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 801–900 of 2,854
Ushizima, D. M., Chen, Y., Alegro, M., Ovando, D., Eser, R. A., Lee, W., Poon, K., Shankar, A., Kantamneni, N., Satrawada, S., et al. (2021) · NeuroImage · doi:10.1016/j.neuroimage.2021.118790 · Cited by 45
Chronic Effects of Mild Neurotrauma: Putting the Cart Before the Horse?
Castellani, R. J., Perry, G., & Iverson, G. L. (2015) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0000000000000193 · Cited by 40
“TAR DNAbinding protein-43 abnormalities) should be documented carefully in future studies using detailed and specific neuropathologic staging for comorbid diseases (65, 66).”
The expression pattern of GDF15 in human brain changes during aging and in Alzheimer’s disease
Chiariello, A., Valente, S., Pasquinelli, G., Baracca, A., Sgarbi, G., Solaini, G., Medici, V., Fantini, V., Poloni, T. E., Tognocchi, M., et al. (2023) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.1058665 · Cited by 40
Brookmeyer, R., Kawas, C. H., Abdallah, N., Paganini‐Hill, A., Kim, R. C., & Corrada, M. M. (2016) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2016.01.004 · Cited by 41
“We recognize that revised criteria for assessing plaque accumulation have been developed based on the Thal phase of Ab distribution in the brain [19]; however, most of autopsies we report here were done before 2013 before the revised criteria were available.”
MethodSpecific patterns of neuronal loss in the pulvinar nucleus in dementia with lewy bodies
Erskine, D., Thomas, A. J., Attems, J., Taylor, J., McKeith, I. G., Morris, C. M., & Khundakar, A. A. (2017) · Movement Disorders · doi:10.1002/mds.26887 · Cited by 40
Population‐based analysis of pathological correlates of dementia in the oldest old
Tanskanen, M., Mäkelä, M., Notkola, I., Myllykangas, L., Rastas, S., Oinas, M., Lindsberg, P. J., Polvikoski, T. M., Tienari, P. J., & Paetau, A. E. (2017) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.389 · Cited by 41
“These criteria have recently been refined and adjusted for the needs of clinical diagnostics, for example, by applying IHC-based methods but the original methods can still be judged reliable indicators of the severity of the pathology.(22,23,24) For the assessment of CAA several methods have been proposed.”
MethodFrancis, P. T., Costello, H., & Hayes, G. M. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180699 · Cited by 44
APOE is a correlate of phenotypic heterogeneity in Alzheimer disease in a national cohort
Weıntraub, S., Teylan, M., Rader, B. M., Chan, K. C. G., Bollenbeck, M., Kukull, W. A., Coventry, C., Rogalski, E. J., Bigio, E. H., & Mesulam, M. M. (2019) · Neurology · doi:10.1212/wnl.0000000000008666 · Cited by 40
“All neuropathologic diagnoses were made using criteria established in the ADC program.(15,16)”
MethodSelf-citationCodron, P., Letournel, F., Marty, S., Renaud, L., Bodin, A. M., Duchesne, M., Verny, C., Lenaers, G., Duyckaerts, C. J., Julien, J., et al. (2020) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12646 · Cited by 40
“STORM images of ~30 lm diameter senile plaques and ~15 lm degenerating neurons with NFTs were © 2020 The Authors.”
InfluentialSelf-citationDifferentiating cognitive impairment due to corticobasal degeneration and Alzheimer disease
Day, G. S., Lim, T. S., Hassenstab, J. J., Goate, A., Grant, E., Roe, C. M., Cairns, N. J., & Morris, J. C. (2017) · Neurology · doi:10.1212/wnl.0000000000003770 · Cited by 45
“%) had low ADNC.”
BackgroundMethodInfluentialSelf-citationTau and TDP-43 synergy: a novel therapeutic target for sporadic late-onset Alzheimer’s disease
Latimer, C. S., & Liachko, N. F. (2021) · GeroScience · doi:10.1007/s11357-021-00407-0 · Cited by 40
Dementia is associated with medial temporal atrophy even after accounting for neuropathologies
Woodworth, D. C., Sheikh‐Bahaei, N., Scambray, K. A., Phelan, M. J., Perez-Rosendahl, M. A., Corrada, M. M., Kawas, C. H., Sajjadi, S. A., & Initiative, A. D. N. (2022) · Brain Communications · doi:10.1093/braincomms/fcac052 · Cited by 39
“…current consensus criteria used for pathological staging and classi fi cation of Alzheimer ’ s disease and related disorders (e.g. NIA-AA criteria 38 ) and potentially highlight the need for more quantitative measures of pathological burden to more fully explain the variability in atrophy…”
Extracellular matrix and synapse formation
Yang, L., Wei, M., Xing, B., & Zhang, C. (2022) · Bioscience Reports · doi:10.1042/bsr20212411 · Cited by 42
Firdaus, Z., & Li, X. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25042320 · Cited by 46
“A neuropathologic diagnosis of AD requires the presence of both amyloid beta (A β ) plaques outside neuronal cell, and neurofibrillary tangles (NFTs) inside the neurons, which can now be easily identified using immunohistochemical stains such as A β and tau, respectively [111].”
