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.
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- 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)
plainstates a cause- Asserted: passes — The authors put it forward as true.
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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
hedgedstates an association- 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)
hedgedstates an association- 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)
hedgedstates a possible cause- 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
plainstates an association- 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
plainstates an association- 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)
plainstates an association- 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)
plainstates an association- 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)
hedgedstates an association- 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
hedgedstates an association- 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
“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]
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
“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 2,401–2,500 of 2,854
Biomarkers used in Alzheimer's disease diagnosis
Mishra, S. K., Singh, R., Chang, H., Obaid, A. A., & Singh, S. K. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-15540-6.00013-6 · Cited by 1
Neuropathology of trisomy 21 mosaicism in a case with early‐onset dementia
Ngo, P. T., Pascual, J. R., Wright, S. T., Williams, C. K., Magaki, S., Yong, W. H., Vinters, H. V., Ringman, J. M., & Head, E. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.14394 · Cited by 1
Self-citationMätlik, K., Pressl, C., & Heintz, N. (2025) · Annual Review of Neuroscience · doi:10.1146/annurev-neuro-112723-025516 · Cited by 1
Sun, J., Shao, X., Wang, X. L., Yin, X., Qiu, W., Qian, X., Liu, F., Chen, Y., & Ma, C. (2025) · Molecular Brain · doi:10.1186/s13041-025-01226-6 · Cited by 4
“Therefore, the “I/H” group provides substantial evidence for dementia [22].”
Corticobasal degeneration preceded by cognitive impairment and apathy: An autopsy case report
Hirose, S., Kobayashi, R., Hatakeyama, S., Kawakatsu, S., Suzuki, A., Kawanishi, C., & Utsumi, K. (2025) · Psychiatry and Clinical Neurosciences Reports · doi:10.1002/pcn5.70174 · Cited by 1
“AD neuropathologic changes, evaluated using the ABC score, 11 were graded as A0B1C0, indicating “ Not AD.”
Alzheimer-Associated Pathology in the Extracellular Space
Braak, H., & Tredici, K. D. (2014) · Advances in anatomy, embryology and cell biology · doi:10.1007/978-3-319-12679-1_8 · Cited by 1
Alzheimer's Disease: Current Clinical and Neuropathologic Diagnostic Criteria
Ka, J. (2014) · Cited by 1
Neuroimaging Advances in Alzheimer's Disease
Schonhaut, D. R., & Rabinovici, G. D. (2016) · Elsevier eBooks · doi:10.1016/b978-0-12-800105-9.00017-2 · Cited by 1
Wijesinghe, P., Gorrie, C. A., Shankar, S. K., et al. (2017) · Indian Journal of Psychiatry · doi:10.4103/psychiatry.indianjpsychiatry_102_16 · Cited by 1
“The diagnostic criteria for Alzheimer’s disease (AD) neuropathologic change was based on National Institute on Aging − Alzheimer’s Association guidelines (NIA‑AA)[10] – a practical approach which included: • Consortium to Establish a Registry for AD (CERAD) protocol for NP scoring[11] • Braak and Braak staging scheme…”
InfluentialNeuropathological Insights Into the Link Between Type 2 Diabetes and Dementia
Pruzin, J. J., Nelson, P. T., Abner, E. L., & Arvanitakis, Z. (2018) · Elsevier eBooks · doi:10.1016/b978-0-12-809454-9.00006-8 · Cited by 1
Self-citationJellinger, K. A. (2015) · EMJ Neurology · doi:10.33590/emjneurol/10311025 · Cited by 1
Background of the neuropathological site in neurocognitive decline in elderly schizophrenic patients
Hirano, M., Iritani, S., Sekiguchi, H., et al. (2020) · Psychogeriatrics · doi:10.1111/psyg.12522 · Cited by 1
An autopsy case of primary lateral sclerosis with Alzheimer's disease
Nakamura, T., Kon, T., Kawarabayashi, T., et al. (2020) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2020.116792 · Cited by 1
Schandl, C. A. (2020) · Cambridge University Press eBooks · doi:10.1017/9781316823040.005 · Cited by 1
Chung, E. J., Cho, H. J., Hur, D. Y., Kim, Y. S., Lee, K., & Kim, S. J. (2022) · Journal of Korean Medical Science · doi:10.3346/jkms.2022.37.e195 · Cited by 1
Epileptic Focus in Drug-Resistant Epilepsy: Structure, Organization, and Pathophysiology
Zabrodskaya, Y. M., Gaykova, O. N., Alexandrov, M. V., et al. (2022) · IntechOpen eBooks · doi:10.5772/intechopen.108395 · Cited by 1
Ellison, D., Love, S., Chimelli, L. M. C., Harding, B. N., Lowe, J. S., Vinters, H. V., Brandner, S., & Yong, W. H. (2013) · Elsevier eBooks · doi:10.1016/b978-0-7234-3515-0.00031-3 · Cited by 1
Self-citationBrain pathological changes from population-based studies
Cao, Y., Huang, M., Shu, M.-J., & Zhu, Y. (2022) · Human Brain · doi:10.37819/hb.001.001.0205 · Cited by 1
Lipidomics for Health and Disease
(2016) · Wiley eBooks · doi:10.1002/9781119085263.ch17 · Cited by 1
Neltner, J. H., & Nelson, P. T. (2017) · Neurodegeneration · doi:10.1002/9781118661895.ch1 · Cited by 1
Self-citationIturria‐Medina, Y., Khan, A. F., Adewale, Q., & Initiative, A. D. N. (2019) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/548974 · Cited by 1
“as Lewy body disease, vascular brain injury, hippocampal sclerosis, and TAR DNA binding protein (TDP) immunoreactive inclusions (Montine et al., 2012).”
