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 1,101–1,200 of 2,854
Neurodegenerative proteinopathies associated with neuroinfections
Danics, K., Forrest, S. L., Kapás, I., Erber, I., Schmid, S., Törő, K., Majtényi, K., & Kovács, G. G. (2021) · Journal of Neural Transmission · doi:10.1007/s00702-021-02371-7 · Cited by 28
Chen, C. D., Joseph‐Mathurin, N., Sinha, N., Zhou, A., Li, Y., Friedrichsen, K. A., McCullough, A. A., Franklin, E. E., Hornbeck, R. C., Gordon, B. A., et al. (2021) · Acta Neuropathologica · doi:10.1007/s00401-021-02342-y · Cited by 27
“All participants met the inclusion criteria, having undergone PiB PET prior to death, and having high AD neuropathologic change (ADNC) upon subsequent postmortem examination [51].”
BackgroundSelf-citationCollusion of α-Synuclein and Aβ aggravating co-morbidities in a novel prion-type mouse model
Lloyd, G. M., Dhillon, J.-K. S., Gorion, K.-M. M., Riffe, C. J., Fromholt, S., Xia, Y., Giasson, B. I., & Borchelt, D. (2021) · Molecular Neurodegeneration · doi:10.1186/s13024-021-00486-9 · Cited by 29
Association of cerebral microvascular dysfunction and white matter injury in Alzheimer’s disease
Bagi, Z. A., Kroenke, C. D., Fopiano, K. A., Tian, Y., Filosa, J. A., Sherman, L. S., Larson, E. B., Keene, C. D., Degener-O’Brien, K., Adeniyi, P. A., et al. (2022) · GeroScience · doi:10.1007/s11357-022-00585-5 · Cited by 27
Pathophysiological evaluation of the LRRK2 G2385R risk variant for Parkinson’s disease
Tezuka, T., Taniguchi, D., Sano, M., Shimada, T., Oji, Y., Tsunemi, T., Ikeda, A., Li, Y., Yoshino, H., Ogata, J., et al. (2022) · npj Parkinson s Disease · doi:10.1038/s41531-022-00367-y · Cited by 27
Alosco, M. L., Su, Y., Stein, T. D., Protas, H. D., Cherry, J. D., Adler, C. H., Balcer, L. J., Bernick, C. B., Pulukuri, S. V., Abdolmohammadi, B., et al. (2022) · European Journal of Nuclear Medicine and Molecular Imaging · doi:10.1007/s00259-022-05963-x · Cited by 28
“Established criteria were used for the neuropathological diagnosis of neurodegenerative diseases [56– 64].”
Self-citationMethylation differences in Alzheimer’s disease neuropathologic change in the aged human brain
Lang, A.-L., Eulalio, T. Y., Fox, E., Yakabi, K., Bukhari, S. A., Kawas, C. H., Corrada, M. M., Montgomery, S. B., Heppner, F. L., Capper, D., et al. (2022) · Acta Neuropathologica Communications · doi:10.1186/s40478-022-01470-0 · Cited by 26
“Neuropathological assessment and clinical diagnosis All cases were scored by a neuropathologist following the National Institute on Aging–Alzheimer’s Association (NIA-AA) guidelines for the neuropathologic assessment of Alzheimer’s disease [15, 16].”
MethodSelf-citationLysosomal polygenic risk is associated with the severity of neuropathology in Lewy body disease
Tunold, J., Tan, M. M. X., Koga, S., Geut, H., Rozemüller, A. J. M., Valentino, R. R., Sekiya, H., Martin, N. B., Heckman, M. G., Brás, J., et al. (2023) · Brain · doi:10.1093/brain/awad183 · Cited by 29
“21,30 Lewy pathology was assessed in the neocortices (frontal, temporal, parietal, visual and motor), cingulate gyrus, transentorhinal cortex, amygdala, basal forebrain, midbrain, pons and medulla using α -syn immunohistochemistry (NACP, 1:3000 rabbit polyclonal, Mayo Clinic antibody).”
Self-citationExpanded vacuum-stable gels for multiplexed high-resolution spatial histopathology
Bai, Y., Zhu, B., Oliveria, J. P., Cannon, B. J., Feyaerts, D., Bosse, M. M., Vijayaragavan, K., Greenwald, N. F., Phillips, D. J., Schürch, C. M., et al. (2023) · Nature Communications · doi:10.1038/s41467-023-39616-w · Cited by 29
Single-Cell Sequencing in Neurodegenerative Disorders
Pozojevic, J., & Spielmann, M. (2023) · Molecular Diagnosis & Therapy · doi:10.1007/s40291-023-00668-9 · Cited by 30
“Pathologically, AD is characterized by the presence of β-amyloid-containing plaques in the cerebral cortex and tau-containing neurofibrillary tangles [40, 41].”
