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
Self-citation
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Sorted by citations
Items 2,001–2,100 of 2,854
Sarti, P., Varrasi, S., Guerrera, C. S., Platania, G. A., Furneri, G., Torre, V., Boccaccio, F. M., Rivi, V., Tascedda, S., Pirrone, C., et al. (2025) · BMC Psychology · doi:10.1186/s40359-024-02239-x · Cited by 5
Multiplexed In-cell Immunoassay for Same-sample Protein Expression Profiling
Shang, J., Zrazhevskiy, P., Postupna, N. O., Keene, C. D., Montine, T. J., & Gao, X. (2015) · Scientific Reports · doi:10.1038/srep13651 · Cited by 5
Self-citationPrimary progressive aphasia with parkinsonism
Doherty, K. A., Rohrer, J. D., Lees, A. J., Holton, J. L., & Warren, J. D. (2013) · Movement Disorders · doi:10.1002/mds.25341 · Cited by 5
“LB pathology corresponded to Braak stage 6 and was classified as diffuse neocortical LB pathology.(2,3) With this extent of LB pathology and an additional diagnosis of AD current classification suggests that there is an intermediate likelihood that the pathological findings are associated with a dementia with LBs clin…”
BackgroundMethodAlzheimer's Disease-Related Lesions
Alafuzoff, I. I. (2012) · Journal of Alzheimer s Disease · doi:10.3233/jad-2012-129024 · Cited by 5
“I. Alafuzoff / emphasizing that in addition to AD neuropathological brain injury, and hippocampal sclerosis should also assessed [14].”
Alzheimer’s disease biomarkers: walk with deliberate haste, don’t run blithely on?
Hu, W. T., Shaw, L. M. J., & Trojanowski, J. Q. (2013) · Acta Neuropathologica · doi:10.1007/s00401-013-1197-3 · Cited by 5
“On the heels of updated definitions for clinical [1, 6, 9] and neuropathologic [7] characterization of AD, this may be an opportune moment to re-visit the goals of AD biomarkers [8].”
BackgroundSelf-citationDoes Alzheimer Disease Pathologic Change Underlie Subjective Cognitive Complaints?
Grill, J. D., Vinters, H. V., & Monsell, S. E. (2015) · Alzheimer Disease & Associated Disorders · doi:10.1097/wad.0000000000000092 · Cited by 6
“Intermediate 38 (23) 11 (33) 49 (25) High 1 (1) 2 (6) 3 (2) Presence of Lewy bodies88 14 (11) 4 (17) 18 (12) 0.”
Self-citationCurrent Pathogenetic Concepts of Vascular Cognitive Impairment
Ka, J. (2016) · Journal of Neurology Neurological Science and Disorders · doi:10.17352/jnnsd.000009 · Cited by 5
“There are several international efforts to defi ne cognitive impairment due to cerebrovascular disease in different stages and subtypes: (1) The Newcastle group suggested a categorization of the cerebrovascular pathology associated with cognitive impairment according to 6 subtyes of CVLs ranging from large or several…”
BackgroundKIF5A and KLC1 expression in Alzheimer’s disease: relationship and genetic influences
Hares, K. M., Miners, J. S., Scolding, N. J., Love, S., & Wilkins, A. (2019) · AMRC Open Research · doi:10.12688/amrcopenres.12861.1 · Cited by 5
Nwabuobi, L., Tomishon, D., Shneider, N. A., Fahn, S., Vonsattel, J. P., & Cortes, E. P. (2019) · Movement Disorders Clinical Practice · doi:10.1002/mdc3.12823 · Cited by 5
“The AD pathological changes in the brain were minimal, and the likelihood of dementia attributable to AD changes were most likely nihil, based on the diagnostic categorization of AD recommended by the National Institute on Aging-Alzheimer’s Association.11”
MethodThe Amyloid-beta rich CNS environment alters myeloid cell functionality independent of their origin
Drost, N., Houtman, J., Cseresnyés, Z., Niesner, R. A., Rinnenthal, J.-L., Miller, K. R., Prokop, S., & Heppner, F. L. (2020) · Scientific Reports · doi:10.1038/s41598-020-63989-3 · Cited by 5
Current clinical approaches in neurodegenerative diseases
Gago, M. F., Machado, Á. S., & Rocha, S. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-818084-6.00004-0 · Cited by 5
Comparison of proteome alterations during aging in the temporal lobe of humans and rhesus macaques
Wang, X., Chen, K., Pan, M., Ge, W., & He, Z. (2020) · Experimental Brain Research · doi:10.1007/s00221-020-05855-2 · Cited by 5
Novel monoclonal antibodies targeting the RRM2 domain of human TDP-43 protein
Trejo‐Lopez, J. A., Sorrentino, Z. A., Riffe, C. J., Lloyd, G. M., Labuzan, S. A., Dickson, D. W., Yachnis, A. T., Prokop, S., & Giasson, B. I. (2020) · Neuroscience Letters · doi:10.1016/j.neulet.2020.135353 · Cited by 5
Self-citationOhno, Y., Ikeda, T., Sakurai, K., et al. (2020) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlaa151 · Cited by 5
Different patterns of hippocampal subfield pathology in Lewy body disease and Alzheimer's disease
Jellinger, K. A. (2021) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12695 · Cited by 5
“2 years); 71% showed high and 29% intermediate ADaffected neuropathological changes [4, 5].”