BackgroundE2F4 as a single multifactorial target against Alzheimer’s diseasePreprint
López‐Sánchez, N., Ramón‐Landreau, M., Trujillo, C., Garrido‐García, A., & Frade, J. M. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.05.08.082784 · Cited by 1
Deep learning from multiple experts improves identification of amyloid neuropathologiesPreprint
Wong, D., & Keiser, M. J. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.17605/osf.io/xh2jd · Cited by 1
Joint ex vivo MRI and histology detect iron-rich cortical gliosis in Tau and TDP-43 proteinopathiesPreprint
Tisdall, M. D., Ohm, D. T., Lobrovich, R., Das, S. R., Mizsei, G., Prabhakaran, K., Ittyerah, R., Lim, S., McMillan, C. T., Wolk, D. A., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.04.14.439064 · Cited by 1
“Neuropathological diagnosis was performed using tissue from the non-scanned hemisphere by experienced neuropathologists (EBL, JQT) using well characterized antibodies(57) and current diagnostic criteria.(58,2,59)”
MethodSelf-citationEarly Detection of Tau PathologyPreprint
Parekh, P. A., Badachhape, A., Mu, Q., Bhavane, R. C., Srivastava, M., Stupin, I. V., Bhandari, P., Devkota, L., Eriksen, J. L., Tanifum, E. A., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.05.14.444233 · Cited by 1
Concomitant AD and DLB pathologies shape subfield microglia responses in the hippocampusPreprint
Fixemer, S., Ameli, C., Hammer, G. P., Salamanca, L., Huarte, O. U., Schwartz, C., Gérardy, J., Mechawar, N., Skupin, A., Mittelbronn, M. G. A., et al. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.01.06.475218 · Cited by 1
Huang, Z., Merrihew, G. E., Larson, E. B., Park, J., Plubell, D. L., Fox, E. J., Montine, K. S., Keene, C. D., Zou, J., MacCoss, M. J., et al. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.10.09.511430 · Cited by 1
“While each of these diseases on its own can cause dementia, in the majority of affected individuals these diseases variably combine in a now widely validated idiosyncratic conspiracy of Alzheimer’s disease (AD), vascular brain injury (VBI), Lewy body disease (LBD), hippocampal sclerosis (HS), and limbic-associated TDP…”
BackgroundMethodInfluentialSelf-citationLi, D., Wang, Y., Ang, T. F. A., Xia, W., Aytan, N., Mez, J., Devine, S., Au, R., Farrer, L. A., Stein, T. D., et al. (2022) · Research Square · doi:10.21203/rs.3.rs-2133099/v1 · Cited by 1
Réveret, L., Manon, L., Vincent, E., Loiselle, A., Bourassa, P., Tremblay, C., Bennett, D. A. A., Sébastien, H., & Frédéric, C. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.01.17.524254 · Cited by 1
FTLD targets brain regions expressing recently evolved genesPreprint
Pasquini, L., Pereira, F. L., Seddighi, S., Zeng, Y., Wei, Y., Illán‐Gala, I., Vatsavayai, S. C., Friedberg, A., Lee, A. J., Brown, J. A., et al. (2023) · medRxiv · doi:10.1101/2023.10.27.23297687 · Cited by 1
Jung, S. H., Roy, R. N., Wang, X., Liu, B., Jaiswal, N., Rai, R. K., Takagi, Y., Gao, C., Zeng, L., Lo, H.-Y., et al. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.12.29.573648 · Cited by 1
Santiago-Ruiz, A. N., Hugelier, S., Bond, C. R., Lee, E. B., & Lakadamyali, M. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.04.24.590893 · Cited by 1
