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Cited by 317Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Hippocampal neurons in pre-clinical Alzheimer's disease.

Open access
West, Mark J, Kawas, Claudia H, Stewart, Walter F, Rudow, Gay L, Troncoso, Juan C·2004·Neurobiology of Aging
DOI 10.1016/j.neurobiolaging.2003.12.005
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Abstract

In a previous study of hippocampal neurons in aging and AD [Lancet 344 (1994) 769], we demonstrated that the loss of neurons in the CA1 region was disease-specific and not related to aging. In the present study, we examined for loss of hippocampal neurons in preclinical AD, a period during which there are abundant amyloid deposits in the brain but no evidence of cognitive decline. We examined the postmortem brains of 33 subjects from the Baltimore Longitudinal Study of Aging and the Johns Hopkins Alzheimer's Disease Research Center. Using unbiased stereology, we estimated the total number of neurons in the granule cell layer, hilus, CA3-2, CA1, and subiculum of AD (n = 14) preclinical AD (n = 8), and age-matched control subjects (n = 11). The results from the present study confirm our previous finding of significant neuronal losses in the CA1 (48%), hilus (14%), and subiculum (24%) in AD [Lancet 344 (1994) 769]. However, we did not observe a significant loss of neurons in CA1 or any of the other subdivisions of the hippocampus in preclinical AD.

Integrity signals

Registry

Crossref · 10.1016/j.neurobiolaging.2003.12.005

Cites

43 of 43 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

3 of 29 cited sources checked · 2 supported · 0 flagged · accuracy not yet measured

  • Findingown data

    In males, the difference in subiculum neuron number between Alzheimer's disease and control groups was not statistically significant.

    “However, the difference in the number of neurons in either hilus or subiculum, in males, was not statistically significant.”
    • Also stated in: § 4. Discussion · plain
      “but not for subiculum or hilus.”
    Quote in the paperSubstantial claim
  • Findingreasoning

    The estimates of total neuron number reported in the present study are slightly lower than those of the earlier study.

    “The estimates of total neuron number reported in the present study are slightly lower than those of the earlier study.”
    Quote in the paperNot a substantial claim
  • Findingown data

    In preclinical Alzheimer's disease, compared to age-matched controls, there are no significant differences in neuron number in any hippocampal subdivision.

    “Compared to the age-matched control group, no differences were observed in any subdivision of the preclinical AD group.”
    • Also stated in: § Abstract · plain
      “However, we did not observe a significant loss of neurons in CA1 or any of the other subdivisions of the hippocampus in preclinical AD.”
    • Also stated in: § 4. Discussion · boosted
      “The present study of the number of neurons in the hippocampus of preclinical AD cases demonstrates that the total number of neurons in CA1, or any other hippocampal subdivision, is not significantly different from those of controls.”
    Quote in the paperSubstantial claim
  • Findingown data

    In males, there are no significant differences between preclinical Alzheimer's disease and Alzheimer's disease groups in hippocampal neuron number.

    “No significant differences were observed between preclinical AD and control groups or between preclinical AD and AD groups when the analysis was restricted to males (Table 4).”
    Quote in the paperNot a substantial claim
  • Findingown data

    In Alzheimer's disease, compared to age-matched controls, there is a significant loss of neurons in the hilus (14% loss; P < 0.05).

    “Compared to age-matched controls, the brains of AD cases had significantly fewer neurons in CA1 (48%; P < 0.001), subiculum (24%; P < 0.05), and hilus (14%; P < 0.05).”
    • Also stated in: § Abstract · boosted
      “The results from the present study confirm our previous finding of significant neuronal losses in the CA1 (48%), hilus (14%), and subiculum (24%) in AD [Lancet 344 (1994) 769].”
    • Also stated in: § 4. Discussion · plain
      “The first major finding of our study is the confirmation of loss of neurons in CA1, subiculum, and hilus in the AD group.”
    Quote in the paperSubstantial claim
  • May combine two claims. 12
  • The quote only partly states this claim. 1
  • Classified as probably not a substantial claim. 11

  • May combine two claims.

    Premisecitation

    The validity of the concept of a preclinical stage in Alzheimer's disease is supported by longitudinal clinical studies of mild memory changes followed by an accelerated decline and by clinical-pathological studies that report the presence of the characteristic lesions of Alzheimer's disease in cognitively normal individuals.