BackgroundBougea, A. M., & Gourzis, P. (2024) · Journal of Clinical Medicine · doi:10.3390/jcm13164661 · Cited by 43
“For example, amyloid PET scans can detect the existence of A β plaques in the brain, which are a hallmark neuropathological feature of AD [80].”
BackgroundFactors Affecting Resilience and Prevention of Alzheimer's Disease and Related Dementias
Masurkar, A. V., Marsh, K., Morgan, B. E., Leitner, D., & Wısnıewskı, T. (2024) · Annals of Neurology · doi:10.1002/ana.27055 · Cited by 42
“124 When comparing the more resilient brain regions (cerebellum, sensory cortex, and motor cortex) to 9 of the more vulnerable brain regions that develop AD pathology, proteomics identi fi ed many similarities in protein changes in both the vulnerable and resistant brain regions.”
Behrouzi, R., Liu, X., Wu, D., Robinson, A., Tanaguchi-Watanabe, S., Rollinson, S. J., Shi, J., Tian, J., Hamdalla, H. H. M., Ealing, J., et al. (2016) · Acta Neuropathologica Communications · doi:10.1186/s40478-016-0301-z · Cited by 43
Pai, M., & Lee, C. (2016) · PLoS ONE · doi:10.1371/journal.pone.0155480 · Cited by 39
Identification of prefrontal cortex protein alterations in Alzheimer’s disease
Garranzo‐Asensio, M., Segundo‐Acosta, P. S., Martínez‐Useros, J., Montero‐Calle, A., Fernández‐Aceñero, M. J., Månberg, A., Peláez‐García, A., Villalba, M., Rábano, A., Nilsson, P., et al. (2018) · Oncotarget · doi:10.18632/oncotarget.24303 · Cited by 40
Li, W., Shen, Y., Tian, D., Bu, X., Zeng, F., Liu, Y.-H., Chen, Y., Yao, X., Li, H.-Y., Chen, D., et al. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-190056 · Cited by 39
“Senile plaques are a hallmark to define the diagnosis of AD, which once depended on postmortem biopsy [4].”
Neuropathological correlates of structural and functional imaging biomarkers in 4-repeat tauopathies
Spina, S., Brown, J. A., Deng, J., Gardner, R. C., Nana, A. L., Hwang, J.-H. L., Gaus, S. E., Huang, E. J., Kramer, J. H., Rosen, H. J., et al. (2019) · Brain · doi:10.1093/brain/awz122 · Cited by 40
FTO: An Emerging Molecular Player in Neuropsychiatric Diseases
Annapoorna, P. K., Iyer, H., Parnaik, T., Narasimhan, H., Bhattacharya, A., & Kumar, A. (2019) · Neuroscience · doi:10.1016/j.neuroscience.2019.08.021 · Cited by 40
Sellés, M. C., Fortuna, J. T. S., Zappa-Villar, M. F., de Faria, Y. P. R., de Souza, A. S., Suemoto, C. K., Leite, R. E. P., Rodriguez, R. D., Grinberg, L. T., Reggiani, P. C., et al. (2019) · Molecular Neurobiology · doi:10.1007/s12035-019-01827-y · Cited by 42
Pires, G., McElligott, S., Drusinsky, S., Halliday, G. M., Potier, M., Wısnıewskı, T., & Drummond, E. (2019) · Acta Neuropathologica Communications · doi:10.1186/s40478-019-0848-6 · Cited by 41
Xu, W., Liu, X., He, X., Jiang, Y., Zhang, J., Zhang, Q., Wang, N., Qin, L., & Xin, H. (2020) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2020.112992 · Cited by 41
Ding, R., Hase, Y., Burke, M., Foster, V., Stevenson, W., Polvikoski, T. M., & Kalaria, R. N. (2021) · Acta Neuropathologica Communications · doi:10.1186/s40478-021-01230-6 · Cited by 39
“Braak staging scores and Alzheimer’s Disease Neuropathologic changes [37] were different in mixed and AD cases compared to all other groups (*P < 0.”
BackgroundResultLongitudinal atrophy in prodromal dementia with Lewy bodies points to cholinergic degeneration
Kantarci, K., Nedelska, Z., Chen, Q., Senjem, M. L., Schwarz, C. G., Gunter, J. L., Przybelski, S. A., Lesnick, T. G., Kremers, W. K., Fields, J. A., et al. (2022) · Brain Communications · doi:10.1093/braincomms/fcac013 · Cited by 39
Self-citationHyman, B. (2023) · Annual Review of Medicine · doi:10.1146/annurev-med-042921-023749 · Cited by 39
“The primary diagnostic criteria for AD depend on the presence of both tau-containing neurofibrillary tangles and A β plaques (1, 2); the biochemical criteria similarly depend on the presence of elevated levels of phosphorylated tau (phospho-tau) (3), which is closely associated with tangles.”