BackgroundKIBRA repairs synaptic plasticity and promotes resilience to tauopathy-related memory loss
Kauwe, G., Pareja-Navarro, K. A., Yao, L., Chen, J. H., Wong, I., Saloner, R., Cifuentes, H., Nana, A. L., Shah, S., Li, Y., et al. (2024) · Journal of Clinical Investigation · doi:10.1172/jci169064 · Cited by 28
Ashby, E. L., Miners, J. S., Kumar, S., Walter, J., Love, S., & Kehoe, P. G. (2014) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12212 · Cited by 26
Fujioka, S., Sundal, C., Strongosky, A. J., Castanedes, M. C., Rademakers, R., Ross, O. A., Vilariño‐Güell, C., Farrer, M. J., Wszołek, Z. K., & Dickson, D. W. (2012) · Acta Neuropathologica · doi:10.1007/s00401-012-1059-4 · Cited by 28
“advanced pathology (A3, B3, C3) using the NIA-AA classification and none had greater than ‘‘intermediate’’ Alzheimer neuropathologic change [39].”
Self-citationGoossens, J., Laton, J., Schependom, J. V., Gielen, J., Struyfs, H., Mossevelde, S. V., den Bossche, T. V., Goeman, J., Deyn, P. P. D., Sieben, A., et al. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160188 · Cited by 43
Progressive ataxia and palatal tremor: Two autopsy cases of a novel tauopathy
Gao, A. F., Faust‐Socher, A., Almurshed, M., Bigio, M. R. D., Lang, A. E., & Muñoz, D. G. (2017) · Movement Disorders · doi:10.1002/mds.27074 · Cited by 27
Quantitative Assessment of Pathological Tau Burden in Essential Tremor: A Postmortem Study
Farrell, K. W., Cosentino, S., Iida, M. A., Chapman, S., Bennett, D. A., Faust, P. L., Louis, E. D., & Crary, J. F. (2018) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nly104 · Cited by 27
Genetic screening in early-onset Alzheimer's disease identified three novel presenilin mutations
Wong, T. H., Seelaar, H., Melhem, S., Rozemüller, A. J. M., & Swieten, J. C. V. (2019) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2019.01.015 · Cited by 27
Coexisting Lewy body disease and clinical parkinsonism in frontotemporal lobar degeneration
Forrest, S. L., Crockford, D. R., Sizemova, A., McCann, H., Shepherd, C. E., McGeachie, A. B., Affleck, A. J., Carew‐Jones, F., Bartley, L., Kwok, J. B., et al. (2019) · Neurology · doi:10.1212/wnl.0000000000007530 · Cited by 27
“).(27) Final neuropathologic diagnoses were reviewed by 3 authors (S.”
MethodInhibition of Polo-like kinase 2 ameliorates pathogenesis in Alzheimer’s disease model mice
Lee, J. S., Lee, Y., André, E. A., Lee, K. J., Nguyen, T., Feng, Y., Jia, N., Harris, B. T., Burns, M. P., & Pak, D. T. S. (2019) · PLoS ONE · doi:10.1371/journal.pone.0219691 · Cited by 30
Jang, H., Kim, H. J., Park, S., Park, Y. H., Choe, Y. S., Cho, H., Lyoo, C. H., Yoon, U., Lee, J. S., Kim, Y., et al. (2019) · European Journal of Nuclear Medicine and Molecular Imaging · doi:10.1007/s00259-019-04498-y · Cited by 27
CSF Biomarkers of Alzheimer Disease in Patients With Concomitant α-Synuclein Pathology
Cousins, K. A. Q., Arezoumandan, S., Shellikeri, S., Ohm, D., Shaw, L. M., Grossman, M., Wolk, D., McMillan, C. T., Chen-Plotkin, A., Lee, E., et al. (2022) · Neurology · doi:10.1212/wnl.0000000000201202 · Cited by 25
“At the same time, low CSF Ng levels may be associated with αSyn with or without ADNC.”
BackgroundMethodInfluentialSelf-citationOllen‐Bittle, N., Pejhan, S., Pasternak, S., Keene, C. D., Zhang, Q., & Whitehead, S. N. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02759-1 · Cited by 33
“…AD follows a predictable pattern, which is the basis for the neuro-pathological staging of the disease, which incorporates Aβ plaque distribution across the brain (Thal Phase [2]), NFT distribution across the brain (Braak stage [3]), and cerebral cortical neuritic plaque density (CERAD score) [4].”
Sweeney, N., Kim, T. Y., Morrison, C. T., Li, L., Acosta, D. M., Liang, J., Datla, N. V., Fitzgerald, J. A., Huang, H., Liu, X., et al. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02810-1 · Cited by 28
Self-citationA guide for blood–brain barrier models
Soliman, Y., Al‐khodor, J., Koken, G. Y., & Mustafaoğlu, N. (2024) · FEBS Letters · doi:10.1002/1873-3468.15053 · Cited by 30
“Notably, an increase in BM thickness has been observed and associated with aging in humans and mice due to the accumulation of collagen IV in the matrix [81,82], as well as in AD patients [83].”
Jamerlan, A., An, S. S. A., & Hulme, J. (2025) · Gut Microbes · doi:10.1080/19490976.2025.2486518 · Cited by 34
Sekiya, H., Matsubara, T., Deture, M. A., & Dickson, D. W. (2025) · Molecular Neurodegeneration · doi:10.1186/s13024-025-00900-6 · Cited by 35
“Additionally, the density of neuritic plaques is assessed using the Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) score [466].”
