanced α-synuclein deposition in dementia with Lewy bodies
Colom‐Cadena, M., Gelpí, E., Martı́, M. J., Charif, S., Dols‐Icardo, O., Blesa, R., Clarimón, J., & Lleó, A. (2012) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2012.06.015 · Cited by 53
“We also applied the National Institute on Aging-Alzheimer’s Association Guidelines for neuropathologic assessment of AD (Montine et al., 2012).”
Asymmetry of neurodegenerative disease-related pathologies: a cautionary note
Stefanits, H., Budka, H., & Kovács, G. G. (2012) · Acta Neuropathologica · doi:10.1007/s00401-011-0936-6 · Cited by 54
“Importantly, the recent criteria suggest to consider bilateral sections if both cerebral hemispheres are available [11].”
Vermeiren, Y., Dam, D. V., Aerts, T., Engelborghs, S., Martin, J., & Deyn, P. P. D. (2015) · Alzheimer s Research & Therapy · doi:10.1186/s13195-014-0090-1 · Cited by 52
“[51] was applied to all AD brains collected after May 2011 (n = 5).”
MethodCykowski, M. D., Takei, H., Eldik, L. J. V., Schmitt, F. A., Jicha, G. A., Powell, S. Z.-E., & Nelson, P. T. (2016) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlw014 · Cited by 52
“HS is characteristically defined as neuronal loss and gliosis in the hippocampus and the subiculum in the absence of correspondingly severe neurofibrillary tangle pathology (32, 34, 39).”
BackgroundMethodSelf-citationVos, A. D., Struyfs, H., Jacobs, D., Fransén, E., Klewansky, T., Roeck, E. E. D., Robberecht, C., Broeckhoven, C. V., Duyckaerts, C. J., Engelborghs, S., et al. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160227 · Cited by 54
“Finally, although neurogranin is also present in plasma, no confounding effects by the high plasma levels of neurogranin could be noted on the CSF levels of the protein, as studied in paired CSF-plasma samples [17, 22].”
Self-citationCrary, J. F. (2016) · Journal of Neurology and Neuromedicine · doi:10.29245/2572.942x/2016/6.1059 · Cited by 55
Angiotensin-III is Increased in Alzheimer’s Disease in Association with Amyloid-β and Tau Pathology
Kehoe, P. G., Hibbs, E., Palmer, L. E., & Miners, J. S. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-161265 · Cited by 53
“All brains had been subjected to detailed neuropathological assessment according to the NIA-AA guidelines [34] and AD pathology was a sufficient explanation for the dementia in these cases.”
Multisite Assessment of Aging-Related Tau Astrogliopathy (ARTAG)
Kovács, G. G., Xie, S. X., Lee, E. B., Robinson, J. L., Caswell, C., Irwin, D. J., Toledo, J. B., Johnson, V. E., Smith, D. H., Alafuzoff, I. I., et al. (2017) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlx041 · Cited by 54
Self-citationThe role of Locus Coeruleus in neuroinflammation occurring in Alzheimer’s disease
Giorgi, F. S., Saccaro, L. F., Galgani, A., Busceti, C. L., Biagioni, F., Frati, A., & Fornai, F. (2019) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2019.08.007 · Cited by 53
Lin, L., Nana, A. L., Hepker, M., Hwang, J., Gaus, S. E., Spina, S., Cosme, C. G., Gan, L., Grinberg, L. T., Geschwind, D. H., et al. (2019) · Acta Neuropathologica Communications · doi:10.1186/s40478-019-0809-0 · Cited by 48
Dysbiosis and Alzheimer’s Disease: Cause or Treatment Opportunity?
Janeiro, M. H., Ramírez, M. J., & Solas, M. (2021) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-020-01024-9 · Cited by 51
Koga, S., Ghayal, N. B., & Dickson, D. W. (2021) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlab005 · Cited by 51
“Pathological diagnosis of AD and assignment of Braak NFT stage and Thal amyloid phase were based on thioflavin S microscopy according to published criteria (24–26).”
MethodSelf-citationLiu, P., Smith, B. R., Montonye, M. L., Kemper, L. J., Leinonen-Wright, K., Nelson, K. M., Higgins, L., Guerrero, C. R., Markowski, T. W., Zhao, X., et al. (2020) · Scientific Reports · doi:10.1038/s41598-020-60777-x · Cited by 51
Sex differences for phenotype in pathologically defined dementia with Lewy bodies
Bayram, E., Coughlin, D. G., Banks, S. J., & Litvan, I. (2021) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp-2020-325668 · Cited by 52
Expression pattern of perilipins in human brain during aging and in Alzheimer's disease
Conte, M., Medici, V., Malagoli, D., Chiariello, A., Cirrincione, A., Davin, A., Chikhladze, M., Vasuri, F., Legname, G., Ferrer, I., et al. (2021) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12756 · Cited by 53
“from patients with different severity of AD (low, intermediate and high, based on neuropathological diagnosis [30]) and from centenarians.”