BackgroundGupta, H., Beach, T. G., Mehta, S. H., Shill, H. A., Driver‐Dunckley, E. D., Sabbagh, M. N., Belden, C. M., Liebsack, C., Dugger, B. N., Serrano, G. E., et al. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-200323 · Cited by 5
Self-citationSakurai, K., Kaneda, D., Uchida, Y., et al. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210535 · Cited by 5
Xu, G. M., Fromholt, S., & Borchelt, D. (2022) · Biomolecules · doi:10.3390/biom12070886 · Cited by 5
Pérez‐García, F., Vázquez‐Morón, S., Burgueño‐García, I., et al. (2022) · The Journal of Infectious Diseases · doi:10.1093/infdis/jiac268 · Cited by 5
Alzheimer’s Disease Neuropathologic Change and Vitamin Supplement Use Decades Earlier
Paganini‐Hill, A., Bukhari, S. A., Montine, T. J., Corrada, M. M., & Kawas, C. H. (2023) · Alzheimer Disease & Associated Disorders · doi:10.1097/wad.0000000000000551 · Cited by 5
“None 57 (76) 3 (2) Sparse 16 (21) 21 (11) Moderate 2 (3) 26 (14) Frequent 0 (0) 139 (73)”
Self-citationPifl, C., Reither, H., Attems, J., & Zecca, L. (2023) · npj Parkinson s Disease · doi:10.1038/s41531-023-00514-z · Cited by 5
“The standardized neuropathological assessment was performed for all cases and included the National Institute on Aging-Alzheimer ’ s Association (NIA-AA) criteria 52”
Koga, S., Murakami, A., Soto‐Beasley, A. I., Walton, R. L., Baker, M., Castanedes‐Casey, M., Josephs, K. A., Ross, O. A., & Dickson, D. W. (2023) · Acta Neuropathologica Communications · doi:10.1186/s40478-023-01611-z · Cited by 5
“Braak neurofibrillary tangle (NFT) stage and Thal amyloid phase were assigned by thioflavin S fluorescent microscopy according to published methods as previously described [34, 7, 26, 20].”
MethodSelf-citationMissense and loss‐of‐function variants at GWAS loci in familial Alzheimer's disease
Gunasekaran, T. I., Reyes‐Dumeyer, D., Faber, K. M., Goate, A., Boeve, B. F., Cruchaga, C., Pericak‐Vance, M. A., Haines, J. L., Rosenberg, R. N., Tsuang, D. W., et al. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.14221 · Cited by 4
Amyloid Deposition in the Central Nervous System
Rodríguez, F. J., Picken, M. M., & Lee, J. M. (2015) · Current clinical pathology · doi:10.1007/978-3-319-19294-9_8 · Cited by 5
Fenouil, T., Fourier, A., Quadrio, I., Streichenberger, N., Bernardini, S., Zima, T., Perret‐Liaudet, A., & Meyronet, D. (2019) · Clinical Biochemistry · doi:10.1016/j.clinbiochem.2019.06.004 · Cited by 5
Restifo, L. L. (2021) · Genetics · doi:10.1093/genetics/iyab185 · Cited by 5
The formation of small aggregates contributes to the neurotoxic effects of tau45-230
Afreen, S., & Ferreira, A. (2021) · Neurochemistry International · doi:10.1016/j.neuint.2021.105252 · Cited by 4
Diffuse Lewy body disease presenting as Parkinson's disease with progressive aphasia
Koga, S., Murakami, A., Josephs, K. A., et al. (2022) · Neuropathology · doi:10.1111/neup.12780 · Cited by 5
Self-citationUnique Lewy pathology in myotonic dystrophy type 1
Sano, T., Kawazoe, T., Shioya, A., Mori‐Yoshimura, M., Oya, Y., Maruo, K., Nishino, I., Hoshino, M., Murayama, S., & Saito, Y. (2022) · Neuropathology · doi:10.1111/neup.12790 · Cited by 5
“†CTG repeat abnormality obtained from frozen brain; > 120, abnormal expansion value of CTG repeats verified by PCR; SP stage: Braak amyloid stage(48)/Thal phase(49)/CERAD.(50,51) +, positive; , negative; CERAD, Consortium to Establish a Registry for Alzheimer’s Disease; DM1, myotonic dystrophy type 1; F, female; M, ma…”
BackgroundPrimary chronic traumatic encephalopathy in an older patient with late-onset AD phenotype
Fredericks, C. A., KOESTLER, M. E., Seeley, W. W., Miller, B. L., Boxer, A. L., & Grinberg, L. T. (2015) · Neurology Clinical Practice · doi:10.1212/cpj.0000000000000161 · Cited by 5
Alegro, M., Chen, Y., Ovando, D., Heinser, H., Eser, R., Ushizima, D., Tosun, D., & Grinberg, L. T. (2019) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/698902 · Cited by 5
“2 trillion by 2050 [1].”