Self-citationZhou, F., Jiang, J., Griffith, C. M., Patrylo, P. R., Cai, H., Chu, Y., & Yan, X. (2018) · Alzheimer s Research & Therapy · doi:10.1186/s13195-018-0370-2 · Cited by 25
Liquid-Liquid Phase Separation of Tau Protein in Neurobiology and Pathology
Wegmann, S. (2019) · Advances in experimental medicine and biology · doi:10.1007/978-981-32-9358-8_25 · Cited by 28
Early epigenetic changes of Alzheimer’s disease in the human hippocampus
Blanco‐Luquin, I., Acha, B., Urdánoz‐Casado, A., de Gordoa, J. S., Vicuña‐Urriza, J., Roldán, M., Labarga, A., Zelaya, M. V., Cabello, C., Méndez-López, I., et al. (2020) · Epigenetics · doi:10.1080/15592294.2020.1748917 · Cited by 28
“ABC score combines histopathologic assessments of β-amyloid deposits determined by the method of Thal (A) [18], staging of neurofibrillary tangles by Braak and Braak classification (B) [14], and scoring of neuritic plaques by the method of CERAD (Consortium to Establish A Registry for 1084 I.”
MethodAbbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains
Poloni, T. E., Medici, V., Carlos, A. F., Davin, A., Ceretti, A., Mangieri, M., Cassini, P., Vaccaro, R., Zaccaria, D., Abbondanza, S., et al. (2020) · Journal of Visualized Experiments · doi:10.3791/60296 · Cited by 28
Chronic Traumatic Encephalopathy and Neuropathological Comorbidities
Stein, T. D., & Crary, J. F. (2020) · Seminars in Neurology · doi:10.1055/s-0040-1713628 · Cited by 28
Regional binding of tau and amyloid PET tracers in Down syndrome autopsy brain tissue
Lemoine, L., Ledreux, A., Mufson, E. J., Perez, S. E., Šimić, G., Doran, E. W., Lott, I. T., Carroll, S. L., Bharani, K., Thomas, S., et al. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00414-3 · Cited by 29
Shaffer, R. M., Li, G., Adar, S. D., Keene, C. D., Latimer, C. S., Crane, P. K., Larson, E. B., Kaufman, J. D., Carone, M., & Sheppard, L. A. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-201005 · Cited by 27
“Combined AD pathology (plaques and NFTs) was assessed with an ABC score, in line with recent National Institute on Aging-Alzheimer’s Association (NIA-AA) recommendations [32, 33].”
Chua, X. Y., Chong, J. R., Cheng, A. L., Lee, J. H., Ballard, C. G., Aarsland, D., Francis, P. T., & Lai, M. K. P. (2021) · Neurochemistry International · doi:10.1016/j.neuint.2021.105251 · Cited by 26
Signature laminar distributions of pathology in frontotemporal lobar degeneration
Ohm, D. T., Cousins, K. A. Q., Xie, S. X., Peterson, C. S., McMillan, C. T., Massimo, L. M., Raskovsky, K., Wolk, D. A., Deerlin, V. M. V., Elman, L. B., et al. (2022) · Acta Neuropathologica · doi:10.1007/s00401-021-02402-3 · Cited by 27
Self-citationWalker, J. M., & Richardson, T. E. (2023) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlac115 · Cited by 26
Driver‐Dunckley, E. D., Zhang, N., Serrano, G. E., et al. (2023) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlad025 · Cited by 26
Self-citationAmyloid fibril proteomics of AD brains reveals modifiers of aggregation and toxicity
Upadhyay, A., Chhangani, D., Rao, N. R., Kofler, J., Vassar, R. J., Rincón-Limas, D. E., & Savas, J. N. (2023) · Molecular Neurodegeneration · doi:10.1186/s13024-023-00654-z · Cited by 27
“S1j, see Table S1 for patient details) [28, 37, 38].”
BackgroundMethodLorca‐Puls, D. L., Gajardo‐Vidal, A., Mandelli, M. L., Illán‐Gala, I., Ezzes, Z., Wauters, L., Battistella, G., Bogley, R., Ratnasiri, B. M., Licata, A. E., et al. (2023) · Brain · doi:10.1093/brain/awad327 · Cited by 26
Pérez‐Grijalba, V., Fandos, N., Canudas, J., Insua, D., Casabona, D., Lacosta, A. M., Montañés, M., Pesini, P., & Sarasa, M. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160325 · Cited by 26
“8 million people worldwide [2], can only be established by postmortem evaluation of these two pathological hallmarks of the disease [3].”
