Cited by 70Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Neuronal loss and neurofibrillary degeneration in the hippocampal cortex in late-onset sporadic Alzheimer’s disease

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Fukutani, Yuken, Cairns, Nigel J, Shiozawa, Masaki, Sasaki, Kazuo, Sudo, Satoru, Isaki, Kiminori, Lantos, Peter L·2000·Psychiatry and Clinical Neurosciences

Abstract

To explore more fully the relationship between neuronal death and neurofibrillary degeneration, unaffected neurons, intracellular neurofibrillary tangles (i-NFT) and extracellular NFT (e-NFT) in 22 patients with late-onset sporadic Alzheimer's disease (AD) were morphometrically evaluated in eight subdivisions of the hippocampal cortex, using the Gallyas hematoxylin-eosin stain. The subdivisions examined included CA4, CA3, CA2, CA1 (CA: cornu ammonis), prosubiculum (PRO), subiculum and presubiculum (PRE), parasubiculum (PARA) and the entorhinal cortex (ENT). The unaffected neuron density was significantly lower and both i-NFT and e-NFT densities were significantly higher in subdivisions other than CA4 and CA3 in AD patients compared with those in the aged controls. Unaffected neuron density was significantly, inversely correlated with e-NFT density and with total NFT density in all subdivisions except for PRE in AD patients. Especially in CA2, CA1, PRO and ENT, there were strong correlations between the neuron density and these NFT densities. Both unaffected neuron and e-NFT densities in CA1 and ENT were significantly correlated with the disease duration. The i/e-NFT ratio, an index of the degree and/or rate of progress of neuronal death via neurofibrillary degeneration, showed the lowest value in ENT in AD patients. The findings suggest that neuronal death via neurofibrillary degeneration starts earliest and/or most rapidly progresses in ENT. Furthermore, the i/e-NFT ratios in both ENT and CA1 were significantly correlated with the disease duration, suggesting that the neuronal death pattern in the two subdivisions parallels disease progression.

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Crossref · 10.1046/j.1440-1819.2000.00747.x

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  • Other brain regions, such as the primary sensory cortices, are relatively resistant to degeneration until later stages of Alzheimer's disease.

    “In contrast, other brain regions, such as the primary sensory cortices, are relatively resistant to degeneration until later stages of the disease (Arnold et al., 1991; Bussière et al., 2003; Fukutani et al., 2000; Gómez-Isla et al., 1996; Hof and Morrison, 1990; Hyman et al., 1984; Morrison and Hof, 1997; West et al., 1994).”

    From Selective Neuronal Vulnerability in Alzheimer’s Disease: A Network-Based Analysis (2020) · cites this paper as Fukutani et al., 2000

  • In early stages of Alzheimer's disease, clinical symptoms such as memory loss are caused by the selective degeneration of principal neurons of the entorhinal cortex layer II (ECII), followed by CA1 pyramidal cells in the hippocampus, and pyramidal neurons in neocortical association areas.

    “In the early stages of Alzheimer’s disease (AD), the most common form of age-related dementia, clinical symptoms (such as memory loss) are caused by the selective degeneration of principal neurons of the entorhinal cortex layer II (ECII), followed by CA1 pyramidal cells in the hippocampus, and pyramidal neurons in neocortical association areas.”

    From Selective Neuronal Vulnerability in Alzheimer’s Disease: A Network-Based Analysis (2020) · cites this paper as Fukutani et al., 2000

  • Several studies have reported a strong negative correlation between neuronal counts and NFT number in the CA1 subfield, suggesting that the progression of brain atrophy and the progression of NFT are strongly associated.

    “Moreover, several studies have reported a strong negative correlation between neuronal counts and NFT number in the CA1 subfield (Fukutani et al., 2000; Von Gunten et al., 2006) suggesting that the progression of brain atrophy and the progression of NFT are strongly associated (Whitwell et al., 2008).”

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Authors
Fukutani, Y., Cairns, N. J., Shiozawa, M., Sasaki, K., Sudo, S., Isaki, K., & Lantos, P. L.
Corresponding author
Fukutani, Yuken
Venue
Psychiatry and Clinical Neurosciences
Publisher
Wiley
Published
2000-10
Volume
54
Issue
5
Pages
523-529
ISSN
  • 1323-1316 (ISSN-L)
  • 1440-1819
OpenAlex
W2030545203
Cited by
70
References
18
Citations by year
2026: 1 · 2025: 8 · 2024: 3 · 2023: 5 · 2022: 4 · 2021: 2 · 2020: 4 · 2019: 1 · 2018: 7 · 2017: 3 · 2016: 2 · 2015: 3 · 2014: 2 · 2013: 2
FWCI
0.82
Type
journal article
Language
en
Open access
Locations
  • Psychiatry and Clinical Neurosciences (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › 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, neuronal loss, hippocampus, entorhinal cortex, disease duration, hippocampal subfields, CA1, presubiculum, parasubiculum, subiculum, cornu ammonis, neuronal density
MeSH terms
Age Factors, Aged, Aged, 80 and over, Alzheimer Disease, Female, Hippocampus, Humans, Male, Nerve Degeneration, Neurons, Severity of Illness Index, Neurofibrillary Tangles

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