    “The validity of the concept of a preclinical stage in AD is supported by longitudinal clinical studies of mild memory changes followed by an accelerated decline [6,15,19,33] and by clinical-pathological studies that report the presence of the characteristic lesions of AD in cognitively normal individuals [1,23,35,36].”
    Quote in the paperSubstantial claim2 of 8 sources checked
    • cites [6] Elias, 2000, The preclinical phase of Alzheimer disease: a 22-year prospective study of the Framingham Cohort, Arch. Neurol. source
    • cites [15] Jacobs, 1995, Neuropsychological detection and characterization of preclinical Alzheimer’s disease, Neurology source
    • cites [19] Masur, 1994, Neuropsychological prediction of dementia and the absence of dementia in healthy elderly persons, Neurology source
    • cites [33] Small, 2000, The course of cognitive impairment in preclinical Alzheimer disease: 3- and 6-year follow-up of a population-based sample, Arch. Neurol. source
    • cites [1] Arriagada, 1992, Distribution of Alzheimer-type pathologic changes in nondemented elderly individuals matches the pattern in Alzheimer’s disease, Neurology source
    • cites [23] Morris, 1996, Cerebral amyloid deposition and diffuse plaques in “normal” aging: evidence for presymptomatic and very mild Alzheimer’s disease, Neurology source
    • cites [35] Troncoso, 1996, Neuropathology in controls and demented subjects from the Baltimore Longitudinal Study of Aging, Neurobiol. Aging source
    • cites [36] Troncoso, 1998, Neuropathology of preclinical and clinical late-onset Alzheimer’s disease, Ann. Neurol. source

      Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Some studies suggest that Aβ deposits in the brain may precede the onset of cognitive decline by a decade or more, indicating a wide temporal window for neuronal protective therapeutic intervention.

    “Some of these studies suggest that the A␤ deposits in the brain may precede the onset of cognitive decline by a decade or more [27,36], indicating the presence of a wide temporal window for neuronal protective therapeutic intervention.”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [27] Sandberg, 2001, The prevalence of the neuropathological lesions of Alzheimer’s disease is independent of race and gender, Neurobiol. Aging source
    • cites [36] Troncoso, 1998, Neuropathology of preclinical and clinical late-onset Alzheimer’s disease, Ann. Neurol. source

  • The quote only partly states this claim.

    Findingown data

    In Alzheimer's disease, compared to age-matched controls, there is no significant difference in neuron number in the CA3-2 subdivision of the hippocampus.

    “However, no differences in neuron number were present between these two groups in either the granule or the CA2-3 subdivision.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    The Alzheimer's disease group in the present study differs from the sample in the previous study with regard to gender composition and severity of disease.

    “With regard to gender composition and severity of disease, the AD group examined in the present study differs from the sample used in our previous study.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    In the original study, all Alzheimer's disease cases were males and in later stages of disease; in the present study, half of the cases were females and 5 out of 14 cases were of mild to moderate severity (MMSE > 16).

    “Whereas in our original study, all the AD cases were males and in the later stages of the disease, in the present study half of the cases were females and 5 out of 14 cases were of mild to moderate severity, i.e., with MMSE > 16.”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim.

    Interpretationreasoning

    The agreement of the present study's observations with those of a previous study [26], also with limited statistical power, strengthens the findings in both.

    “Although our study had limited power to detect a difference in the number of hippocampal neurons between controls and preclinical AD cases, it should be underscored that the agreement of our observations with those of a previous study [26], also with limited statistical power, strengthens the findings in both.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [26] Price, 2001, Neuron number in the entorhinal cortex and CA1 in preclinical Alzheimer’s disease, Arch. Neurol. source

  • Classified as probably not a substantial claim.

    Study design and conductreasoning

    The optical fractionator was chosen for the present study in order to reduce potential biases related to defining the anatomical borders of regions of interest.

    “The optical fractionator was chosen for the present study in order to reduce potential biases related to defining the anatomical borders of regions of interest.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Interpretationreasoning

    This explanation is a distinct possibility because the clinical data in that report was retrospective and it is not clear if the clinical evaluations were designed to detect changes in mental status or cognitive decline.

