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Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer's disease
Abstract
We studied the accumulation of neurofibrillary tangles (NFTs) and senile plaques (SPs) in 10 Alzheimer's disease patients who had been examined during life. We counted NFTs and SPs in 13 cytoarchitectural regions representing limbic, primary sensory, and association cortices, and in subcortical neurotransmitter-specific areas. The degree of neuropathologic change was compared with the severity of dementia, as assessed by the Blessed Dementia Scale and duration of illness. We found that (1) the severity of dementia was positively related to the number of NFTs in neocortex, but not to the degree of SP deposition; (2) NFTs accumulate in a consistent pattern reflecting hierarchic vulnerability of individual cytoarchitectural fields; (3) NFTs appeared in the entorhinal cortex, CA1/subiculum field of the hippocampal formation, and the amygdala early in the disease process; and (4) the degree of SP deposition was also related to a hierarchic vulnerability of certain brain areas to accumulate SPs, but the pattern of SP distribution was different from that of NFT.
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In the citing paper
“Studies have shown that their number and location correlates with neuronal loss, disease severity and clinical course [65, 66].”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [66]
In the citing paper
“Neurofibrillary tangles and quantitative neuronal loss, but not amyloid plaques, have been found to correlate with disease severity and dementia duration [21–23].”
From Clinical trials of new drugs for Alzheimer disease (2020) · cites this paper as [22]
In the citing paper
“to correlate with measures of cognitive decline (Arriagada et al., 1992) in humans.”
From Network analysis identifies strain-dependent response to tau and tau seeding-associated genes (2023) · cites this paper as Arriagada et al., 1992
In the citing paper
“In AD patients, the clinical severity of dementia strongly correlates with the load of pathological tau aggregates. 3 , 4”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [3]
In the citing paper
“Correlations between NFT density and clinical symptoms, such as a cognitive decline in AD, have been demonstrated [11, 12].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [11]
In the citing paper
“Increasing evidence demonstrates that the cognitive dysfunction and severity of the disease are more related to tau pathology [11–14].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [11]
In the citing paper
“Tau has received increasing attention as a potential therapeutic target, since evidence indicates that tau pathology is more associated with cognitive dysfunction.”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [11]
In the citing paper
“NFTs and quantitative neuronal loss may be more closely correlated with disease severity and dementia progression than the amyloid plaque burden [20–22].”
From Clinical trials of new drugs for Alzheimer disease: a 2020–2023 update (2023) · cites this paper as [21]
In the citing paper
“the best pathological correlate for clinical symptoms to date is the extent of NFT formation (Arriagada et al., 1992; Brier et al., 2016; Giannakopoulos et al., 2003)”
From Selective Neuronal Vulnerability in Alzheimer’s Disease: A Network-Based Analysis (2020) · cites this paper as Arriagada et al., 1992
In the citing paper
“a large number of studies have arrived at a common finding, namely, there is a strong link between neocortical NFTs and cognitive decline (Tomlinson et al., 1970; Duyckaerts et al., 1990, 1997, 1998; Mckee et al., 1991; Arriagada et al., 1992;”
From Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models (2014) · cites this paper as Arriagada et al., 1992
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Metadata
- Authors
- Arriagada, P. V., Growdon, J. H., Hedley-Whyte, E. T., & Hyman, B. T.
- Affiliations
- Harvard University (US)
- ORCID
- Hyman, Bradley T.
- Venue
- Neurology
- Published
- 1992-03
- Volume
- 42
- Issue
- 3
- Pages
- 631-631
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- OpenAlex
- W2053116497
- Cited by
- 2,668
- References
- 0
- Citations by year
- 2026: 54 · 2025: 89 · 2024: 81 · 2023: 101 · 2022: 89 · 2021: 141 · 2020: 135 · 2019: 131 · 2018: 96 · 2017: 112 · 2016: 132 · 2015: 101 · 2014: 106 · 2013: 93 · 2012: 97
- FWCI
- 28.79
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (AG-08487, P50 AG05134, P50AG005134)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, neurofibrillary tangles, amyloid plaques, dementia severity, disease duration, neuropathology, entorhinal cortex, hippocampal formation, amygdala, regional vulnerability, cytoarchitecture
- MeSH terms
- Aged, Alzheimer Disease, Amygdala, Brain, Female, Hippocampus, Humans, Male, Middle Aged, Neurofibrillary Tangles
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