Shepherd, C. E., McGeachie, A. B., Affleck, A. J., & Halliday, G. M. (2019) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlz069 · Cited by 5
“We would like to clarify that our Condensed Protocol encompasses a total of 5 paraffin tissue blocks which each contain 4 tissue samples to include all 20 of the brain regions described in the original 2012 NIA-AA guidelines (2,3).”
MethodResultInfluentialPrakash, R. S., McKenna, M. R., Gbadeyan, O., Andridge, R., Scharre, D. W., & Initiative, A. D. N. (2020) · medRxiv · doi:10.1101/2020.10.13.20211375 · Cited by 5
Mladinov, M., Oh, J. Y., Petersen, C., Eser, R. A., Li, S. H., Theofilas, P., Spina, S., Seeley, W. W., Bittencourt, J. C., Neylan, T. C., et al. (2021) · medRxiv · doi:10.1101/2021.01.27.21250608 · Cited by 5
Perivascular SPP1 Mediates Microglial Engulfment of Synapses in Alzheimer’s Disease ModelsPreprint
Schepper, S. D., Ge, J. Z., Crowley, G., Ferreira, L. S. S., Garceau, D. T., Toomey, C. E., Sokolova, D., Childs, T., Lashley, T., Burden, J. J., et al. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.04.04.486547 · Cited by 5
A limbic-predominant amnestic neurodegenerative syndrome associated with TDP-43 pathologyPreprint
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. (2023) · medRxiv · doi:10.1101/2023.11.19.23298314 · Cited by 5
Self-citationResistance and Resilience to Alzheimer's DiseasePreprint
Latimer, C. S., Prater, K. E., Postupna, N. O., & Keene, C. D. (2023) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a041201 · Cited by 8
Koutarapu, S., Ge, J., Dulewicz, M., Srikrishna, M., Szadziewska, A., Wood, J. I., Blennow, K., Zetterberg, H., Michno, W., Ryan, N. S., et al. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.06.03.596890 · Cited by 5
“All these tools have significant shortcomings with respect to specificity, sensitivity, bias, and throughput that provide solely discrete readout variables that comprehensively form the basis of pathological staging (Montine et al. 2012; Mirra et al. 1991).”
BackgroundMethodLogue, M. W., Labadorf, A. T., O’Neill, N. K., Dickson, D. W., Dugger, B. N., Flanagan, M. E., Frosch, M. P., Gearing, M., Jin, L., Kofler, J., et al. (2024) · medRxiv · doi:10.1101/2024.10.29.24316311 · Cited by 6
Self-citationTitze‐de‐Almeida, R., Gomes, G. D. M. O., dos Santos, T. C., & Titze-de-Almeida, S. S. (2025) · Pharmaceuticals · doi:10.3390/ph19010026 · Cited by 5
Mao, C., Wang, W., Huang, X., Wu, M., Wang, Y., Wang, T., Qiu, Y., Chu, S., Jin, W., Jiang, Y., et al. (2026) · Alzheimer s Research & Therapy · doi:10.1186/s13195-025-01943-z · Cited by 7
“The pathological hallmarks of AD are the accumulation of amyloid-β (Aβ) plaques and neurofibrillary tangles containing hyperphosphorylated tau protein [1].”