BackgroundIn vivo [ 18 F]-AV-1451 tau-PET imaging in sporadic Creutzfeldt-Jakob disease
Day, G. S., Gordon, B. A., Perrin, R. J., Cairns, N. J., Beaumont, H., Schwetye, K., Ferguson, C., Sinha, N., Bucelli, R., Musiek, E. S., et al. (2018) · Neurology · doi:10.1212/wnl.0000000000005064 · Cited by 26
Self-citationβ‐amyloid and tau pathology in the aging feline brain
Fiock, K. L., Smith, J. D., Crary, J. F., & Hefti, M. M. (2019) · The Journal of Comparative Neurology · doi:10.1002/cne.24741 · Cited by 31
“This included the assessment of β-amyloid distribution by Thal phase (Alafuzoff et al., 2009) and neuritic plaque density by CERAD criteria (Montine et al., 2012).”
MethodOhm, D. T., Peterson, C. S., Lobrovich, R., Cousins, K. A. Q., Gibbons, G. S., McMillan, C. T., Wolk, D. A., Deerlin, V. M. V., Elman, L. B., Spindler, M., et al. (2020) · Acta Neuropathologica · doi:10.1007/s00401-020-02210-1 · Cited by 26
Self-citationGDAP2 mutations implicate susceptibility to cellular stress in a new form of cerebellar ataxia
Eidhof, I., Baets, J., Kamsteeg, E.-J., Deconinck, T., van Ninhuijs, L., Martin, J.-J., Schüle, R., Züchner, S., De Jonghe, P., Schenck, A., et al. (2018) · Brain · doi:10.1093/brain/awy198 · Cited by 25
“Using Montine’s scoring system (Montine et al., 2012) for”
Cervantes González, A., Irwin, D. J., Alcolea, D., McMillan, C. T., Chen-Plotkin, A., Wolk, D., Sirisi, S., Dols-Icardo, O., Querol-Vilaseca, M., Illán-Gala, I., et al. (2022) · Molecular Neurodegeneration · doi:10.1186/s13024-022-00534-y · Cited by 19
Self-citationCharacterizing Amyloid-Positive Individuals With Normal Tau PET Levels After 5 Years
Josephs, K. A., Weigand, S. D., & Whitwell, J. L. (2022) · Neurology · doi:10.1212/wnl.0000000000200287 · Cited by 39
“We identified 45 individuals meeting criteria for ALT and 157 meeting criteria for biomarker AD.”
BackgroundInfluentialInsights into the pathological basis of dementia from population‐based neuropathology studies
Wharton, S. B., Simpson, J. E., Ince, P. G., Richardson, C. D., Merrick, R. L., Matthews, F. E., Brayne, C., & CFAS (2023) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12923 · Cited by 27
“This is reflected in current neuropathological diagnostic approaches to dementia, such as the CERAD and ABC systems for Alzheimer’s disease, which are focused on determining if AD is the cause of dementia in the situation of known dementia.(33,97) The incor-”
MethodAuger, C. A., Perosa, V., Greenberg, S. M., van Veluw, S. J., & Kozberg, M. G. (2023) · Journal of Neuroinflammation · doi:10.1186/s12974-023-02872-0 · Cited by 25
“Brains were also screened for Lewy bodies and hippocampal sclerosis as per [32].”
BackgroundMethodInfluentialRole of GBA variants in Lewy body disease neuropathology
Walton, R. L., Koga, S., Soto‐Beasley, A. I., White, L. J., Griesacker, T., Murray, M. E., Kasanuki, K., Hou, X., Fiesel, F. C., Springer, W., et al. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02699-w · Cited by 27
“…were assessed with thioflavin S fluorescence microscopy, a method validated in our prior work and recognized by the National Institute on Aging-Alzheimer’s Association guidelines for its consistency with tau immunohistochemistry results, particularly in large-scale studies [5, 22, 25, 29, 38].”
Self-citationAlmeida, F., Santos, A. C., Jesus, T., Coelho, A., Quintas-Neves, M., Gauthreaux, K. M., Mock, C., Kukull, W. A., Crary, J. F., & Oliveira, T. G. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.14191 · Cited by 28
“46 PART was defined as the presence of NFTs in the absence of NPs. 2”
The association of seizure control with neuropathology in dementia
Zawar, I., Łuniewski, A., Gundlapalli, R., Manning, C. A., Parikh, P., Kapur, J., & Quigg, M. (2025) · Brain · doi:10.1093/brain/awaf017 · Cited by 29
Cacace, R., den Bossche, T. V., Engelborghs, S., Geerts, N., Laureys, A., Dillen, L., Graff, C., Thonberg, H., Chiang, H., Pástor, P., et al. (2015) · Human Mutation · doi:10.1002/humu.22908 · Cited by 25
“In the EOAD patient cohort, average onset age was 63.6 ± 6.3 years (range 37–70; in addition, two autosomal dominant AD probands had a later onset age of 76 and 77 years, respectively), 58% were women, and 37 of the patients received a definite diagnosis of AD at autopsy.”
BackgroundMethodInfluentialJavanshiri, K., Haglund, M., & Englund, E. M. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-190485 · Cited by 25
“, not studied here) and were defined as follows, according to established criteria referenced in that study [22] and more recent, expanded criteria [24]—in brief:”
BackgroundDerby, C. A. (2020) · Current Epidemiology Reports · doi:10.1007/s40471-020-00231-8 · Cited by 27
The Significance of Tau Aggregates in the Human Brain
Castellani, R. J. (2020) · Brain Sciences · doi:10.3390/brainsci10120972 · Cited by 25
“There are no data as yet to suggest that people with medial temporal p-tau aggregates without Aβ will invariably progress to full-blown dementia, although once initiated, AD encompasses medial temporal p-tau aggregates as well as Aβ pathology [2,3].”