Self-citationNeuropsychological Markers of Cognitive Decline in Persons With Alzheimer Disease Neuropathology
Hassenstab, J. J., Monsell, S. E., Mock, C., Roe, C. M., Cairns, N. J., Morris, J. C., & Kukull, W. A. (2015) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0000000000000254 · Cited by 40
Self-citationNeurogranin as biomarker in CSF is non-specific to Alzheimer's disease dementia
Willemse, E. A. J., Sieben, A., Somers, C., Vermeiren, Y., De Roeck, N., Timmers, M., Van Broeckhoven, C., De Vil, B., Cras, P., De Deyn, P. P., et al. (2021) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2021.08.002 · Cited by 34
Synapses, Microglia, and Lipids in Alzheimer’s Disease
Paasila, P. J., Aramideh, J. A., Sutherland, G. T., & Graeber, M. B. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2021.778822 · Cited by 40
“Importantly, the density and anatomical spread of NFTs remain criteria for diagnostic and staging purposes (Montine et al., 2012).”
BackgroundC-terminal TMEM106B fragments in human brain correlate with disease-associated TMEM106B haplotypes
T. Vicente, C., Perneel, J., Wynants, S., Heeman, B., Van den Broeck, M., Baker, M., Cheung, S., Faura, J., Mackenzie, I. R. A., & Rademakers, R. (2023) · Brain · doi:10.1093/brain/awad133 · Cited by 38
“26 The FTLD-TDP cases were classified into pathological subgroups according to current pathological criteria.”
MethodLevin, J., Baiardi, S., Quadalti, C., Rossi, M., Mammana, A., Vöglein, J., Bernhardt, A. M., Perrin, R. J., Jucker, M., Preische, O., et al. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.13818 · Cited by 39
“%) showed the Amg-LBP variantpattern(#19,21,22,25),three (25%)had immunore-activityrestrictedtotheolfactoryarea(piriformcortex,olfactorytract, and peduncle; participants #16, 23, 24), two were negative (#17 and 20) and one virtually negative (#27).”
BackgroundSelf-citationRavikumar, S., Denning, A. E., Lim, S., Chung, E. P., Sadeghpour, N., Ittyerah, R., Wisse, L. E. M., Das, S. R., Xie, L., Robinson, J. L., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-49205-0 · Cited by 47
“This is in line with the CA1 sub fi eld showing robust atrophy, particularly with hippocampal sclerosis associated with TDP-43 pathology 43 .”
InfluentialClinical criteria for a limbic-predominant amnestic neurodegenerative syndrome
Corriveau‐Lecavalier, N., Botha, H., Graff‐Radford, J., Switzer, A. R., Przybelski, S. A., Wiste, H. J., Murray, M. E., Reichard, R. R., Dickson, D. W., Nguyen, A. T., et al. (2024) · Brain Communications · doi:10.1093/braincomms/fcae183 · Cited by 47
“ADNC was diagnosed according to the ABC ranking score 40 which includes the Thal staging of amyloid plaques, Braak staging of neurofibrillary tangles 41 and the density measurement of neuritic plaques.”
MethodSelf-citationTau protein profiling in tauopathies: a human brain study
Lantero‐Rodriguez, J., Camporesi, E., Montoliu‐Gaya, L., Gobom, J., Piotrowska, D., Olsson, M., Matečko‐Burmann, I., Becker, B., Brinkmalm, A., Burmann, B. M., et al. (2024) · Molecular Neurodegeneration · doi:10.1186/s13024-024-00741-9 · Cited by 42
“The neuropathological assessment of the AD cases fulfilled the 2012 National Institute on Aging and the Alzheimer’s Association (NIA-AA) guidelines [54] and the clinical evaluation met the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) criteria for probable AD…”
MethodPittsburgh compound B and the postmortem diagnosis of alzheimer disease
Niedowicz, D. M., Beckett, T. L., Matveev, S., Weidner, A. M., Baig, I., Kryscio, R. J., Mendiondo, M. S., LeVine, H., Keller, J. N., & Murphy, M. P. (2012) · Annals of Neurology · doi:10.1002/ana.23633 · Cited by 37
“Although what these changes mean for the AD brain is unknown, it is worth noting that recent guidelines for the neuropathologic assessment of AD take into account cerebellar pathology.(32,33) Oligomeric Ab failed to reach overall statistical significance (p < 0.”
BackgroundMcMillan, C. T., & Wolk, D. A. (2016) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp-2015-312690 · Cited by 39
Emerging Diagnostic and Therapeutic Strategies for Tauopathies
Coughlin, D. G., & Irwin, D. J. (2017) · Current Neurology and Neuroscience Reports · doi:10.1007/s11910-017-0779-1 · Cited by 42
Chronic Traumatic Encephalopathy in Professional American Football Players: Where Are We Now?