Koss, D. J., Todd, O., Menon, H., Anderson, Z., Yang, T., Attems, J., LeBeau, F. E. N., Erskine, D., & Outeiro, T. F. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.04.24.590825 · Cited by 1
Kim, B., Blam, K., Elser, H. C., Xie, S. X., Deerlin, V. M. V., Penning, T. M., Weintraub, D. A., Irwin, D. J., Massimo, L. M., McMillan, C. T., et al. (2024) · medRxiv · doi:10.1101/2024.07.18.24310646 · Cited by 1
Pathologic subtyping of Alzheimer’s disease brain tissue reveals disease heterogeneityPreprint
Lam, T. G., Ross, S. K., Ciener, B., Xiao, H., Flaherty, D., Lee, A., Dugger, B. N., Reddy, H., & Teich, A. F. (2024) · medRxiv · doi:10.1101/2024.10.14.24315458 · Cited by 1
Compensatory Plasticity Defines a Vulnerable Neuronal State in Alzheimer’s Disease with PsychosisPreprint
Victor, M. B., Sun, N., Galani, K., Leary, N., Tanigawa, Y., Scannail, A. N., Ho, L., Prosper, S., Liu, L., Kofler, J., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.04.30.651435 · Cited by 1
“At the time of autopsy, the brain was bisected and the left hemisphere fixed in formalin for subsequent diagnostic evaluation using consensus guidelines 85–88 .”
Simonetti, F., Zhong, W., Hutten, S., Uliana, F., Schifferer, M., Rezaei, A., Ramirez, L. M., Hochmair, J., Sankar, R., Gopalan, A. B., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.07.07.662960 · Cited by 1
Piras, I. S., Bonfitto, A., Song, S., Aldabergenova, A., Sloan, J., Trejo, A., Troncoso, J. C., Geula, C., Rogalski, E. J., Kawas, C. H., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.10.19.683343 · Cited by 3
Self-citationInfluenza A infection accelerates disease-associated microglia formation during physiological agingPreprint
Grant, R. A., Runyan, C. E., Minogue, G., Stoolman, J. S., Watanabe, S., Chen, F., Senkow, K. J., Cusick, L., Schleck, M. J., Nafikova, R. A., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2025.12.11.693336 · Cited by 1
Microglial reactivity in the hippocampal CA2 is associated with advanced neuronal α-synucleinopathyPreprint
Luna, E., Cousins, K. A. Q., Emrani, S., Xie, S. X., Trotman, W., Weintraub, D. A., Chen‐Plotkin, A. S., Lee, E. B., & Irwin, D. J. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.02.06.704430 · Cited by 1
“We performed a large-scale detailed digital histopathological study using almost 300 slides from >70 autopsied patients to test the hypothesis that microglial abnormalities classically associated with a pro-inflammatory state are associated with increasing distribution and severity of n-asyn across the interconnected…”
InfluentialCasamitjana, A., Lorenzi, M., Ferraris, S., Peter, L., Marc Modat, A., Stevens, A. A., Fischl, B. R., Vercauteren, T. K., & Iglesias, J. E. (2021) · Medical Image Analysis · doi:10.1016/j.media.2021.102265
Nomethiazoles: PK/PD Study of a Novel Class of Alzheimer’s Disease Therapeutics
Tavassoli, E. (2012) · Figshare
Balasa, M. (2013) · Dipòsit Digital de la Universitat de Barcelona (Universitat de Barcelona)
Reexamination casts doubt on brain tissue classified as healthy
Chakradhar, S. (2015) · Nature Medicine · doi:10.1038/nm0415-296
Correlati neurobiologici nell'anziano con malattia di alzheimer e altre demenze
Guaita, A. (2013) · RICERCHE DI PSICOLOGIA · doi:10.3280/rip2012-002016
O4‐02‐05: Neuropathologic basis of white matter hyperintensity accumulation