BackgroundMethodInfluentialProvost, K., Iaccarino, L., Soleimani‐Meigooni, D. N., Baker, S. L., Edwards, L., Eichenlaub, U., Hansson, O., Jagust, W. J., Janabi, M., Joie, R. L., et al. (2021) · European Journal of Nuclear Medicine and Molecular Imaging · doi:10.1007/s00259-020-05152-8 · Cited by 27
“Using intermediate-to-high ADNC [52] as a gold standard, the highest overall accuracy was with FTP visual assessment (1.”
MethodInfluentialJia, Y., Wang, X., Chen, Y., Qiu, W., Ge, W., & Ma, C. (2021) · Molecular Neurobiology · doi:10.1007/s12035-021-02356-3 · Cited by 25
“score defined by the NIA-AA guidelines was used for the neuropathological assessment of each AD patient[35].”
MethodIncreased VLCFA-lipids and ELOVL4 underlie neurodegeneration in frontotemporal dementia
He, Y. Z., Phan, K., Bhatia, S., Pickford, R., Fu, Y., Yang, Y., Hodges, J. R., Piguet, O., Halliday, G. M., & Kim, W. S. (2021) · Scientific Reports · doi:10.1038/s41598-021-00870-x · Cited by 26
Biyong, E. F., Tremblay, C., Leclerc, M., Caron, V., Alfos, S., Helbling, J., Rodriguez, L., Pernet, V., Bennett, D. A., Pallet, V., et al. (2021) · Neurobiology of Disease · doi:10.1016/j.nbd.2021.105542 · Cited by 29
Verheijen, M. C. T., Krauskopf, J., Caiment, F., Nazaruk, M., Wen, Q. F., van Herwijnen, M. H. M., Hauser, D. A., Gajjar, M. K., Verfaillie, C. M., Vermeiren, Y., et al. (2021) · Toxicology Letters · doi:10.1016/j.toxlet.2021.12.009 · Cited by 25
Dysregulation of ACE-1 in Normal Aging and the Early Stages of Alzheimer’s Disease
MacLachlan, R. A., Kehoe, P. G., & Miners, J. S. (2022) · The Journals of Gerontology Series A · doi:10.1093/gerona/glac083 · Cited by 27
“A neuropathological diagnosis of AD was made according to NIA-AA guidelines (23).”
Wang, S. J., Guo, Y., Ervin, J. F., Lusk, J. B., & Luo, S. (2022) · Acta Neuropathologica · doi:10.1007/s00401-022-02432-5 · Cited by 28
Hase, Y., Ameen‐Ali, K. E., Waller, R., Simpson, J. E., Stafford, C., Mahesh, A., Ryan, L., Pickering, L., Bodman, C., Hase, M., et al. (2022) · Brain Pathology · doi:10.1111/bpa.13101 · Cited by 27
“neuropathologic changes [28] were not different (p > 0.”
BackgroundMethodTena, J., Maezawa, I., Barboza, M., et al. (2022) · Molecular & Cellular Proteomics · doi:10.1016/j.mcpro.2022.100427 · Cited by 25
“For postmortem diagnosis, we followed the National Institute on Aging-Alzheimer’s Association guideline for the neuropathologic assessment of AD (29).”
MethodDefining the phenotypic spectrum of sporadic Creutzfeldt–Jakob disease MV2K: the kuru plaque type
Baiardi, S., Mammana, A., Dellavalle, S., Rossi, M., Redaelli, V., Colaizzo, E., Fede, G. D., Ladogana, A., Capellari, S., & Parchi, P. (2023) · Brain · doi:10.1093/brain/awad074 · Cited by 25
Katsumata, Y., Wu, X., Aung, K. Z., Gauthreaux, K. M., Mock, C., Forrest, S. L., Kovács, G. G., & Nelson, P. T. (2024) · Neurobiology of Disease · doi:10.1016/j.nbd.2024.106412 · Cited by 27
“Open questions remain about other pathological correlates between ARTAG and common neurodegenerative pathologies, e.g., tauopathies such as Alzheimer ’ s disease neuropathologic change (ADNC) (Montine et al., 2012) and primary age-related tauopathy (PART) (Crary et al., 2014).”
Self-citationRenziehausen, J., Hiebel, C., Nagel, H., Kundu, A., Kins, S., Kögel, D., Behl, C., & Hajieva, P. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-140600 · Cited by 25
“∗Correspondence to: Christian Behl, PhD, Institute for Pathobiochemistry, University Medical Center of the Johannes Gutenberg University Mainz, Duesbergweg 6, 55099 Mainz, Germany.”