Tharmaratnam, T., Iskandar, M. M. A., Tabobondung, T., Tobbia, I., Gopee‐Ramanan, P., & Tabobondung, T. A. (2018) · Frontiers in Neurology · doi:10.3389/fneur.2018.00445 · Cited by 44
“Owing to the irregularities in lesion distribution however, additional sampling may also be required based on Alzheimer Disease Centers (National Institute on Aging-Alzheimer’s Association (NIA-AA) criteria (64).”
MethodSpectrum of tau pathologies in Huntington's disease
Baskota, S. U., López, O. L., Greenamyre, J. T., & Kofler, J. (2018) · Laboratory Investigation · doi:10.1038/s41374-018-0166-9 · Cited by 38
“(A2, B1, C1) following the 2012 NIA-AA criteria for the neuropathologic assessment of AD [33, 34].”
Buciuc, M., Wennberg, A. M. V., Weigand, S. D., Murray, M. E., Senjem, M. L., Spychalla, A. J., Boeve, B. F., Knopman, D. S., Jack, C. R., Kantarci, K., et al. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-191040 · Cited by 38
“phases [58] and therefore might not represent a direct association between A and atrophy in subcortical regions, e.”
BackgroundSelf-citationBourassa, P., Tremblay, C., Schneider, J. A., Bennett, D. A., & Calon, F. (2020) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12599 · Cited by 38
Self-citationEede, P., Obst, J., Benke, E., Yvon‐Durocher, G., Richard, B. C., Gimber, N., Schmoranzer, J., Böddrich, A., Wanker, E. E., Prokop, S., et al. (2020) · EMBO Reports · doi:10.15252/embr.201948530 · Cited by 39
“Extracellular amyloid-b (Ab) deposits are one of the prominent hallmarks of the disease [1], and a dysregulation of Ab metabolism is thought to be one of the earliest pathological changes observable in AD patients, decades before first clinical symptoms occur [4,5].”
Wijesinghe, P., Steinbusch, H. W. M., Shankar, S. K., Yasha, T. C., & de Silva, K. R. D. (2020) · Journal of Chemical Neuroanatomy · doi:10.1016/j.jchemneu.2020.101772 · Cited by 40
Applications of 3D Bioprinted-Induced Pluripotent Stem Cells in Healthcare
Soman, S. S., & Vijayavenkataraman, S. (2020) · International Journal of Bioprinting · doi:10.18063/ijb.v6i4.280 · Cited by 40
“68 International Journal of Bioprinting (2020)–Volume 6, Issue 4 attention, and memory[120].”
BackgroundAberrant interaction between FUS and SFPQ in neurons in a wide range of FTLD spectrum diseases
Ishigaki, S., Riku, Y., Fujioka, Y., Endo, K., Iwade, N., Kawai, K., Ishibashi, M., Yokoi, S., Katsuno, M., Watanabe, H., et al. (2020) · Brain · doi:10.1093/brain/awaa196 · Cited by 40
“, 2007) and demonstrated neurofibrillary tangle of Braak stage IV or more and amyloid deposits of Thal phase 4 or more (Montine et al., 2012).”
BackgroundCousins, K. A. Q., Phillips, J. S., Irwin, D. J., Lee, E. B., Wolk, D. A., Shaw, L. M. J., Zetterberg, H., Blennow, K., Burke, S., Kinney, N. G., et al. (2020) · Alzheimer s & Dementia · doi:10.1002/alz.12233 · Cited by 38
Self-citationGiannini, L., Peterson, C. S., Ohm, D. T., Xie, S. X., McMillan, C. T., Raskovsky, K., Massimo, L. M., Suh, E. R., Deerlin, V. M. V., Wolk, D. A., et al. (2021) · Acta Neuropathologica Communications · doi:10.1186/s40478-021-01129-2 · Cited by 37
“Our sampling extends beyond traditional neuropathological sampling optimized for the diagnosis of AD [47], but we have relatively limited availability of regional sampling compared to the entire set of regions that comprise whole-brain in vivo imaging approaches.”
BackgroundMethodInfluentialSelf-citationTisdall, 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) · NeuroImage Clinical · doi:10.1016/j.nicl.2021.102913 · Cited by 41
“(Mack-enzie et al., 2011; Mackenzie et al., 2010; Montine et al., 2012) We included only sporadic FTLD patients, genotyped based on pedigree-analysis, using a custom targeted next-generation sequencing panel for neurodegenerative diseases including MAPT, GRN and repeat-primed PCR for C9orf72 , as…”
InfluentialSelf-citationNeuropathological comorbidity associated with argyrophilic grain disease
Yokota, O., Miki, T., Ikeda, C., Nagao, S., Takenoshita, S., Ishizu, H., Haraguchi, T., Kuroda, S., Terada, S., & Yamada, N. (2018) · Neuropathology · doi:10.1111/neup.12429 · Cited by 38
“AGD case had high-level AD pathology according to the pathological criteria of AD because the distribution of neuritic changes was frequently limited in the limbic regions.(43) Thal et al.”