BackgroundMethodMontoliu‐Gaya, L., Alosco, M. L., Yhang, E., Tripodis, Y., Sconzo, D., Ally, M., Grötschel, L., Ashton, N. J., Lantero‐Rodriguez, J., Sauer, M., et al. (2023) · Acta Neuropathologica · doi:10.1007/s00401-023-02660-3 · Cited by 57
“Alzheimer’s disease (AD) neuropathological changes include the intracellular accumulation of hyperphosphorylated tau (p-tau) as neurofibrillary tangles (NFTs) and neuropil threads as well as the aggregation of extracellular amyloid beta (Aβ) plaques [17].”
BackgroundEvolutional Aspects of Alzheimer's Disease Pathogenesis
Braak, H., & Tredici, K. D. (2012) · Journal of Alzheimer s Disease · doi:10.3233/jad-2012-129029 · Cited by 54
“It is not possible to make a definitive diagnosis based on antemortem evidence alone [1].”
CRTC1 gene is differentially methylated in the human hippocampus in Alzheimer’s disease
Mendióroz, M., Celarain, N., Altuna, M., de Gordoa, J. S., Zelaya, M. V., Roldán, M., Rubio, I., Larumbe, R., Erro, M. E., Méndez-López, I., et al. (2016) · Alzheimer s Research & Therapy · doi:10.1186/s13195-016-0183-0 · Cited by 51
“Neuropathological examination was completed following the usual recommendations [27] and assessment of AD was performed according to the updated National Institute on Aging-Alzheimer's Association guidelines [26].”
MethodA Decade of Cerebrospinal Fluid Biomarkers for Alzheimer’s Disease in Belgium
Somers, C., Struyfs, H., Goossens, J., Niemantsverdriet, E., Luyckx, J., Roeck, N. D., Roeck, E. E. D., Vil, B. B. D., Cras, P. P., Martin, J., et al. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-151097 · Cited by 50
Chen, M., Lee, H. K., Moo, L. R., Hanlon, E. B., Stein, T. D., & Xia, W. (2018) · Journal of Proteomics · doi:10.1016/j.jprot.2018.04.032 · Cited by 53
“Alzheimer’s disease “ABC” scoring system was used for neuropathological assessment of the post-mortem human brains, showing a high degree of Alzheimer’s neuropathological change according to the NIA Alzheimer Association’s guidelines and is sufficient to account for the patient’s dementia [39].”
MethodMoreno‐Rodríguez, M., Perez, S. E., Nadeem, M., Malek‐Ahmadi, M. H., & Mufson, E. J. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-1723-x · Cited by 53
“The RROS neuropathology core includes the transactive response DNA-binding protein of 43 kDa (TDP-43) [65] in their diagnosis.”
Distinct clinicopathologic clusters of persons with TDP-43 proteinopathy
Katsumata, Y., Abner, E. L., Karanth, S. D., Teylan, M., Mock, C., Cykowski, M. D., Lee, E. B., Boehme, K. L., Mukherjee, S., Kauwe, J. S. K., et al. (2020) · Acta Neuropathologica · doi:10.1007/s00401-020-02211-0 · Cited by 48
Self-citationThomas, D. X., Bajaj, S., McRae‐McKee, K., Hadjichrysanthou, C., Anderson, R. M., & Collinge, J. (2020) · Scientific Reports · doi:10.1038/s41598-020-71305-2 · Cited by 53
Lexical and Acoustic Speech Features Relating to Alzheimer Disease Pathology
Cho, S., Cousins, K. A. Q., Shellikeri, S., Ash, S., Irwin, D. J., Liberman, M. Y., Grossman, M., & Nevler, N. (2022) · Neurology · doi:10.1212/wnl.0000000000200581 · Cited by 51
“Thirteen patients of 15 with autopsy data had a high probability of having AD pathologic change on the basis of established ABC scoring.(25) Four patients with posterior cortical atrophy and 3 patients with nonamnestic mild cognitive impairment who did not meet the criteria for lvPPA(18) were excluded from the analysi…”
BackgroundLimbic-Predominant Age-Related TDP-43 Encephalopathy
Gauthreaux, K. M., Teylan, M., Katsumata, Y., Mock, C., Culhane, J. E., Chen, Y., Chan, K. C. G., Fardo, D. W., Dugan, A. J., Cykowski, M. D., et al. (2022) · Neurology · doi:10.1212/wnl.0000000000200001 · Cited by 50
“HS pathology is diagnosed routinely with hematoxylin & eosin stains at autopsy, and HS has been defined as “severe pyramidal cell loss and gliosis in CA1 and subiculum of the hippocampal formation that is out of proportion to ADNC in the same structures”.(8) This definition lacks rigorous practical criteria or samplin…”