Vallortigara, J., Rangarajan, S., Whitfield, D., Alghamdi, A. A., Howlett, D. R., Hortobágyi, T., Johnson, M. A., Attems, J., Ballard, C. G., Thomas, A. J., et al. (2014) · F1000Research · doi:10.12688/f1000research.3786.1 · Cited by 27
STED imaging of tau filaments in Alzheimer’s disease cortical grey matter
Benda, A., Aitken, H., Davies, D., Whan, R. M., & Goldsbury, C. S. (2016) · Journal of Structural Biology · doi:10.1016/j.jsb.2016.07.003 · Cited by 24
Cystatin F is a biomarker of prion pathogenesis in mice
Nuvolone, M., Schmid, N., Miele, G., Sorce, S., Moos, R., Schori, C., Beerli, R. R., Bauer, M., Saudan, P., Dietmeier, K., et al. (2017) · PLOS ONE · doi:10.1371/journal.pone.0171923 · Cited by 25
“Neuropathologic assessment of Alzheimer type brain pathology was made according to the NIA/AA criteria [7].”
BackgroundMethodXia, C., & Dickerson, B. C. (2017) · PET Clinics · doi:10.1016/j.cpet.2017.02.005 · Cited by 28
Nasaruddin, M. L., Pan, X., McGuinness, B., Passmore, P., Kehoe, P. G., Hölscher, C., Graham, S. F., & Green, B. D. (2018) · Metabolites · doi:10.3390/metabo8040069 · Cited by 26
“The AD was classified as moderate (“intermediate” AD neuropathological change [48], and also Braak tangle stage III–IV; n = 16) or severe (“high” AD neuropathological change [48], and also Braak tangle stage V–VI; n = 30).”
BackgroundMethodHeritability in frontotemporal tauopathies
Forrest, S. L., Halliday, G. M., McCann, H., McGeachie, A. B., McGinley, C. V., Hodges, J. R., Piguet, O., Kwok, J. B., Spillantini, M. G., & Kril, J. J. (2019) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1016/j.dadm.2018.12.001 · Cited by 25
“Specifically, FTLD-tau cases were excluded if they had high or intermediate AD neuropathological change according to NIA-AA criteria [23,25] or any Lewy body pathology [24,25].”
BackgroundMethodInfluentialGiannini, L., Xie, S. X., Peterson, C. S., Zhou, C., Lee, E. B., Wolk, D. A., Grossman, M., Trojanowski, J. Q., McMillan, C. T., & Irwin, D. J. (2019) · Frontiers in Neuroscience · doi:10.3389/fnins.2019.00682 · Cited by 25
“Indeed, this quantitative approach to measuring pathological burden provides increased sensitivity to detect clinicopathological correlations (Neltner et al., 2012; Walker et al., 2015, 2017; Irwin et al., 2016b; Ferman et al., 2018), which are critical to improve the antemortem diagnosis of…”
BackgroundMethodSelf-citationImaging Biomarkers of Alzheimer Disease in Multiple Sclerosis
Zeydan, B., Lowe, V. J., Reichard, R. R., Przybelski, S. A., Lesnick, T. G., Schwarz, C. G., Senjem, M. L., Gunter, J. L., Parisi, J. E., Machulda, M. M., et al. (2020) · Annals of Neurology · doi:10.1002/ana.25684 · Cited by 27
“Hippocampal sclerosis was present with associated TAR DNA-binding protein 43 immunoreactive lesions (Fig 4).(31)”
BackgroundInfluentialIncreased glutaminyl cyclase activity in brains of Alzheimer’s disease individuals
Gunn, A. P., Wong, B. X. W., McLean, C., Fowler, C. J., Barnard, P. J., Duce, J. A., & Roberts, B. R. (2020) · Journal of Neurochemistry · doi:10.1111/jnc.15114 · Cited by 28
Gefen, T. D., Kawles, A., Makowski‐Woidan, B., Engelmeyer, J., Ayala, I. A. D. L., Abbassian, P., Zhang, H., Weıntraub, S., Flanagan, M. E., Mao, Q., et al. (2021) · Cerebral Cortex · doi:10.1093/cercor/bhaa409 · Cited by 25
“The Consortium to Establish a Registry for AD (CERAD) protocol was used to determine neuritic plaque scoring (Mirra et al. 1991; Montine et al. 2012).”