Wan, L., Ai, J.-Q., Yang, C. G., Jiang, J., Zhang, Q., Luo, Z., Huang, R., Tu, T., Pan, A., Tu, E., et al. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.717263 · Cited by 37
“diagnosis of AD (Braak and Braak, 1991; Thal et al., 2002; Braak et al., 2006; Montine et al., 2012); ****chronic obstructive pulmonary disease.”
BackgroundSordo, L., Qian, T., Bukhari, S. A., Nguyen, K. M., Woodworth, D. C., Head, E., Kawas, C. H., Corrada, M. M., Montine, T. J., & Sajjadi, S. A. (2023) · Acta Neuropathologica · doi:10.1007/s00401-023-02606-9 · Cited by 36
“MVLs were scored positive if there were two or more MVLs in the screening sections [35].”
BackgroundMethodInfluentialSelf-citationα-Synuclein pathology in post-mortem retina and optic nerve is specific for α-synucleinopathies
de Ruyter, F. J. H., Morrema, T. H. J., den Haan, J., Gase, G., Twisk, J. W. R., de Boer, J. F., Scheltens, P., Bouwman, F. H., Verbraak, F. D., Rozemüller, A. J. M., et al. (2023) · npj Parkinson s Disease · doi:10.1038/s41531-023-00570-5 · Cited by 37
“…to the guidelines of the BrainNet Europe Consortium 34 , including assessment of Braak-stage for Lewy bodies (Braak LB stage) 27 Alzheimer ’ s disease neuropathological changes 35 , including Thal-phase for A β 36,37 , Braak-stage for NFTs 38 and CERAD score for neuritic plaque pathology 39 .”
Padilla-Godínez, F. J., Vázquez-García, E. R., Trujillo-Villagrán, M. I., Soto-Rojas, L. O., Palomero‐Rivero, M., Hernández-González, O., Pérez-Eugenio, F., Collazo-Navarrete, O., Arias-Carrión, Ó., & Guerra‐Crespo, M. (2025) · Frontiers in Neuroscience · doi:10.3389/fnins.2025.1570553 · Cited by 42
Amyloid or tau: the chicken or the egg?
Mann, D. M. A., & Hardy, J. (2013) · Acta Neuropathologica · doi:10.1007/s00401-013-1162-1 · Cited by 39
Amyloid β‐abrogated TrkA ubiquitination in PC 12 cells analogous to Alzheimer's disease
Chen, Z., Geetha, T., Gearing, M., & Babu, J. R. (2015) · Journal of Neurochemistry · doi:10.1111/jnc.13076 · Cited by 38
Hippocampal Sclerosis of Aging Can Be Segmental
Ighodaro, E. T., Jicha, G. A., Schmitt, F. A., Neltner, J. H., Abner, E. L., Kryscio, R. J., Smith, C. D., Duplessis, T., Anderson, S., Patel, E., et al. (2015) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0000000000000204 · Cited by 37
“based criteria (1, 7); these include cell loss, gliosis, and atrophy”
BackgroundMethodInfluentialSelf-citationAltered neurofilament protein expression in the lateral vestibular nucleus in Parkinson’s disease
Wellings, T. P., Brichta, A. M., & Lim, R. (2017) · Experimental Brain Research · doi:10.1007/s00221-017-5092-3 · Cited by 37
Complement Activation in Capillary Cerebral Amyloid Angiopathy
Matsuo, K., Shindo, A., Niwa, A., Tabei, K., Akatsu, H., Hashizume, Y., Akiyama, H., Ayaki, T., Maki, T., Sawamoto, N., et al. (2017) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000486091 · Cited by 35
Wren, M. C., Lashley, T., Årstad, E., & Sander, K. (2018) · Acta Neuropathologica Communications · doi:10.1186/s40478-018-0535-z · Cited by 43
Initiative, A. D. N., Wei, H., Kong, M., Zhang, C., Guan, L., & Ba, M. (2018) · Quantitative Imaging in Medicine and Surgery · doi:10.21037/qims.2018.10.08 · Cited by 37
McAleese, K. E., Graham, S., Dey, M., Walker, L., Erskine, D., Johnson, M. A., Johnston, E., Thomas, A. J., McKeith, I. G., DeCarli, C. S., et al. (2018) · Brain Pathology · doi:10.1111/bpa.12685 · Cited by 38
Bezdíček, O., Ballarini, T., Herman Buschke, L., Růžička, F., Roth, J., Albrecht, F., Růžička, E., Mueller, K., Schroeter, M. L., & Jech, R. (2019) · Neuropsychology · doi:10.1037/neu0000503 · Cited by 38
Ghisays, V., Goradia, D. D., Protas, H. D., Bauer, R. J., III, Devadas, V., Tariot, P. N., Lowe, V. J., Knopman, D. S., Petersen, R. C., Jack, C. R., et al. (2019) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2019.08.195 · Cited by 35
Yamoah, A., Tripathi, P., Sechi, A. S., Köhler, C. N., Guo, H., Chandrasekar, A., Nolte, K. W., Wruck, C. J., Katona, I., Anink, J. J., et al. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-190722 · Cited by 35
ATN status in amnestic and non-amnestic Alzheimer’s disease and frontotemporal lobar degeneration