    “This is a distinct possibility since the clinical data in that report was retrospective and it is not clear if the clinical evaluations were designed to detect changes in mental status or cognitive decline.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Study design and conductcitation

    The Alzheimer's disease subjects had clinical histories of dementia and their brains contained sufficient neuritic Aβ plaques (CERAD plaques scores B or C) to meet CERAD criteria for definite Alzheimer's disease.

    “The AD (n = 14) subjects had clinical histories of dementia and their brains contained a sufficient number of neuritic A␤ plaques (CERAD plaques scores B or C) to meet the CERAD criteria for definite AD [21].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [21] Mirra, 1991, The consortium to establish a registry for Alzheimer’s disease (CERAD). Part II. Standardization of the neuropathologic assessment of Alzheimer’s disease, Neurology source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    The clinical diagnosis was made without knowledge of the pathologic diagnosis.

    “The clinical diagnosis was made without knowledge of the pathologic diagnosis.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationreasoning

    The relatively mild clinical severity of the disease in male Alzheimer's disease cases, together with large variability in the preclinical group and reduced group sizes in male comparisons, may be responsible for the inability to demonstrate significant differences in hippocampal neuron number between preclinical Alzheimer's disease and Alzheimer's disease groups.

    “The relatively mild clinical severity of the disease in the male AD cases, together with the large variability in the preclinical group and the reduction in the size of the groups when making comparisons among the males, may also be responsible for our inability to demonstrate significant differences in the number of hippocampal neurons between preclinical AD and AD groups (Table 4).”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim.

    Study design and conductcitation

    The optical fractionator method was used to estimate the total number of neurons in each hippocampal subdivision of each individual.

    “The optical fractionator method [38] was used to estimate the total number of neurons in each hippocampal subdivision of each individual used in the study.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [38] West, 1991, Unbiased stereological estimation of the total number of neurons in the subdivisions of the rat hippocampus using the optical fractionator, Anat. Rec. source

  • Classified as probably not a substantial claim.

    Study design and conductcitation

    The neuropathological diagnosis of Alzheimer's disease followed CERAD guidelines.

    “The neuropathological diagnosis of AD followed CERAD [21] guidelines.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [21] Mirra, 1991, The consortium to establish a registry for Alzheimer’s disease (CERAD). Part II. Standardization of the neuropathologic assessment of Alzheimer’s disease, Neurology source

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    In a previous study, the authors described the pattern of loss of hippocampal neurons in normal aging and Alzheimer's disease and concluded that the most distinctive lesion of Alzheimer's disease was the loss of neurons in the CA1 region.

    “In a previous study we described the pattern of loss of hippocampal neurons in normal aging and AD [39] and concluded that the most distinctive lesion of AD was the loss of neurons in the CA1 region.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [39] West, 1994, Differences in the pattern of hippocampal neuronal loss in normal ageing and Alzheimer’s disease, Lancet source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Another study failed to show Alzheimer's disease-related changes in CA1.

    “However, another study [32] failed to show AD-related changes in CA1.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [32] Simic, 1997, Volume and number of neurons of the human hippocampal formation in normal aging and Alzheimer’s disease, J. Comp. Neurol. source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Interpretationreasoning

    The failure of another study to show Alzheimer's disease-related changes in CA1 may be explained by contamination of the age-matched control group with mild Alzheimer's disease cases.

    “This result may be explained by contamination of the age-matched control group with mild AD cases.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Study design and conductcitation

    The preclinical Alzheimer's disease subjects were cognitively intact with MMSE scores ≥26, but their brains contained substantial numbers of neuritic Aβ plaques (CERAD plaque scores B or C).

    “The preclinical AD subjects (n = 8) were cognitively intact and their MMSE scores were ≥26, but their brains contained substantial numbers of neuritic A␤ plaques (CERAD plaque scores B or C) [21].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [21] Mirra, 1991, The consortium to establish a registry for Alzheimer’s disease (CERAD). Part II. Standardization of the neuropathologic assessment of Alzheimer’s disease, Neurology source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductcitation

    Silver stains were used to determine Braak neurofibrillary scores.

    “Silver stains were used to determine Braak neurofibrillary scores [4].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [4] Braak, 1991, Neuropathological stageing of Alzheimer-related changes, Acta Neuropathol. source

  • May combine two claims.