MethodSelf-citationHendrickx, J. O., Martinet, W., Dam, D. V., & Meyer, G. R. Y. D. (2021) · Frontiers in Molecular Biosciences · doi:10.3389/fmolb.2021.651215 · Cited by 28
Neighborhood disadvantage reduces cognitive reserve independent of neuropathologic change
Kim, B.-R., Yannatos, I., Blam, K., Wiebe, D. J., Xie, S. X., McMillan, C. T., Mechanic-Hamilton, D. J., Wolk, D. A., & Lee, E. B. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.13736 · Cited by 25
Wang, D., Honnorat, N., Toledo, J. B., Li, K., Charisis, S., Rashid, T., Nirmala, A. B., Brandigampala, S. R., Mojtabai, M., Seshadri, S. S., et al. (2024) · Brain · doi:10.1093/brain/awae388 · Cited by 26
Multitarget Compounds Designed for Alzheimer, Parkinson, and Huntington Neurodegeneration Diseases
Katsoulaki, E.-E., Dimopoulos, D., & Hadjipavlou‐Litina, D. (2025) · Pharmaceuticals · doi:10.3390/ph18060831 · Cited by 30
Laser-Induced In-Source Decay Applied to the Determination of Amyloid-Beta in Alzheimer’s Brains
Kelley, A. R., Perry, G. L., Castellani, R. J., & Bach, S. B. H. (2015) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.5b00295 · Cited by 23
Herline, K., Prelli, F., Mehta, P. D., MacMurray, C., Goñi, F., & Wısnıewskı, T. (2018) · Alzheimer s Research & Therapy · doi:10.1186/s13195-018-0384-9 · Cited by 24
Bartoletti‐Stella, A., Corrado, P., Mometto, N., Baiardi, S., Durrenberger, P. F., Arzberger, T., Reynolds, R., Kretzschmar, H. A., Capellari, S., & Parchi, P. (2018) · Molecular Neurobiology · doi:10.1007/s12035-018-1421-1 · Cited by 24
Sinclair, L. I., Kumar, A., Darreh‐Shori, T., & Love, S. (2019) · Alzheimer s Research & Therapy · doi:10.1186/s13195-019-0519-7 · Cited by 24
Miki, T., Yokota, O., Haraguchi, T., Ishizu, H., Hasegawa, M., Ishihara, T., Ueno, S., Takenoshita, S., Terada, S., & Yamada, N. (2020) · Brain Pathology · doi:10.1111/bpa.12843 · Cited by 24
“The AD group was composed of cases having intermediate or high level AD pathology (Braak stage V–VI, Thal phase 3–5) (52).”
BackgroundLongitudinal anatomic, functional, and molecular characterization of Pick disease phenotypes
Whitwell, J. L., Tosakulwong, N., Schwarz, C. C., Senjem, M. L., Spychalla, A. J., Duffy, J. R., Graff-Radford, J., Machulda, M. M., Boeve, B. F., Knopman, D. S., et al. (2020) · Neurology · doi:10.1212/wnl.0000000000010948 · Cited by 23
“The PiB-PET scan failed to identify Aβ deposition in the one other case that showed sparse neuritic plaques and moderate diffuse plaques in the cortex; this case also met criteria for low AD neuropathologic change.(21) Previous studies have shown that PiB-PET can detect diffuse Aβ plaques,(32) that the global PiB SUVR…”
MethodResultSelf-citationPatterns of Mixed Pathologies in Down Syndrome
Ichimata, S., Yoshida, K., Visanji, N. P., Lang, A. E., Nishida, N., & Kovacs, G. G. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-215675 · Cited by 24
“Based on these results, the level of AD neuropathological change was divided into four categories (Not, Low, Intermediate, High) following the National Institute on Aging-Alzheimer’s Association (NIA-AA) guidelines [37].”
Latimer, C. S., Melief, E. J., Ariza, J., et al. (2022) · Methods in molecular biology · doi:10.1007/978-1-0716-2655-9_1 · Cited by 24
Kotari, V., Southekal, S. S., Navitsky, M. A., Kennedy, I. A., Lu, M., Morris, A., Zimmer, J. A., Fleisher, A., Mintun, M. A., Devous, M. D., et al. (2023) · Alzheimer s Research & Therapy · doi:10.1186/s13195-023-01160-6 · Cited by 25
The Landscape of m6A Regulators in Multiple Brain Regions of Alzheimer’s Disease
Liu, Z., Xia, Q. H., Zhao, X. L., Zheng, F., Xiao, J., Ge, F., Wang, D., & Gao, X. (2023) · Molecular Neurobiology · doi:10.1007/s12035-023-03409-5 · Cited by 25
“The NINCDS-ADRDA guideline includes Aβ, neurofibrillary tangles, tau protein phosphorylation, and neuritic plaques as pathological diagnostic markers [5], which are also the most recognized hypotheses for Zi Jie Liu and Qing Xia contributed equally to this work.”
BackgroundWhole genome deconvolution unveils Alzheimer’s resilient epigenetic signature
Berson, E., Sreenivas, A., Phongpreecha, T., Perna, A., Grandi, F. C., Xue, L., Ravindra, N. G., Payrovnaziri, S. N., Mataraso, S. J., Kim, Y., et al. (2023) · Nature Communications · doi:10.1038/s41467-023-40611-4 · Cited by 25
“…’ brain samples from both ATAC-seq datasets were carefully fi ltered according to clinical diagnosis of cognitive status proximatetodeathandassessmentofADneuropathologicchangeand other neuropathologic comorbidities (see Supplementary Table 1) using current consensus guidelines 24,65 – 69 .”