Plasma eMTBR-tau243 and %p-tau217 for Biological Staging of Alzheimer Disease
Salvadó, G., Horie, K., Barthélemy, N. R., Schindler, S. E., Janelidze, S., Dolado, A. O., Bali, D., Perrin, R. J., Morris, J. C., Benzinger, T. L. S., et al. (2026) · JAMA Neurology · doi:10.1001/jamaneurol.2026.1405 · Cited by 8
Therriault, J., Gauthier, S. G., & Rosa‐Neto, P. (2023) · The Journal of Prevention of Alzheimer s Disease · doi:10.14283/jpad.2023.52 · Cited by 4
“Staging systems are currently employed in the diagnosis of AD at autopsy (1, 2).”
BackgroundMethodNeuropsychological and clinical indicators of Lewy body and Alzheimer's pathology
Simpson, A., Wyman‐Chick, K. A., & Daniel, M. S. (2025) · Journal of Alzheimer s Disease Reports · doi:10.1177/25424823241304386 · Cited by 4
“…to the reduced sample size for the DLB group, our rigorous neuropathological selection criteria (according to DLB Consortium 3 and the NIAA-AA 39 ) and exclusion of other disease processes was indeed a signi fi cant strength of our study, allowing the potential to eliminate confounding…”
InfluentialYoussef, H., Gatto, R. G., Pham, N. T. T., Jones, D. T., Petersen, R. C., Machulda, M. M., Whitwell, J. L., & Josephs, K. A. (2025) · Neuropathology · doi:10.1111/neup.70000 · Cited by 4
“The neuropathological diagnosis was conducted following the National Institute on Aging and Alzheimer's Association (NIA-AA) guidelines [16, 17].”
A Review Article on Oxidative Stress Markers F2-Isoprostanes and Presenilin-1 in Alzheimer’s Disease
Timalsina, D. R., Abichandani, L. G., & Ambad, R. S. (2025) · Journal of Pharmacy And Bioallied Sciences · doi:10.4103/jpbs.jpbs_1784_24 · Cited by 4
“[8] The brain is highly vulnerable to oxidation due to its high oxygen use and content of polyunsaturated fatty acids.”
Takeda, K., Fujishiro, H., Torii, Y., Sekiguchi, H., Arafuka, S., Habuchi, C., Miwa, A., Ozaki, N., Yoshida, M., Iritani, S., et al. (2025) · Psychiatry and Clinical Neurosciences · doi:10.1111/pcn.13814 · Cited by 4
“23 According to the fourth CDLB neuropathological criteria, 1 immunostaining with α -synuclein and phosphorylated α -synuclein were used to assess Lewy-related pathology, such as LBs and the other α -synuclein-positive structures.”
“The DESCRIBE-ALS-FTD study: a prospective multicenter observational study of the ALS-FTD spectrum”
Hermann, A., Prudlo, J., Kasper, E., Synofzik, M., Peters, O., Priller, J., Dinter, E., Wiltfang, J., Zerr, I., Flöel, A., et al. (2025) · Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration · doi:10.1080/21678421.2025.2509617 · Cited by 4
“For all cases, assessment includes reporting of Alzheimer ’ s disease neuropathological changes (31) and presence/ regional distribution of Lewy pathology (32).”
Performance of novel tau antibodies across multiple modalities for Alzheimer's disease assessment
Trivedi, P., Forrest, K., Fisher, D. W., Winstone, J. K., McMillan, P. J., Valentine, M., Postupna, N. O., Wilson, A. M., Bajwa, T. S., MacCoss, M. J., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70481 · Cited by 6
“51,52 For pT181, pT217, and pT231 immunostains, p-tau was not present in either aged or young unimpaired donors and showed staining in high ADNCandADNC,anexpectedfindingbasedontheAT8-stainedslides (Figure 3A).”
Characterization of neurodegenerative pathologies in adult and pediatric subjects with Down syndrome
Canan, F., Wick, N., Raisanen, J. M., Burns, D. K., Hatanpaa, K. J., Richardson, T. E., White, C. L., & Daoud, E. V. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251362762 · Cited by 4
“13 Widely accepted neuropathological criteria for the diagnosis of AD were fi rst established by the National Institute on Aging in 1985 14 and went through a revision by the Consortium to Establish a Registry for Alzheimer ’ s Disease (CERAD) in 1991.”
Ha, H.-Y., Han, S.-H., & Cho, S. (2025) · Innovations in Acupuncture and Medicine · doi:10.1186/s44424-025-00017-z · Cited by 4
“In accordance with the previous studies on the association between these two key pathological proteins, we confirmed the regulatory effect of PLE on Aβ levels and hyperphosphorylation of tau [41].”