Cousins, K. A. Q., Irwin, D. J., Wolk, D. A., Lee, E. B., Shaw, L. M. J., Trojanowski, J. Q., Re, F. D., Gibbons, G. S., Grossman, M., & Phillips, J. S. (2020) · Brain · doi:10.1093/brain/awaa165 · Cited by 39
Self-citationHansen, D., Ling, H., Lashley, T., Foley, J. A., Strand, C., Eid, T. M., Holton, J. L., & Warner, T. T. (2020) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12648 · Cited by 38
Amyloid‐ β PET and CSF in an autopsy‐confirmed cohort
Reimand, J., Boon, B. D. C., Collij, L. E., Teunissen, C. E., Rozemüller, A. J. M., van Berckel, B. N. M., Scheltens, P., Ossenkoppele, R., & Bouwman, F. H. (2020) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.51195 · Cited by 40
“org) and the applicable diagnostic criteria.(24,25) For this particular study, every case also without suspicion of AD pathology during life, was scored by AR and BB for AD neuropathological changes according to the ABC scoring system by AR and BB,(24) in which the A stands for amyloid-β Thal phase,(26) B for Braak st…”
MethodLiu, H., Kim, C., Haldiman, T., Sigurdson, C. J., Nyström, S., Nilsson, K. P. R., Cohen, M. L., Wısnıewskı, T., Hammarström, P., & Safar, J. (2021) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2021.101267 · Cited by 37
Frigerio, I., Boon, B. D. C., Lin, C., Graaf, Y. G.-D., Bol, J. G. J. M., Preziosa, P., Twisk, J. W. R., Barkhof, F., Hoozemans, J. J. M., Bouwman, F. H., et al. (2021) · Brain Communications · doi:10.1093/braincomms/fcab281 · Cited by 38
Motor neuron TDP-43 proteinopathy in progressive supranuclear palsy and corticobasal degeneration
Riku, Y., Iwasaki, Y., Ishigaki, S., Akagi, A., Hasegawa, M., Nishioka, K., Li, Y., Riku, M., Ikeuchi, T., Fujioka, Y., et al. (2022) · Brain · doi:10.1093/brain/awac091 · Cited by 37
Wolframin is a novel regulator of tau pathology and neurodegeneration
Chen, S., Acosta, D. M., Li, L., Liang, J., Chang, Y., Wang, C., Fitzgerald, J., Morrison, C. T., Goulbourne, C. N., Nakano, Y., et al. (2022) · Acta Neuropathologica · doi:10.1007/s00401-022-02417-4 · Cited by 40
“All samples are classified according to the ABC scoring method described in the National Institute of Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of AD (NIA-AA AD) [51] Case ID Sex Age (yr) AD Other NDs Amyloid Thal phase (A) Braak NFT stage (B) CERAD neuritic plaque score (C) Section t…”
MethodSelf-citationNeocortical Lewy Body Pathology Parallels Parkinson's Dementia, but Not Always
Martin, W. R. W., Younce, J. R., Campbell, M. C., Racette, B. A., Norris, S. A., Ushe, M., Criswell, S. R., Davis, A. A., Alfradique‐Dunham, I., Maiti, B., et al. (2022) · Annals of Neurology · doi:10.1002/ana.26542 · Cited by 44
“Neuropathologic diagnoses were based on standard criteria.(2,12,13) The diagnosis of PD was based on the presence of LBs within and the loss of pigmented neurons from the substantia nigra.”
BackgroundMethodResultInfluentialSelf-citation[11C]Martinostat PET analysis reveals reduced HDAC I availability in Alzheimer’s disease
Pascoal, T. A., Chamoun, M., Lax, E., Wey, H.-Y., Shin, M., Ng, K. P., Kang, M. S., Mathotaarachchi, S., Benedet, A. L., Therriault, J., et al. (2022) · Nature Communications · doi:10.1038/s41467-022-30653-5 · Cited by 43
Self-citationMaldonado‐Díaz, C., Hiya, S., Yokoda, R. T., Farrell, K. W., Marx, G. A., Kauffman, J., Daoud, E. V., Gonzales, M. M., Parker, A. S., Canbeldek, L., et al. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02716-y · Cited by 38
“In instances where NPADNC was not available, ADNC levels were derived from a combination of Braak stage (NAC-CBRAA), Thal phase (NPTHAL), and CERAD neuritic plaque (NP) score (NACCNEUR) [12, 32, 52, 83].”
BackgroundMethodInfluentialNascimento, C. F., Suemoto, C. K., Rodriguez, R. D., Alho, A. T. D. L., Leite, R. P., Farfel, J. M., Pasqualucci, C. A., Filho, W. J., & Grinberg, L. T. (2015) · Brain Pathology · doi:10.1111/bpa.12296 · Cited by 37
“A neuropathological diagnosis of AD was made when individuals met the criteria for intermediate AD neuropathologic change, according to the latest National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of AD (NIA-AA criteria) (45).”