Erten‐Lyons, D., Woltjer, R. L., Dodge, H. H., Stanfield, S., Reese, L. C., Tran, H. T. D., Quinn, J. F., Wild, K., Oken, B., Kaye, J. A., et al. (2012) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2012.05.1644
Darlington, D. (2014) · Digital Commons - University of South Florida (University of South Florida)
Microtubules and the Protein Tau
Braak, H., & Tredici, K. D. (2014) · Advances in anatomy, embryology and cell biology · doi:10.1007/978-3-319-12679-1_4
Abner, E. L. (2013) · UKnowledge (University of Kentucky)
Understanding Conflicting Neuropathological Findings
Jellinger, K. A. (2016) · JAMA Neurology · doi:10.1001/jamaneurol.2015.4879
Dexter, D. T., Al‐Sarraj, S., Seilhean, D., et al. (2015)
Alafuzoff, I. I., Pikkarainen, M., & Parkkinen, L. (2014) · Cambridge University Press eBooks · doi:10.1017/cbo9781107588660.009
Pathological diagnosis of coexistence of ALS with Alzheimer’s disease
Yamamoto, T. (2015) · Rinsho Shinkeigaku · doi:10.5692/clinicalneurol.cn-000604
Munger, E. L. (2016) · OhioLink ETD Center (Ohio Library and Information Network)
Inhibition of Alzheimer’s type toxic aggregates of tau with fungal secondary metabolites
Paranjape, S. R. (2015) · KU ScholarWorks (University of Kansas)
Immunopathology of the Nervous System
Remick, A. K., Pershing, M. L., Papenfuss, T. L., Lanigan, L. G., Beck, M. J., & Toot, J. (2017) · Molecular and integrative toxicology · doi:10.1007/978-3-319-47385-7_5 · Cited by 1
SHORT COMMUNICATION Acetylated Tau Neuropathology in Sporadic and Hereditary Tauopathies
Irwin, D. J., Cohen, T. J., Grossman, M., Arnold, S. E., Deerlin, V. M. V., Lee, Y., & Trojanowski, J. Q. (2013)
Self-citationMisquitta, K. (2017) · TSpace (University of Toronto)
Methods for Pathological Classification of Alzheimer’s Disease
Attems, J., McAleese, K. E., & Walker, L. (2018) · Neuromethods · doi:10.1007/978-1-4939-7674-4_5
Neuropathological Assessment as an Endpoint in Clinical Trial Design
Gentleman, S., & Liu, A. K. L. (2018) · Methods in molecular biology · doi:10.1007/978-1-4939-7704-8_18
Iwasaki, Y., Deguchi, A., Mori, K., Ito, M., Kawai, Y., Akagi, A., Mimuro, M., Miyahara, H., & Yoshida, M. (2018) · Neuropathology · doi:10.1111/neup.12521
“ever, autopsy is required to arrive at a definite diagnosis.(1,2) The neuropathological criteria of AD are based on”
BackgroundInfluentialArmstrong, R. A. (2018) · EMJ Neurology · doi:10.33590/emjneurol/10312487
Moon, Y., & Kim, E. J. (2019) · Journal of the Korean Neurological Association · doi:10.17340/jkna.2019.2.25
“베타아밀로이드신경과-moderate, C3: 베타아밀로이드신경판-frequent) (Table 2).(5,6) 각 병리 변화, 즉 A, B, C별 단계는 0-3으로 표시되므로 A0B0C0부”
Alzheimer’s Disease and Overview of Dementia
Trittschuh, E. H., & Wang, L. L. (2019) · Springer eBooks · doi:10.1007/978-1-4939-8722-1_12
Assessing circular RNAs in Alzheimer diseasePreprint
Cervera‐Carles, L., Dols‐Icardo, O., González, A. C., Molina‐Porcel, L., Muñoz, L., & Clarimón, J. (2019) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/800342
Laton, J., Schependom, J. V., Goossens, J., et al. (2019) · medRxiv · doi:10.1101/19009316
“Subgroups of definite dementia patients were defined by genetic carrier status and/or post-mortem confirmation of brain pathology (Mackenzie et al., 2011; MacKenzie et al., 2010; Montine et al., 2012).”