BackgroundSelf-citationGrau‐Rivera, O., Gelpí, E., Nos, C., Gaig, C., Ferrer, I., Saiz, A., Lladó, A., Molinuevo, J. L., Graus, F., Sánchez‐Valle, R., et al. (2015) · Neurodegenerative Diseases · doi:10.1159/000439251 · Cited by 51
Vermeiren, Y., Janssens, J., Aerts, T., Martin, J., Sieben, A., Dam, D. V., & Deyn, P. P. D. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160320 · Cited by 51
Prospects for strain-specific immunotherapy in Alzheimer’s disease and tauopathies
Bittar, A., Sengupta, U., & Kayed, R. (2018) · npj Vaccines · doi:10.1038/s41541-018-0046-8 · Cited by 50
Characteristics of the tissue section that influence the staining outcome in immunohistochemistry
Libard, S., Cerjan, D., & Alafuzoff, I. I. (2018) · Histochemistry and Cell Biology · doi:10.1007/s00418-018-1742-1 · Cited by 52
Baiardi, S., Abu‐Rumeileh, S., Rossi, M., Zenesini, C., Bartoletti‐Stella, A., Polischi, B., Capellari, S., & Parchi, P. (2018) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.697 · Cited by 53
“The pathological hallmarks of Alzheimer’s disease (AD) include the extracellular deposition of protein amyloid beta (Ab) in brain parenchyma and blood vessel walls, and the intraneuronal accumulation of hyperphosphorylated tau (p-tau).(1) According to the prevailing amyloid hypothesis, aggregation and tissue depositio…”
BackgroundMethodJonkman, L. E., Graaf, Y. G.-D., Bulk, M., Kaai, E., Pouwels, P. J. W., Barkhof, F., Rozemüller, A. J. M., van der Weerd, L., Geurts, J. J. G., & van de Berg, W. D. J. (2019) · NeuroImage Clinical · doi:10.1016/j.nicl.2019.101698 · Cited by 44
“These susceptibility-weighted changes are closely related to myelin and iron allowing detection of cortical lamination and iron-associated pathology (Bulk et al., 2018; Nabuurs et al., 2010; van Rooden et al., 2009).”
Kou, X., Chen, D., & Chen, N. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20071591 · Cited by 52
“The pathological changes of AD are diffuse atrophy of the cerebral cortex, deepening of cortical sulci, and narrowing of cerebral gyri, in which the loss of neurons, the extracellular deposition of amyloid-beta (Aβ) peptide as senile plaques (SPs), and the formation of neurofibrillary tangles (NFTs) are characteristic…”
BackgroundThe Na+/Ca2+exchanger in Alzheimer’s disease
Pannaccione, A., Piccialli, I., Secondo, A., Ciccone, R., Molinaro, P., Boscia, F., & Annunziato, L. (2020) · Cell Calcium · doi:10.1016/j.ceca.2020.102190 · Cited by 52
Pasquini, L., Nana, A. L., Toller, G., Brown, J. A., Deng, J., Staffaroni, A. M., Kim, E. J., Hwang, J., Li, L., Park, Y., et al. (2020) · Cerebral Cortex · doi:10.1093/cercor/bhaa119 · Cited by 51
Aphasia in Progressive Supranuclear Palsy: As Severe as Progressive Non-Fluent Aphasia
Burrell, J. R., Ballard, K. J., Halliday, G. M., & Hodges, J. R. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-170743 · Cited by 49
Bigio, E. H., Weıntraub, S., Rademakers, R., Baker, M. C., Ahmadian, S. S., RADEMAKER, A. W., Weitner, B. B., Mao, Q., Lee, K. ‐., Mishra, M., et al. (2012) · Neuropathology · doi:10.1111/j.1440-1789.2012.01332.x · Cited by 47
“Using the new criteria, 15 were “not AD,” two had low AD neuropathologic change (ADNC), and three had intermediate ADNC.21,22 There was no difference between groups in the presence of AD pathology.”
MethodInfluentialSelf-citationNeocortical and hippocampal TREM2 protein levels during the progression of Alzheimer's disease
Perez, S. E., Nadeem, M., He, B., Miguel, J. C., Malek‐Ahmadi, M. H., Chen, K., & Mufson, E. J. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.02.012 · Cited by 51
“Recent neuropathological guidelines for AD require the transactive response DNA-binding protein of 43 kDa (TDP-43) inclusions (Montine et al., 2012).”