MethodMaking the Diagnosis of Frontotemporal Lobar Degeneration
Bigio, E. H. (2013) · Archives of Pathology & Laboratory Medicine · doi:10.5858/arpa.2012-0075-ra · Cited by 38
“All sections should be stained with routine hematoxylin-eosin (H&E) and evaluated according to NIA-AA revised criteria for regional neuronal loss and gliosis, vascular brain injury, microvascular lesions, and hippocampal sclerosis.(5,6) Whereas in AD the most striking neuronal loss and gliosis is in the entorhinal cor…”
InfluentialSelf-citationRabinovici, G. D., Karlawish, J. H., Knopman, D. S., Snyder, H. M., Sperling, R. A., & Carrillo, M. C. (2016) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2016.03.002 · Cited by 35
“Brain beta-amyloid PET imaging can detect betaamyloid plaques in the brain, a pathological hallmark of AD [2].”
BackgroundLópez-López, A., Gelpí, E., Lopategui, D. M., & Vidal-Taboada, J. M. (2017) · Molecular Neurobiology · doi:10.1007/s12035-017-0489-3 · Cited by 35
“The diagnosis of LOAD was defined as an age of onset or diagnosis ≥65 years according to clinical charts and required a high or intermediate score of AD neuropathological change according to the current National Institute on Aging, Alzheimer’s Association guidelines, characterized by the presence of moderate or severe…”
MethodJanssens, J., Vermeiren, Y., Fransén, E., Aerts, T., Dam, D. V., Engelborghs, S., & Deyn, P. P. D. (2018) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1016/j.dadm.2018.01.002 · Cited by 36
“Further evidence supporting these findings can be found in the fact that the LC is initially involved in DLB/ PDD neuropathology, while AD patients at first show Ab plaques in neo- and allocortical brain regions, with amyloid pathology only reaching the brainstem nuclei in more advanced stages, that is, Thal stages 4…”
ResultRegion- and Cell-specific Aneuploidy in Brain Aging and Neurodegeneration
Shepherd, C. E., Yang, Y., & Halliday, G. M. (2018) · Neuroscience · doi:10.1016/j.neuroscience.2018.01.050 · Cited by 36
White-matter commissures: a clinically focused anatomical review
Lavrador, J. P., Ferreira, V., Lourenço, M., Alexandre, I., Rocha, M., Oliveira, E., Kailaya-Vasan, A., & Neto, L. L. (2019) · Surgical and Radiologic Anatomy · doi:10.1007/s00276-019-02218-7 · Cited by 36
Donega, V., Burm, S. M., van Strien, M. E., van Bodegraven, E. J., Paliukhovich, I., Geut, H., van de Berg, W. D. J., Li, K. W., Smit, A. B., Başak, O., et al. (2019) · Acta Neuropathologica Communications · doi:10.1186/s40478-019-0736-0 · Cited by 36
Evidence of corticofugal tau spreading in patients with frontotemporal dementia
Kim, E., Hwang, J., Gaus, S. E., Nana, A. L., Deng, J., Brown, J. A., Spina, S., Lee, M. J., Ramos, E. M., Grinberg, L. T., et al. (2019) · Acta Neuropathologica · doi:10.1007/s00401-019-02075-z · Cited by 33
Can post-mortem MRI be used as a proxy for in vivo? A case study
Boon, B. D. C., Pouwels, P. J. W., Jonkman, L. E., Keijzer, M. J., Preziosa, P., van de Berg, W. D. J., Geurts, J. J. G., Scheltens, P., Barkhof, F., Rozemüller, A. J. M., et al. (2019) · Brain Communications · doi:10.1093/braincomms/fcz030 · Cited by 35
“Neuropathology confirmed Alzheimer’s disease pathology, with maximum stages for Ab plaques, neurofibrillary tangles and neuritic plaques resulting in an A3B3C3 score (Montine et al., 2012).”