MethodSelf-citationLyu, X., Duong, M. T., Xie, L., de Florès, R., Richardson, H., Hwang, G., Wisse, L. E. M., DiCalogero, M., McMillan, C. T., Robinson, J. L., et al. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.13559 · Cited by 22
Riku, Y., Watanabe, H., Yoshida, M., Mimuro, M., Iwasaki, Y., Masuda, M., Ishigaki, S., Katsuno, M., & Sobue, G. (2016) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlw053 · Cited by 24
“We excluded patients who fulfilled the diagnostic criteria for other neurological disorders, including either intermediate or high grade Alzheimer disease (AD), according to the 2012 neuropathologic guidelines for AD, dementia with Lewy bodies in either the limbic or neocortical stage, argyrophilic grain disease (AGD)…”
MethodMao, Q., Wang, D., Li, Y., Kohler, M., Wilson, J., Parton, Z., Shmaltsuyeva, B., Gursel, D. B., Rademakers, R., Weıntraub, S., et al. (2017) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlx085 · Cited by 24
Self-citationFactors influencing accuracy of cortical thickness in the diagnosis of Alzheimer's disease
Mahanand, B. S., Fischl, B. R., Salat, D. H., & Initiative, A. D. N. (2017) · Human Brain Mapping · doi:10.1002/hbm.23922 · Cited by 23
“The current gold standard for a conclusive diagnosis of AD is through postmortem examination to identify the disease-defining regional patterns of neurofibrillary tau tangles and amyloid plaque deformities in the brain (Arnold, Hyman, Flory, Damasio, & Van Hoesen, 1991; Braak and Braak, 1991; Brun and Gustafson, 1976;…”
BackgroundChronic Traumatic Encephalopathy in Football Players—Reply
McKee, A. C., Mez, J. B., & Abdolmohammadi, B. (2017) · JAMA · doi:10.1001/jama.2017.16687 · Cited by 25
Sánchez, S. M., Duarte-Abritta, B., Abulafia, C., Pino, G. D., Bocaccio, H., Castro, M. N., Sevlever, G. E., Fonzo, G. A., Nemeroff, C. B., Gustafson, D., et al. (2020) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2019.12.019 · Cited by 27
Malpas, C. B., Sharmin, S., & Kalinčík, T. (2020) · International Journal of Neuroscience · doi:10.1080/00207454.2020.1758087 · Cited by 25
“Only standard blocks were used to assign histopathological staging as described by Montine and colleagues [17].”
MethodNeuropathological findings in multiple system atrophy with cognitive impairment
Jellinger, K. A. (2020) · Journal of Neural Transmission · doi:10.1007/s00702-020-02201-2 · Cited by 25
Metadata
- Authors
- Montine, T. J., Phelps, C. H., Beach, T. G., Bigio, E. H., Cairns, N. J., Dickson, D. W., Duyckaerts, C., Frosch, M. P., Masliah, E., Mirra, S. S., Nelson, P. T., Schneider, J. A., Thal, D. R., Trojanowski, J. Q., Vinters, H. V., & Hyman, B. T.
- Affiliations
- University of Washington (US)
- National Institutes of Health (US)
- Banner Sun Health Research Institute (US)
- Northwestern University (US)
- Washington University in St. Louis (US)
- Mayo Clinic (US)
- Pitié-Salpêtrière Hospital (FR)
- Harvard University (US)
- University of California San Diego (US)
- SUNY Downstate Health Sciences University (US)
- University of Kentucky (US)
- Rush University Medical Center (US)
- Universität Ulm (DE)
- University of Pennsylvania (US)
- University of California, Los Angeles (US)
- Corresponding author
- Montine, Thomas J.
- ORCID
- Venue
- Acta Neuropathologica
- Published
- 2011-11-20
- Volume
- 123
- Issue
- 1
- Pages
- 1-11
- ISSN
- 0001-6322 (ISSN-L)
- 1432-0533
- PMC
- PMC3268003
- OpenAlex
- W2128228199
- Cited by
- 2,894
- References
- 66
- Citations by year
- 2026: 254 · 2025: 290 · 2024: 329 · 2023: 251 · 2022: 284 · 2021: 257 · 2020: 244 · 2019: 183 · 2018: 164 · 2017: 148 · 2016: 144 · 2015: 136 · 2014: 92 · 2013: 69 · 2012: 46
- FWCI
- 39.19
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Acta Neuropathologica (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5u01ag024904-10)
- National Institute on Aging (U01-AG-024904, R01AG017917, AG18840, AG-15819, R01AG015866, P30AG028383, R01AG042210, R01AG018440, U01AG016976, P50AG005131, P50AG016570, P01AG003949, P30AG010124, R01AG015819, P30AG010161, AG24904, P50AG005681, P30AG019610, P01AG003991, P50AG005136, P50AG005134, P30AG013854, U19AG010483, RF1AG015819, P01AG012435, U19AG024904, P30AG062421)
- National Institute of Neurological Disorders and Stroke (P50NS062684)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, amyloid-beta deposition, neurofibrillary tangles, neuritic plaques, ABC score, Lewy body disease, vascular brain injury, hippocampal sclerosis, TDP-43 inclusions, staining techniques, clinicopathological correlation, preclinical Alzheimer's disease
- MeSH terms
- Alzheimer Disease, Brain, Cerebrovascular Disorders, DNA-Binding Proteins, Hippocampus, Humans, Sclerosis, United States, Cerebrovascular Trauma, Lewy Body Disease, National Institute on Aging (U.S.)
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