    Study design and conductcitation

    The mean coefficients of error for individual estimates in each subdivision were less than 0.10, indicating adequate precision for the stereological analysis.

    “The mean CEs, for the individual estimates made in each subdivision, were less than 0.10, indicating that the precision of the estimates derived with this sampling scheme were adequate for the stereological analysis described here [38].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [38] West, 1991, Unbiased stereological estimation of the total number of neurons in the subdivisions of the rat hippocampus using the optical fractionator, Anat. Rec. source

  • May combine two claims.

    Premisecitation

    The development of neurofibrillary tangles and senile plaques has been described in preclinical Alzheimer's disease, but there is only a single stereological study of the number of neurons in the hippocampus in preclinical Alzheimer's disease.

    “The development of NFT and SP has been described in preclinical AD [25], but there is only a single stereological study of the number of neurons in the hippocampus in preclinical AD [26].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [25] Price, 1999, Tangles and plaques in nondemented aging and “preclinical” Alzheimer’s disease, Ann. Neurol. source
    • cites [26] Price, 2001, Neuron number in the entorhinal cortex and CA1 in preclinical Alzheimer’s disease, Arch. Neurol. source

  • Classified as probably not a substantial claim.

    Premisecitation

    In the previous study, the authors found that the degeneration in CA1 was disease-specific and not related to aging, per se.

    “Moreover, we found that the degeneration in CA1 was disease-specific and not related to aging, per se.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [39] West, 1994, Differences in the pattern of hippocampal neuronal loss in normal ageing and Alzheimer’s disease, Lancet source

  • May combine two claims.

    Study design and conductcitation

    The age-matched controls were cognitively intact with MMSE scores ≥26, and their brains had no or minimal pathologic changes ranging from no Aβ deposits to sparse neuritic Aβ plaques (CERAD neuritic plaque score 0 or A).

    “The age-matched controls (n = 11) were cognitively intact and their MMSE were ≥26, and their brains had no or minimal pathologic changes that ranged from no A␤ deposits, to a few diffuse A␤ plaques, to sparse neuritic A␤ plaques (CERAD neuritic plaque score 0 or A).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [21] Mirra, 1991, The consortium to establish a registry for Alzheimer’s disease (CERAD). Part II. Standardization of the neuropathologic assessment of Alzheimer’s disease, Neurology source
22 of 22

  • The authors state this as an assumption.

    Individuals with preclinical Alzheimer's disease (cognitively intact with substantial AD neuropathology) would have developed clinical Alzheimer's disease had they lived long enough.

    “An important caveat with the concept of preclinical AD is that we are making the assumption that those individuals, had they live long enough, would have developed clinical AD.”
1 of 1

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?

  • Neuron loss is not present in pre-clinical AD and may be responsible for the onset of the adverse symptoms occurring with the transition to AD.

    “Unlike A b and Tau pathology, neuron loss is not present in pre-clinical AD and thus may be responsible for the onset of the adverse symptoms occurring with the transition to AD [23].”

    From Transient intraneuronal Aβ rather than extracellular plaque pathology correlates with neuron loss in the frontal cortex of APP/PS1KI mice (2008) · cites this paper as [23]

  • Some studies have reported preserved neuronal numbers and synaptic densities in the hippocampus in "preclinical/resilient AD" compared with normal and clinical AD cases.

    “Some studies have reported preserved neuronal numbers and synaptic densities in the hippocampus in “preclinical/resilient AD” compared with normal and clinical AD cases [62], [108], [109].”

    From Repair of Oxidative DNA Damage, Cell-Cycle Regulation and Neuronal Death May Influence the Clinical Manifestation of Alzheimer’s Disease (2014) · cites this paper as [108]

  • Neuronal loss in the entorhinal cortex or hippocampal field CA1 is absent in preclinical npAD, whereas cases with equivalent neuropathological lesion burden but symptomatic very mild DAT (CDR = 0.5) show substantial cell loss.