BackgroundMethodLlibre‐Guerra, J. J., Li, Y., Schindler, S. E., Gordon, B. A., Fagan, A. M., Morris, J. C., Benzinger, T. L. S., Hassenstab, J. J., Wang, G., Allegri, R., et al. (2019) · JAMA Network Open · doi:10.1001/jamanetworkopen.2019.17126 · Cited by 40
Proteopathic Seed Amplification Assays for Neurodegenerative Disorders
Ferreira, N., & Caughey, B. W. (2020) · Clinics in Laboratory Medicine · doi:10.1016/j.cll.2020.04.002 · Cited by 35
Analysis of 3-O-Sulfated Heparan Sulfate Using Isotopically Labeled Oligosaccharide Calibrants
Wang, Z., Arnold, K., Dhurandahare, V. M., Xu, Y., Pagadala, V., Labra, E., Jeske, W. P., Fareed, J., Gearing, M., & Liu, J. (2022) · Analytical Chemistry · doi:10.1021/acs.analchem.1c04965 · Cited by 37
Plasma GFAP associates with secondary Alzheimer's pathology in Lewy body disease
Cousins, K. A. Q., Irwin, D. J., Chen‐Plotkin, A. S., Shaw, L. M. J., Arezoumandan, S., Lee, E. B., Wolk, D. A., Weintraub, D. A., Spindler, M., Deik, A., et al. (2023) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.51768 · Cited by 38
Patterns of Hippocampal Tau Pathology Differentiate Neurodegenerative Dementias
Milenković, I., Petrov, T., & Kovács, G. G. (2014) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000365548 · Cited by 36
Erskine, D., Thomas, A. J., Taylor, J., Savage, M. A., Attems, J., McKeith, I. G., Morris, C. M., & Khundakar, A. A. (2017) · American Journal of Geriatric Psychiatry · doi:10.1016/j.jagp.2017.01.005 · Cited by 36
Plasma phosphorylated tau181 predicts cognitive and functional decline
Tropea, T. F., Waligórska, T., Xie, S. X., Nasrallah, I. M., Cousins, K. A. Q., Trojanowski, J. Q., Grossman, M., Irwin, D. J., Weintraub, D. A., Lee, E. B., et al. (2022) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.51695 · Cited by 39
“Postmortem examination of the brains from people with AD during life, show significant cortical and medial temporal lobe atrophy; amyloid-b (Ab) plaques and neurofibrillary tangles (NFT) of hyperphosphorylated tau confirm the neuropathological diagnosis.(2) Biofluid and neuroimaging biomarkers of axonal degeneration (…”
BackgroundSelf-citationValentin‐Escalera, J., Leclerc, M., & Calon, F. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-230118 · Cited by 37
Neuroinflammation is associated with Alzheimer’s disease co-pathology in dementia with Lewy bodies
van Wetering, J., Geut, H., Bol, J. G. J. M., Galis, Y., Timmermans, E., Twisk, J. W. R., Hepp, D. H., Morella, M. L., Pihlstrøm, L., Lemstra, A. W., et al. (2024) · Acta Neuropathologica Communications · doi:10.1186/s40478-024-01786-z · Cited by 41
Progressive amnestic dementia, hippocampal sclerosis, and mutation in C9ORF72
Murray, M. E., Bieniek, K. F., Greenberg, M. B., DeJesus‐Hernandez, M., Rutherford, N. J., van Blitterswijk, M., Niemantsverdriet, E., Ash, P. E. A., Gendron, T. F., Kouri, N., et al. (2013) · Acta Neuropathologica · doi:10.1007/s00401-013-1161-2 · Cited by 34
“The neuritic plaque score was assigned by retrospectively assessing neuropathologic reports to determine distribution on thioflavin S stains of the most affected cortices according to the recent neuropathologic guidelines recommended by the National Institutes on Aging and the Alzheimer’s Association [17, 28].”
MethodSelf-citationBeach, T., Schneider, J., Sue, L., Serrano, G., Dugger, B., Monsell, S. E., & Kukull, W. (2014) · Journal of Neuropathology and Experimental Neurology · doi:10.1097/nen.0000000000000114 · Cited by 37
“The revised NIA Alzheimers’ Association recommendations for the neuropathologic assessment of AD include the Thal-Braak staging of A-amyloid plaques (defined as any plaque type that is immunoreactive to A-amyloid) as 1 arm of the tripartite histologic assessment (15, 21); the accumulation of sufficient postmortem data…”
Self-citationCuyvers, E., van der Zee, J., Bettens, K., Engelborghs, S., Vandenbulcke, M., Robberecht, C., Dillen, L., Merlin, C., Geerts, N., Graff, C., et al. (2015) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2015.02.014 · Cited by 36
“Diagnosis of pathology confirmed patients was based on currently accepted diagnostic criteria (Montine et al., 2012).”
Decreased Levels of VAMP2 and Monomeric Alpha-Synuclein Correlate with Duration of Dementia
Vallortigara, J., Whitfield, D., Quelch, W., Alghamdi, A. A., Howlett, D. R., Hortobágyi, T., Johnson, M. A., Attems, J., O'Brien, J. T., Thomas, A. J., et al. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-150707 · Cited by 35
“on Aging-Alzheimer’s Association (NIA-AA) guidelines and phases of amyloid-β (Aβ) deposition (Aβ-phases) [2, 26-29].”
BackgroundMezache, L., Mikhail, M., Garofalo, M., & Nuovo, G. J. (2015) · Applied immunohistochemistry & molecular morphology · doi:10.1097/pai.0000000000000147 · Cited by 34
“20 Hyperphosphorylated tau was basically absent in normal brain and very rare in some cerebral sections of Alzheimer disease, even though each Alzheimer disease case we studied had a Braak and Braak overall score of 3 using the “ABC” evaluation criteria.(21) This finding underscores the importance when studying Alzhei…”
Method
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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