Neuropathologic Changes in People With Essential Tremor With Dementia
Wainman, E., Berry, D. S., Hernandez, N. C., Guy, T. O., Cosentino, S., Faust, P. L., & Louis, E. D. (2025) · Neurology · doi:10.1212/wnl.0000000000214310 · Cited by 5
Neuropsychiatric symptoms and severity of dementia
Caldas, G. H. D. O., Pires, S. L., & Gorzoni, M. L. (2013) · Dementia & Neuropsychologia · doi:10.1590/s1980-57642013dn70200006 · Cited by 4
Arezoumandan, S., Cai, X., Kalkarni, P., Davis, S. A., Wilson, K. I., Ferris, C. F., Cairns, N. J., & Gitcho, M. A. (2021) · Neuroscience Letters · doi:10.1016/j.neulet.2021.136010 · Cited by 4
Self-citationFernandes, Z., Sahana, K. D., & Dattatreya, K. S. (2022) · International Journal of Drug Delivery Technology · doi:10.25258/ijddt.12.3.13 · Cited by 4
Nagaraja, N., Wang, W., Duara, R., DeKosky, S. T., & Vaillancourt, D. E. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-220624 · Cited by 4
Hirsch‐Reinshagen, V., Hercher, C., Vila‐Rodriguez, F., Neumann, M., Rademakers, R., Honer, W. G., Hsiung, G. R., & Mackenzie, I. R. (2023) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12921 · Cited by 4
“Cases included in this study had at most stage Braak IV neurofibrillary pathology with no more than moderate numbers of senile neuritic plaques (classified as moderate Alzheimer’s disease [AD] and corresponding to an intermediate level of Alzheimer’s disease neuropathologic change using NIA-AA criteria [38]).”
Malik, N., Miah, M.-U., Galgani, A., McAleese, K. E., Walker, L., LeBeau, F. E. N., Attems, J., Outeiro, T. F., Thomas, A. J., & Koss, D. J. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02691-4 · Cited by 5
“…diagnoses were based on assessment of brain tissue according to the National Institute of Ageing-Alzheimer’s Association (NIA-AA) criteria [52], including Braak NFT staging [12], Thal phases [63], and Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) scoring [31], as well…”
MethodLearning precise segmentation of neurofibrillary tangles from rapid manual point annotations
Ghandian, S., Albarghouthi, L., Nava, K., Sharma, S. R. R., Minaud, L., Beckett, L. A., Saito, N. H., DeCarli, C. S., Rissman, R. A., Teich, A. F., et al. (2026) · Scientific Reports · doi:10.1038/s41598-026-61605-4 · Cited by 4
“All cases met the pathological criteria for Alzheimer disease (AD), meeting NIA Reagan or NIA-AA intermediate/high criteria 25,26 . www.nature.com/scientificreports”
Unveiling the Intricate Link Between Anaerobe Niche and Alzheimer Disease Pathogenesis
Drakes, N., Kondrikova, G., Pytel, D., & Hamlett, E. D. (2024) · The Journal of Infectious Diseases · doi:10.1093/infdis/jiae312 · Cited by 4
Taniguchi, D., Shimonaka, S., Ahmed, I., Elahi, M., Hatano, T., Imai, Y., & Hattori, N. (2024) · Neurobiology of Disease · doi:10.1016/j.nbd.2024.106686 · Cited by 5
“The diagnosis was confirmed using a neuropathological examination (Dickson et al., 2002; Litvan et al., 1996; Montine et al., 2012).”
MethodPlasma proteomics-based brain aging signature and incident dementia risk
Kou, M., Ma, H., Wang, X., Heianza, Y., & Qi, L. (2024) · GeroScience · doi:10.1007/s11357-024-01407-6 · Cited by 5
“For example, multiple proteinopa-thies coexisted in human brains with dementia [32], including the presence of amyloid-β plaques and tau neurofibrillary tangles which biologically defined AD [33].”
Houwer, J. F. H. D., Dopper, E. G. P., Rajicic, A., van Buuren, R., Arcaro, M., Galimberti, D., Breedveld, G. J., Wilke, M., van Minkelen, R., Jiskoot, L. C., et al. (2024) · Journal of Neurology · doi:10.1007/s00415-024-12758-7 · Cited by 4
Ortega‐Cruz, D., Rábano, A., & Strange, B. A. (2025) · Alzheimer s Research & Therapy · doi:10.1186/s13195-024-01633-2 · Cited by 4
Sánchez‐Aced, É., Moya‐Llamas, B., Escabias, J. A., Torres, S., Colom‐Cadena, M., Pegueroles, J., de Quintana-Schmidt, C. J., Bayés, À., Molina‐Porcel, L., Aldecoa, I., et al. (2025) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.70010 · Cited by 4
“All samples were processed using previously described methods [15] and generally recommended [8].”
