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Inflammation, Aβ Deposition, and Neurofibrillary Tangle Formation as Correlates of Alzheimer's Disease Neurodegeneration
Abstract
We evaluated entorhinal cortex and superior frontal gyrus for hallmarks of Alzheimer's disease (AD) pathology, including inflammation, in three patient sets: AD patients, nondemented elderly patients with few or no neurofibrillary tangles (NFTs) and amyloid β peptide (Aβ) deposits, i.e. normal controls (NC), and nondemented elderly patients with profuse entorhinal cortex NFTs and neocortical Aβ deposits, i.e. high pathology controls (HPC). Membrane attack complex (C5b-9) immunoreactivity and immune activation of microglia (MHCII expression) were used as general markers for inflammation. Compared to NC patients, AD patients exhibited significant cortical synapse loss, Aβ deposition, NFT formation, and inflammation. HPC patients also had significantly elevated Aβ deposition and NFT formation, but there was no evidence of synapse loss and little or no evidence of inflammation. Across patients and brain regions the measures of inflammation each accounted for significant percentages of the variance in synaptophysin immunoreactivity and each was more highly correlated with synapse estimates than NFT formation or Aβ deposition.
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“Increased MHCII staining, counts or expression was noted in: the entorhinal cortex,7, 18, 20, 35, 43, 47 frontal and temporal gyri,7, 19, 24, 32, 33, 39, 45, 56 hippocampus20, 25, 27, 30, 32, 33, 34, 35, 36, 37, 38, 40, 42, 43, 44, 47 and frontal,18, 21, 25, 40, 41, 44, 46, 48, 49, 52 temporal16, 17, 18, 28, 30, 35, 43, 44, 48, 52 and occipital cortices.25, 35, 41, 43, 44”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [7]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“major histocompatibility complex II (36/43 studies)”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [7]
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“Nearly identical results were obtained in our previous research with six other HPC patients.5”
From Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer's Disease (1999) · cites this paper as [5]
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“Elevations in neuroinflammatory markers are widely reported in Alzheimer’s disease (AD), both in animal models1, 2, 3 and human subjects.4, 5, 6, 7”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [7]
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“Five of these studies reported higher levels of microglia markers in AD, three using HLA-DR,7, 33, 40 one using CD68,83 and one using both TREM2 and Iba1.61”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [7]
In the citing paper
“As in our previous research, 5 counts of the various elements at ϫ100 final magnification were recorded by an observer blind to disease state.”
From Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer's Disease (1999) · cites this paper as [5]
In the citing paper
“We have also found that HPC patients show little or no evidence of neocortical or limbic synapse loss, 5 underscoring the critical relationship of neuritic degeneration to dementia.”
From Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer's Disease (1999) · cites this paper as [5]
In the citing paper
“As in our previous study, 5 HPC patients had significantly higher (Ͼ36%) synaptophysin immunoreactivity on Western blot analysis compared with AD patients (F 1,14 ϭ 25.8, P Ͻ 0.0003), whereas they did not differ from ND patients on this measure (F 1,14 ϭ 1.9, P Ͼ 0.50, 7% difference; Table 1).”
From Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer's Disease (1999) · cites this paper as [5]
In the citing paper
“Similar results on brain regional changes in AD pathology were obtained in our previous study of ND, HPC, and AD patients.5”
From Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer's Disease (1999) · cites this paper as [5]
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Research works printed but not linked: 21
- [1]1. Brachova L, Lue L-F, Byttner S, Civin WH, Schultz J, Tuohy J, Rogers J. Reduced complement activation in nondemented patients with excessive β-amyloid peptide deposition. (Abstract) Neurosci Abst 1992;19:833
- [2]2. Katzman R, Terry R, DeTeresa R, et al. Clinical, pathological, and neurochemical changes in dementia: A subgroup with preserved mental status and numerous neocortical plaques. Ann Neurol 1988;23:138-44
- [3]3. Terry RD, Masliah E, Salmon DP, et al. Physical basis of cognitive alterations in Alzheimer's disease: Synapse loss is the major correlate of cognitive impairment. Ann Neurol 1991;30:572–80
- [4]4. Crystal H, Dickson D, Fuld P, et al. Clinico-pathologic studies in dementia: Nondemented subjects with pathologically confirmed Alzheimer's disease. Neurol 1998;38:1682–87