BackgroundUnderstanding and improving the diagnosis of dementia with Lewy bodies
Kane, J. P. M. (2019)
Khatun, A., Paterson, R. W., & Schöll, M. (2020) · Alzheimer s Research & Therapy · doi:10.1186/s13195-020-0583-z
Neuropathology of Alzheimer’s Disease and Vascular Dementia
Kapasi, A., & Schneider, J. A. (2020) · Oxford University Press eBooks · doi:10.1093/oso/9780190634230.003.0015
Self-citationReview: Role of Autophagy in Nervous System Injury
Xie, Z., & Shen, E. (2020) · Molecular Biology & Nanomedicine · doi:10.37813/j.mbn.2707-4692.005
Neurodegenerative Diseases in Elders
Reichard, R. R., Iles, L. E., Swanson, A. A., & Crain, B. J. (2020) · Cambridge University Press eBooks · doi:10.1017/9781316823040.019
Fine Particulate Matter, Neuropathologies, & Dementia
Shaffer, R. M. (2020) · ResearchWorks at the University of Washington (University of Washington)
Joo, K. E., 김현우, 강태호, et al. (2013)
The aging brain and brain banking
Jeżewski, R. C., Halliday, G. M., & Shepherd, C. E. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-818000-6.00010-x
Dendritic spine remodeling and aging
Boros, B. D., & Herskowitz, J. H. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-817990-1.00022-6
Small Vessel Diseases: 3D Characteristics of the Vasculature and White MatterPreprint
Saito, R., Tainaka, K., Nozaki, H., Uemura, M., Toyoshima, Y., Suzuki, M., Tanaka, M., Hasegawa, A., Abe, T., Sato, A., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.06.30.450101
Gut Dysbiosis and Neurological Disorders—An Eclectic Perspective
Bostancıklıoğlu, M., & Demir, T. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-819265-8.00041-3 · Cited by 1
A TREM2 -derived circRNA is upregulated in the entorhinal cortex of Alzheimer’s disease patientsPreprint
Urdánoz‐Casado, A., de Gordoa, J. S., Robles, M., Roldán, M., Zelaya, M. V., Blanco‐Luquin, I., & Mendióroz, M. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.06.23.449571
“Neuropathological examination was completed following the usual recommendations 138 (49) and according to the updated National Institute on Aging-Alzheimer’s Association guidelines 139 (50).”
MethodPixley, L. D. (2020) · ResearchWorks at the University of Washington (University of Washington)
Genetic analyses of SERPINA5 in Alzheimer’s diseasePreprint
Matchett, B. J., Lincoln, S., Baker, M. C., Tamvaka, N., Cabrera-Rodriguez, J. N., Labuzan, S. A., Helminger, J., Hinkle, K. M., Duara, R., Graff‐Radford, N. R., et al. (2021) · Research Square · doi:10.21203/rs.3.rs-769744/v1
Self-citationGonzález, A. C., Irwin, D. J., Alcolea, D. A., McMillan, C. T., Chen‐Plotkin, A. S., Wolk, D. A., Sirisi, S., Dols‐Icardo, O., Querol‐Vilaseca, M., Illán‐Gala, I., et al. (2021) · Research Square · doi:10.21203/rs.3.rs-885718/v1
Self-citationPitman, J., & Chiang, G. C.-Y. (2021) · Springer eBooks · doi:10.1007/978-3-030-82367-2_25
Heat Acclimation for Special Populations
(2020) · Frontiers research topics · doi:10.3389/978-2-88966-018-6 · Cited by 1
Jiang, Y., Zhang, L., Li, Y., et al. (2021) · IEEE International Conference on Bioinformatics and Biomedicine (BIBM) · doi:10.1109/bibm52615.2021.9669322
An overview of Alzheimer's disease and its diagnosis using conventional and novel methods
Zhao, X. (2021) · International Conference on Bioinformatics and Biomedical Science (ICBBS) · doi:10.1145/3498731.3498761
“Microscopic examination of multiple brain regions with staining methods can detect Alzheimer type neuropathologic changes, and diagnoses are based upon the morphology and density of lesions and their topographic distribution [17].”
Deramecourt, V. (2022) · La Presse Médicale Formation · doi:10.1016/j.lpmfor.2022.01.014
(2020) · Emerald Group Publishing Limited eBooks · doi:10.1108/978-1-83867-691-920201009
Rujescu, D., & Jung, M. (2019) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.725966450.793557761
Schleicher, E. M. (2021) · eDiss (Georg-August-Universität Göttingen) · doi:10.53846/goediss-8990
Advancing the Characterization of Neuronal Cyto-Architecture by X-ray Phase-Contrast Tomography
Eckermann, M. (2021) · Göttingen series in x-ray physics · doi:10.17875/gup2021-1830
Saldanha, N. M. (2021) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/d.5.2021.tde-31032022-162126
OLIVEIRA, P. S. D., & Urbano, J. V. F. (2022) · Editora Pasteur eBooks · doi:10.29327/561131.1-19
Rosenzweig, S. A. (2020) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.727123638.793572332
Mrak, R. E., & Angtuaco, E. J. (2017) · Cambridge University Press eBooks · doi:10.1017/9781139696401.010
Ashford, J. W. (2018) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.734280398.793553881
Petersen, R. B. (2019) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.734510478.793555621
Age-related cytoskeletal pathologies
Wijesinghe, P. (2020) · doi:10.26481/dis.20202508pk
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 ›
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