Kim, Y., Andreasson, T., Vishupad, N., Benegal, A., Pizzo, D. P., Hansen, L. A., Hiniker, A. O., & Coughlin, D. G. (2025) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlaf047 · Cited by 4
“2,4,5,15,16 Thus, currently accepted methods are adaptations of earlier works that have evolved over time, have variable inter-rater reliability and tend to emphasize topology over regional severity.”
Schaffert, J., Iyengar, N., Magill, R., LoBue, C., Chiang, H., White, C. L., Hart, J., Didehbani, N., & Cullum, C. M. (2025) · Neurology · doi:10.1212/wnl.0000000000214012 · Cited by 5
The China Brain Multi-omics Atlas Project (CBMAP)
Zhou, D., Zhou, Y., Sun, Z., Ji, F., Zhang, D., Wang, Q., Ruan, Y., Wang, Y., Zhu, Y., Sun, X., et al. (2025) · Molecular Psychiatry · doi:10.1038/s41380-025-03250-3 · Cited by 6
“These uniformly applied pathological diagnostic procedures are organized by the National Health and Disease Human Brain Tissue Resource Center at Zhejiang University, following a uni fi ed process of quality controls [32, 34 – 36].”
Early subtypes and progressions of progressive supranuclear palsy: a data-driven brain bank study
Ono, D., Sekiya, H., Ghayal, N. B., Maier, A. R., Roemer, S. F., Uitti, R. J., Litvan, I., Josephs, K. A., Wszołek, Z. K., & Dickson, D. W. (2025) · Journal of Neurology · doi:10.1007/s00415-025-13459-5 · Cited by 4
Self-citationMultiproteinopathy, neurodegeneration and old age: a case study
Rojas, J. C., Stephens, M. L., Rabinovici, G. D., Kramer, J. H., Miller, B. L., & Seeley, W. W. (2018) · Neurocase · doi:10.1080/13554794.2017.1420199 · Cited by 3
“Immunohistochemical analyses revealed a complex pathological picture, showing a high level of AD pathology (Montine et al., 2012), with frequent neuritic plaques and neurofibrillary tangles in clinically implicated regions, but also FTLD-TDP, and, more variably, LBD pathology in vulnerable regions (Table 2).”
BackgroundJang, J., & Kim, S. (2019) · Journal of the Korean Neurological Association · doi:10.17340/jkna.2019.1.1 · Cited by 4
“와 병적 타우를 반영하는 지표로, 즉 아밀로이드병증(A)과 병적 타 우(T)로 알츠하이머병을 정의하기로 결정하였다.(21,22) 대상자가 베 타아밀로이드 침착과 관련된 생물표지자의 변화만을 보인다면 ‘알 츠하이머의 병적 변화(Alzheimer’s pathologic change)’ 단계이며 병적 타우 지표의 변화까지 확인되면 ‘알츠하이머병(Alzheimer’s disease)’ 단계로 명명하기로 하였다(Table 2).”
Lack of Association of Locus Coeruleus Pathology with Orthostatic Hypotension in Parkinson’s Disease
Tong, Q., & Chen, L. (2020) · Journal of Parkinson s Disease · doi:10.3233/jpd-202325 · Cited by 4
Klotz, S., & Gelpí, E. (2021) · Wiener Medizinische Wochenschrift · doi:10.1007/s10354-021-00848-4 · Cited by 4
Vervuurt, M., Zhu, X., Schrader, J. M., de Kort, A. M., Marques, T. M., Kersten, I., van Ton, A. M. P., Abdo, W. F., Schreuder, F. H. B. M., Rasing, I., et al. (2022) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12804 · Cited by 4
“CSF of CAA patients and controls was used to determine Aβ40 levels through the Lumipulse G β-[1-40] chemiluminescent immunoassay (Fujirebio, Gent, Belgium).”