- [5]5. Dickson DW, Crystal HA, Mattiace LA, et al. Identification of normal and pathological aging in prospectively studied nondemented elderly humans. Neurobiol Aging 1991;13:179–89
- [6]6. Arriagada PV, Marzloff K, Hyman BT. Distribution of Alzheimertype pathologic changes in nondemented elderly individuals matches the pattern in Alzheimer's discase. Neurol 1992;42:1681–88
- [7]7. Markesbery WR. The diagnosis of Alzheimer's disease. Arch Pathol Lab Med 1993;117:129-31
- [8]8. Hyman BT, Tanzi RE, Marzloff KM, Barbour R, Schenk D. Kunitz -rom nug os r S os nnoo reactivity in Alzheimer's disease. J Neuropathol Exp Neurol 1992;51:76–83
- [9]9. Webster S, O'Barr S, Rogers J. Enhanced aggregation and β structure of amyloid β peptide after co-incubation with C1q. J Neurosci Res 1994;39:448–56
- [11]11. Rogers J, Lue L-F, Brachova L, Webster S, Schultz J. Inflammation as a response and a cause of Alzheimer's pathophysiology. Dementia (Japan) 1995;9:133–38
- [12]12. Rogers J, Cooper NR, Schultz J, et al. Complement activation by β-amyloid in Alzheimer's disease. Proc Nat Acad Sci USA 1992;89:10016–20
- [13]13. Perlmutter LS, Scott SA, Barron E, Chui HC. MHC Class II-positive microglia in human brain: Association with Alzheimer lesions. J Neurosci Res 1992;33:549–58
- [14]14. Neurobiol Aging 1992;15:793–98
- [15]15. characterization of HLA-DR immunoreactivity in normal elderly and Alzheimer's disease brain. Exp Neurol 1990;110:93–104
- [16]16. Lett 1988;94:17-22
- [17]17. Brachova L, Lue L-F, Clark TD, Walker DG, Lorton D, Rogers J matory mediators by cultured microglia from Alzheimer's disease and nondemented elderly patients. (Abstract) Neurosci Abst 1995;21:740
- [18]18. Rogers J, Webster S, Lue L-F, et al. Inflammation and Alzheimer disease pathogenesis. Neurobiol Aging (in press)
- [20]20. Hyman BT, Van Hoesen GW, Damasio AR, Barnes CL. Alzheimer's Science 1984;225:1168-70
- [21]21. thology in Alzheimer's disease. Hippocampus 1991;1:1–8
- [23]23. robiol Aging 1993;14:1-16
- [24]24. heimer's disease. Brain Res 1992;569:141–45 Reccived June 20, 1996 Accepted August 1, 1996 Downloaded from https://academic.oup.com/jnen/article/55/10/1083/2610495 by guest on 03 September 2023
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Sorted by citations
Neuropathological alterations in Alzheimer disease
Serrano-Pozo, A., Frosch, M. P., Masliah, E., & Hyman, B. T. (2011) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a006189 · Cited by 3,345
Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer's Disease
Lue, L.-F., Kuo, Y.-M., Roher, A. E., Brachova, L., Shen, Y., Sue, L., Beach, T., Kurth, J. H., Rydel, R. E., & Rogers, J. (1999) · The American Journal of Pathology · doi:10.1016/s0002-9440(10)65184-x · Cited by 1,530
Self-citationVascular contributions to cognitive impairment and dementia including Alzheimer's disease
Snyder, H. M., Corriveau, R. A., Craft, S., Faber, J. E., Greenberg, S. M., Knopman, D., Lamb, B. T., Montine, T. J., Nedergaard, M., Schaffer, C. B., et al. (2015) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2014.10.008 · Cited by 603
“Lue and colleagues reported that plaques and tangles appear only to cause neurodegeneration when inflammation is also present [29].”
BackgroundLi, Y., Liu, L., Barger, S. W., & Griffin, W. S. T. (2003) · The Journal of Neuroscience · doi:10.1523/jneurosci.23-05-01605.2003 · Cited by 563
“Furthermore, in a study comparing neuropathology in AD patients with that in cognitively normal individuals with abundant A deposits, the latter group was found to have normal synapse densities and scant evidence of inflammation ( Lue et al., 1996 ), suggesting that inflammatory events contribute to neuronal abnormali…”
Hopperton, K. E., Mohammad, D., Trépanier, M. O., Giuliano, V, & Bazinet, R. P. (2018) · Molecular Psychiatry · doi:10.1038/mp.2017.246 · Cited by 567
Metadata
- Authors
- Lue, L.-F., Brachova, L., Civin, H. W., & Rogers, J.
- Affiliations
- Banner Sun Health Research Institute (US)
- Corresponding author
- Rogers, Joseph
- ORCID
- Lue, Lih-Fen
- Venue
- Journal of Neuropathology and Experimental Neurology
- Publisher
- Oxford University Press (OUP)
- Published
- 1996-10
- Volume
- 55
- Issue
- 10
- Pages
- 1083-1088
- ISSN
- 0022-3069 (ISSN-L)
- OpenAlex
- W4296391647
- Cited by
- 246
- References
- 0
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 7 · 2023: 10 · 2022: 9 · 2021: 14 · 2020: 13 · 2019: 10 · 2018: 7 · 2017: 9 · 2016: 6 · 2015: 10 · 2014: 8 · 2013: 8 · 2012: 7
- FWCI
- 4.27
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuropathology & Experimental Neurology (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, neuroinflammation, amyloid-beta deposition, neurofibrillary tangles, entorhinal cortex, superior frontal gyrus, synaptic loss, synaptophysin, microglial activation, MHC class II, neurodegeneration, non-demented elderly
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