    “Neuronal loss in the entorhinal cortex or hippocampal field CA1 has been shown to be absent in preclinical npAD compared with substantial cell loss in cases with equivalent neuropathological lesion burden but with symptomatic very mild DAT (CDR = 0.5).(Gomez-Isla et al., 1996; Price et al., 2001; West et al., 2004)”

    From Neuropathology of nondemented aging: presumptive evidence for preclinical Alzheimer disease (2009) · cites this paper as West et al., 2004

  • There appears to be little neuronal degeneration in preclinical AD.

    “Because there appears to be little neuronal degeneration in preclinical AD,(Gomez-Isla et al., 1996; Price et al., 2001; West et al., 2004) this stage of the illness could be an attractive target for treatment with agents developed to modify or arrest the AD process.”

    From Neuropathology of nondemented aging: presumptive evidence for preclinical Alzheimer disease (2009) · cites this paper as West et al., 2004

  • In brains from cognitively intact subjects, hippocampal CA1 neuron counts do not correlate with age.

    “In brains from cognitively intact subjects, hippocampal CA1 neuron counts do not correlate with age [47–49].”

    From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [48]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • CA1 total sampling fraction does not match its components

    Minor

    The listed CA1 sampling fractions imply a reciprocal total fraction of 36,846, not the reported 34,500.

    Reported 34500 · recomputed 36846

  • Only four AD cases exceed the stated MMSE threshold

    Minor

    The paper says five AD cases had MMSE scores above 16. Table 1 shows that the fifth-highest score is exactly 16, leaving only four cases above the threshold.

  • Male-only table includes all 11 controls

    Minor

    Table 4 is labeled as an analysis of males and lists 11 controls, but Table 1 identifies one of the 11 controls as female. A male-only control group would contain 10 subjects.

  • Section sampling fraction has two incompatible definitions

    Minor

    Table A.1 lists the section sampling fraction as 1/30, but its explanatory note defines ssf as 30. Those are reciprocals, so the notation is inconsistent.

4 of 4

Cites

Flagged first, then by citations

Research works printed but not linked: 3

  1. Folstein MF, Bylsma FW. Noncognitive symptoms of Alzheimer disease. In: Terry RD, Katzman R, Bick KL, Sisodia SS, editors. Alzheimer disease. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 1999. p. 25–37.
  2. Morris JC. Clinical presentation and course of Alzheimer disease. In: Terry RD, Katzman R, Bick KL, Sisodia SS, editors. Alzheimer disease. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 1999. p. 11–24.
  3. Terry RD, Masliah E, Hansen L. The neuropathology of Alzheimer disease and the structural basis of its cognitive alterations. In: Terry RD, Katzman R, Bick KL, Sisodia SS, editors. Alzheimer disease. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 1999. p. 187–206.

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Related

Authors
West, M. J., Kawas, C. H., Stewart, W. F., Rudow, G. L., & Troncoso, J. C.
Affiliations
  • Aarhus University (DK)
  • University of California, Irvine (US)
  • Johns Hopkins University (US)
Corresponding author
Troncoso, Juan C
ORCID
Venue
Neurobiology of Aging
Publisher
Elsevier BV
Published
2004-10
Volume
25
Issue
9
Pages
1205-1212
ISSN
0197-4580 (ISSN-L)
DOI
10.1016/j.neurobiolaging.2003.12.005
OpenAlex
W2048251539
Semantic Scholar
d7a5f54add413fc89de46d57890d3772e96aeec0
Cited by
317
References
43
Citations by year
2026: 4 · 2025: 12 · 2024: 9 · 2023: 5 · 2022: 10 · 2021: 6 · 2020: 20 · 2019: 11 · 2018: 19 · 2017: 22 · 2016: 17 · 2015: 24 · 2014: 20 · 2013: 18 · 2012: 16
FWCI
7.20
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Neurobiology of Aging (publishedVersion)
  • PubMed (publishedVersion)
  • eScholarship (California Digital Library) (submittedVersion, cc-by)
Funders
National Institute on Aging (P50AG005146, AG 05146)
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
preclinical Alzheimer's disease, hippocampal neurons, neuronal loss, CA1 region, subiculum, hilus, amyloid deposits, postmortem brain, stereology, aging
MeSH terms
Aged, Aged, 80 and over, Alzheimer Disease, Cell Count, Female, Hippocampus, Humans, Male, Middle Aged, Nerve Degeneration, Neurons, Cell Death, Disease Progression, Dentate Gyrus

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