MethodBenedusi, V. (2018) · Materials and Methods · doi:10.13070/mm.en.8.2665 · Cited by 5
Coughlin, D. G., Coslett, H. B., Peterson, C. S., et al. (2022) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1002/trc2.12294 · Cited by 4
Self-citationHuman Brain Banking as a Convergence Platform of Neuroscience and Neuropsychiatric Research
Liu, F., Yin, X., Cong, C., Wang, Y., & Ma, C. (2022) · Human Brain · doi:10.37819/hb.001.001.0204 · Cited by 5
“Dementia, which is characterised by the deposition of argyrophilic senile plaques and NFTs in the brain, was named Alzheimer’s disease (AD) (Montine et al., 2012).”
BackgroundLaton, J., Schependom, J. V., Goossens, J., Wiels, W. A., Sieben, A., Deyn, P. P. D., Goeman, J., Streffer, J. R., van der Zee, J., Martin, J., et al. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220693 · Cited by 4
Artifacts in magnetic force microscopy of histological sections
Walsh, K. J., Shiflett, O., Shah, S. V., Renner, T., Soulas, N., Scharre, D. W., McTigue, D. M., & Agarwal, G. (2022) · Journal of Magnetism and Magnetic Materials · doi:10.1016/j.jmmm.2022.170116 · Cited by 4
Journe‐Mallet, I., Gouju, J., Etcharry‐Bouyx, F., Chauviré, V., Guillet, V., Scherer‐Gagou, C., Prundean, A., Godard, S., Lecluse, A., Cassereau, J., et al. (2022) · Brain Pathology · doi:10.1111/bpa.13138 · Cited by 4
Riluzole is associated with decreasing neuritic plaque severity in amyotrophic lateral sclerosis
Mazumder, S., McCann, H., D’Silva, S., et al. (2022) · Brain · doi:10.1093/brain/awac467 · Cited by 4
“AD neuropathological change was assessed according to the National Institute of Ageing and Alzheimer’s Disease Association Recommendations which includes an amyloid-β plaque (A) score, Braak neurofibrillary tangle (B) score and neuritic plaque (C) score.(4) Statistical analysis was performed using SPSS (Version 25) wi…”
MethodCarlos, A. F., Koga, S., Graff‐Radford, N. R., Baker, M., Rademakers, R., Ross, O. A., Dickson, D. W., & Josephs, K. A. (2023) · Neuropathology · doi:10.1111/neup.12938 · Cited by 4
“4 A subset of senile plaques, called neuritic plaques, are associated with tau-immunoreactive neurites.”
BackgroundSelf-citationMiyahara, H., Tamai, C., Inoue, M., Sekiguchi, K., Tahara, D., Tahara, N., Takeda, K., Arafuka, S., Moriyoshi, H., Koizumi, R., et al. (2023) · Brain Pathology · doi:10.1111/bpa.13199 · Cited by 5
“Based on each diagnostic criteria, Alzheimer ’ s disease was assessed using PHF-Tau and amyloid β [4 – 6, 9, 10, 12 – 24] IHC of the temporal lobe [20, 25], Lewy body disease was assessed using α -synuclein IHC of the substantia nigra, locus coeruleus, and dorsal nucleus of the vagus nerve [ 19],…”
Cross-species comparative analysis of single presynapses
Berson, E., Gajera, C. R., Phongpreecha, T., Perna, A., Bukhari, S. A., Becker, M., Chang, A. L., Francesco, D. D., Espinosa, C. A., Ravindra, N. G., et al. (2023) · Scientific Reports · doi:10.1038/s41598-023-40683-8 · Cited by 4
Self-citationBackman, E. A., Saari, L., Parkkola, R. K., Koikkalainen, J. R., Gardberg, M., & Kaasinen, V. (2023) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2023.122804 · Cited by 4
“Postmortem tissue sampling and neuropathological evaluations were performed using conventional methods to detect neurodegenerative disorders, with minor modifications [14].”
MethodFocused review: Clinico-neuropathological aspects of late onset epilepsies
Rácz, Á., Galvis-Montes, D. S., Borger, V., Becker, A. J., & Pitsch, J. (2024) · Seizure · doi:10.1016/j.seizure.2024.06.015 · Cited by 5
“…for Alzheimer ’ s disease neuropathological changes and related disorders suggest HS neuropathology to be ‘defined by severe pyramidal cell loss and gliosis in CA1 and subiculum of the hippocampal formation that is out of proportion to AD neuropathologic change in the same structures ’ [56].”
BackgroundIchimata, S., Hata, Y., Nomoto, K., et al. (2024) · Diagnostic Pathology · doi:10.1186/s13000-024-01519-9 · Cited by 4
“Neuropathological examination revealed edematous change and an intermediate level of Alzheimer’s disease-related pathology based on the National Institution on Aging-Alzheimer’s Association guideline (A3B2C3) (Supplementary Figure S3) [13].”