BackgroundHase, Y., Polvikoski, T. M., Firbank, M., Craggs, L., Hawthorne, E., Platten, C., Stevenson, W., Deramecourt, V., Ballard, C. G., Kenny, R. A., et al. (2019) · Brain Pathology · doi:10.1111/bpa.12769 · Cited by 53
“The clinical diagnosis of AD was confirmed on evidence of significant Alzheimer’s-type pathology incorporating Braak stages V–VI, moderate-severe CERAD (26) and high ABC scores per National Institute of Aging-Alzheimer’s Association guidelines ((36)), in the general absence of significant vascular pathology (Table 2).”
BackgroundMethodIdentification of the function and mechanism of m6A reader IGF2BP2 in Alzheimer’s disease
Deng, Y., Zhu, H., Xiao, L., Liu, C., Liu, Y., & Gao, W. (2021) · Aging · doi:10.18632/aging.203652 · Cited by 48
Tau Pathology in Chronic Traumatic Encephalopathy is Primarily Neuronal
Butler, M. L. M. D., Dixon, E., Stein, T. D., Alvarez, V. E., Huber, B. R., Buckland, M. E., McKee, A. C., & Cherry, J. D. (2022) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlac065 · Cited by 54
Liu, F., Sun, J., Wang, X., Jin, S., Sun, F., Wang, T., Yuan, B., Qiu, W., & Ma, C. (2022) · Neuroscience Bulletin · doi:10.1007/s12264-022-00927-5 · Cited by 48
“A neuropathological AD score of I/H indicates that the donor is very likely to have AD and can be considered a sufficient explanation for dementia [36].”
BackgroundInfluentialLong, J. M., Coble, D. W., Xiong, C., Schindler, S. E., Perrin, R. J., Gordon, B. A., Benzinger, T. L. S., Grant, E., Fagan, A. M., Harari, O., et al. (2022) · Brain · doi:10.1093/brain/awac250 · Cited by 49
Cross-disorder and disease-specific pathways in dementia revealed by single-cell genomics
Rexach, J. E., Cheng, Y., Chen, L., Polioudakis, D., Lin, L., Mitri, V., Elkins, A., Han, X., Yamakawa, M., Yin, A., et al. (2024) · Cell · doi:10.1016/j.cell.2024.08.019 · Cited by 59
Self-citationSpatial proteomics of Alzheimer’s disease-specific human microglial states
Mrdjen, D., Cannon, B. J., Amouzgar, M., Kim, Y., Liu, C. C., Vijayaragavan, K., Fullaway, C. C., Spence, A., McCaffrey, E., Bharadwaj, A., et al. (2025) · Nature Immunology · doi:10.1038/s41590-025-02203-w · Cited by 58
“Donors were age-matched and selected based on their clinical diagnosis and neuropathological scores evaluated by National Institute on Aging–Alzheimer’s Association guidelines 93 .”
Self-citationKalimo, H., Lalowski, M. M., Bogdanović, N., Philipson, O., Bird, T. D., Nochlin, D., Schellenberg, G. D., Brundin, R., Olofsson, T., Soliymani, R., et al. (2013) · Acta Neuropathologica Communications · doi:10.1186/2051-5960-1-60 · Cited by 52
“When the ABC system of the new 2012 NIA-AA criteria [23,25] is applied, the distribution of Aβ plaques, i.”
BackgroundMethodNeuroleptic‐induced P arkinsonism: C linicopathological study
Shuaib, U., Rajput, A. H., Robinson, C. A., & Rajput, A. H. (2015) · Movement Disorders · doi:10.1002/mds.26467 · Cited by 48
“Tau immunostaining revealed changes consistent with an Alzheimer’s disease neuropathological score of “low” according to 2012 National Institute on Aging-Alzheimer’s Association guidelines.(18) Thus, although not ruled out, a definite diagnosis of Alzheimer’s disease could not be made, and the cause for his dementia c…”
BackgroundThe rise and fall of insulin signaling in Alzheimer’s disease
Chami, B., Steel, A. J., de la Monte, S. M., & Sutherland, G. T. (2016) · Metabolic Brain Disease · doi:10.1007/s11011-016-9806-1 · Cited by 48
Beach, T. G., Thal, D. R., Zanette, M., Smith, A. P. L., & Buckley, C. J. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-150732 · Cited by 48
“low, intermediate or high) [21, 22], by the amyloid”
BackgroundSelf-citation
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.
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