BackgroundTayran, H., Yılmaz, E., Bhattarai, P., Min, Y., Wang, X., Ma, Y., Nelson, N. N., Kassara, N., Coşacak, M. İ., Dogru, R. M., et al. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.089273 · Cited by 6
Zhu, H., Xue, Z., Qiu, W., et al. (2015) · Experimental Gerontology · doi:10.1016/j.exger.2015.06.003 · Cited by 4
Aβ Imaging in Aging, Alzheimer’s Disease and Other Neurodegenerative Conditions
Villemagne, V. L., Fodero‐Tavoletti, M. T., Yates, P. A., Masters, C. L., & Rowe, C. C. (2014) · Springer eBooks · doi:10.1007/978-3-642-54307-4_10 · Cited by 4
Biopsy Pathology of Neurodegenerative Disorders in Adults
Joe, M. (2010) · Elsevier eBooks · doi:10.1016/b978-0-443-06982-6.00025-0 · Cited by 4
Emergence of exosomal DNA in molecular neuropathology
Kraus, T. F. J. (2018) · Journal of Laboratory Medicine · doi:10.1515/labmed-2017-0065 · Cited by 4
“Alzheimer’s disease (AD) is classified by evaluating the amount of amyloid β and τ deposits [32, 34, 36], Parkinson’s disease (PD) is classified by evaluating the amount of α-synuclein [38, 133, 134] and Creutzfeldt-Jacob disease (CJD) is diagnosed by detecting deposits of prion protein in different brain regions usin…”
BackgroundJankovská, N., Olejár, T., Kukal, J., & Matěj, R. (2021) · Current Alzheimer Research · doi:10.2174/1875692117999201215162043 · Cited by 4
Rini, J. F., Asken, B. M., Geier, E. G., Rankin, K. P., Kramer, J. H., Boxer, A. L., Miller, B. L., Yokoyama, J. S., & Spina, S. (2021) · Neurocase · doi:10.1080/13554794.2021.1879869 · Cited by 4
“IHC for TDP-43, FUS, and alphasynuclein were negative (Montine et al., 2012).”
BackgroundBrady, C. B., Robey, I., Stein, T. D., Huber, B. R., Riley, J., Rauf, N. A., Spencer, K. R., Walt, G. S., Adams, L., Averill, J. G., et al. (2021) · Brain Sciences · doi:10.3390/brainsci11101349 · Cited by 4
“We perform assessments of vascular disease, Braak and Braak staging for neurofibrillary tangles, Braak staging and NIA-AA classification [37] for Lewy bodies, CERAD staging and Thal phasing for Aβ, and evaluation for TDP-43 pathology [38,39] and age-related tau astrogliopathy [40].”
MethodDecision-Making Deficits Associated with Amyloidosis in Lewy Body Disorders
Spotorno, N., McMillan, C. T., Irwin, D. J., et al. (2017) · Frontiers in Human Neuroscience · doi:10.3389/fnhum.2016.00693 · Cited by 4
“This region is a critical node of a decision-making network as well as a region previously associated with comorbid α-synuclein and Aβ in LBD. Conclusions: These preliminary findings suggest that cognitive difficulties in LBD extend to include deficits in social decision-making and that this may be…”
BackgroundSelf-citationJellinger, K. A. (2016) · Journal of Clinical & Cellular Immunology · doi:10.4172/2155-9899.1000480 · Cited by 4
“Thus, PART does not meet the formal criteria for sporadic AD according to the NIA-AA guidelines [11].”
BackgroundDeafferentation of Olfactory Bulb in Subjects Dying with COVID-19Preprint
Tremblay, C., Beach, T. G., Intorcia, A. J., Walker, J. E., Arce, R. A., Sue, L. I., Nelson, C. M., Borja, C. I., Suszczewicz, K. E., Cline, M. P., et al. (2021) · medRxiv · doi:10.1101/2021.12.21.21268119 · Cited by 4
Self-citationTropea, T. F., Waligórska, T., Xie, S. X., Nasralah, I. M., Cousins, K. A. Q., Trojanowski, J. Q., Grossman, M., Irwin, D. J., Weintraub, D. A., Lee, E. B., et al. (2022) · SSRN Electronic Journal · doi:10.2139/ssrn.4007185 · Cited by 4
Self-citationIngrassia, L., Boluda, S., Jiménez, G., Kar, A., Racoceanu, D., Delatour, B., & Stimmer, L. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.10.31.564976 · Cited by 4
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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