The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index; 3 of the 29 sources its claims cite were checked for support.
Hippocampal neurons in pre-clinical Alzheimer's disease.
Open accessAbstract
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.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 3. Results
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § 4. Discussion · plain
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The estimates of total neuron number reported in the present study are slightly lower than those of the earlier study.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 3. Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Abstract · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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).”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 3. Results
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 3. Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Abstract · boosted
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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).”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 3. Results
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 3. Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Abstract · boosted
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, no differences in neuron number were present between these two groups in either the granule or the CA2-3 subdivision.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 3. Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In contrast, the comparison between the preclinical AD group and the AD group revealed significantly lower numbers of neurons in the CA1 (44%; P < 0.05), but not in other subdivisions of the AD group (Table 3).”
- Also stated in: § 4. Discussion · plain
“However, we found a significant loss (P < 0.05) in CA1 cell count in cases of AD compared to preclinical cases.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 3. Results
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § 4. Discussion · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The significant loss of neurons in CA1, detected between controls and AD, persisted (37%; P < 0.05) when the analysis was limited to the brains of males (Table 4).”
- Also stated in: § 4. Discussion · boosted
“This analysis demonstrated a significant difference between males in the AD and control groups for CA1 neurons (P = 0.02), but not for subiculum or hilus.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 3. Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § 4. Discussion · boosted
- It may state two separate claims as one. 12
- The quote only partly states this claim. 1
- Probably not a substantial claim. 11
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“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].”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 1. Introduction
What the sources say
- Not checked — no full text of the sourcecites [6] Elias, 2000, The preclinical phase of Alzheimer disease: a 22-year prospective study of the Framingham Cohort, Arch. Neurol. source
- Not checked — no full text of the sourcecites [15] Jacobs, 1995, Neuropsychological detection and characterization of preclinical Alzheimer’s disease, Neurology source
- Not checked — no full text of the sourcecites [19] Masur, 1994, Neuropsychological prediction of dementia and the absence of dementia in healthy elderly persons, Neurology source
- Not checked — no full text of the sourcecites [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
- Not checked — no full text of the sourcecites [1] Arriagada, 1992, Distribution of Alzheimer-type pathologic changes in nondemented elderly individuals matches the pattern in Alzheimer’s disease, Neurology source
- Not checked — no full text of the sourcecites [23] Morris, 1996, Cerebral amyloid deposition and diffuse plaques in “normal” aging: evidence for presymptomatic and very mild Alzheimer’s disease, Neurology source
- Supportedcites [35] Troncoso, 1996, Neuropathology in controls and demented subjects from the Baltimore Longitudinal Study of Aging, Neurobiol. Aging source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Partly supportedcites [36] Troncoso, 1998, Neuropathology of preclinical and clinical late-onset Alzheimer’s disease, Ann. Neurol. sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“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.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 1. Introduction
What the sources say
- Not checked — no full text of the sourcecites [27] Sandberg, 2001, The prevalence of the neuropathological lesions of Alzheimer’s disease is independent of race and gender, Neurobiol. Aging source
- Supportedcites [36] Troncoso, 1998, Neuropathology of preclinical and clinical late-onset Alzheimer’s disease, Ann. Neurol. source
The Discussion (page not specified in our copy) says that perineuronal Aβ deposition is an early event that precedes clinical onset by several decades. It also identifies these early abnormalities as having therapeutic implications, supporting the citing sentence’s proposed intervention window. (LLM, conf=0.89)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, no differences in neuron number were present between these two groups in either the granule or the CA2-3 subdivision.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 3. Results
Strength:plain· not yet calibratedn = 7Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe quote only partly states this claim.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“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.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
What the sources say
- Not checked — no full text of the sourcecites [26] Price, 2001, Neuron number in the entorhinal cortex and CA1 in preclinical Alzheimer’s disease, Arch. Neurol. source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“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.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“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].”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 2.1. Subjects
What the sources say
- Not checked — no full text of the sourcecites [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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The clinical diagnosis was made without knowledge of the pathologic diagnosis.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 2.2. Clinical diagnoses
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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).”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“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.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 2.5. Estimating the total number of neurons in a hippocampal subdivision
What the sources say
- Not checked — no full text of the sourcecites [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
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
In the paper
“The neuropathological diagnosis of AD followed CERAD [21] guidelines.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 2.3. Neuropathology
What the sources say
- Not checked — no full text of the sourcecites [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
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
In the paper
“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.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 1. Introduction
What the sources say
- Not checked — no full text of the sourcecites [39] West, 1994, Differences in the pattern of hippocampal neuronal loss in normal ageing and Alzheimer’s disease, Lancet source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
In the paper
“However, another study [32] failed to show AD-related changes in CA1.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
What the sources say
- Not checked — no full text of the sourcecites [32] Simic, 1997, Volume and number of neurons of the human hippocampal formation in normal aging and Alzheimer’s disease, J. Comp. Neurol. source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This result may be explained by contamination of the age-matched control group with mild AD cases.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“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].”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 2.1. Subjects
What the sources say
- Not checked — no full text of the sourcecites [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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Silver stains were used to determine Braak neurofibrillary scores [4].”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 2.3. Neuropathology
What the sources say
- Not checked — no full text of the sourcecites [4] Braak, 1991, Neuropathological stageing of Alzheimer-related changes, Acta Neuropathol. source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“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].”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > Additional information
What the sources say
- Not checked — no full text of the sourcecites [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
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
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
“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].”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 1. Introduction
What the sources say
- Not checked — no full text of the sourcecites [25] Price, 1999, Tangles and plaques in nondemented aging and “preclinical” Alzheimer’s disease, Ann. Neurol. source
- Not checked — no full text of the sourcecites [26] Price, 2001, Neuron number in the entorhinal cortex and CA1 in preclinical Alzheimer’s disease, Arch. Neurol. source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Moreover, we found that the degeneration in CA1 was disease-specific and not related to aging, per se.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 1. Introduction
What the sources say
- Not checked — no full text of the sourcecites [39] West, 1994, Differences in the pattern of hippocampal neuronal loss in normal ageing and Alzheimer’s disease, Lancet source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
In the paper
“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).”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 2.1. Subjects
What the sources say
- Not checked — no full text of the sourcecites [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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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.”
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?
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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
In the citing paper
“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 the citing paper
“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]
In the citing paper
“However, the three studies that provided neuronal counts in the hippocampal subfields of patients with AD report discrepant data.”
From Atrophy of presubiculum and subiculum is the earliest hippocampal anatomical marker of Alzheimer's disease (2015) · cites this paper as [12]
In the citing paper
“both the proline‐rich domain and the microtubule‐binding domain of tau are known to contribute to its interaction with DNA 107.”
From Altered Machinery of Protein Synthesis in Alzheimer's: From the Nucleolus to the Ribosome (2016) · cites this paper as [107]
In the citing paper
“This change has been mainly interpreted as being the result of loss of afferents to the DG and to the loss of neurons in the CA1 region of the hippocampus 107.”
From Altered Machinery of Protein Synthesis in Alzheimer's: From the Nucleolus to the Ribosome (2016) · cites this paper as [107]
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
MinorThe listed CA1 sampling fractions imply a reciprocal total fraction of 36,846, not the reported 34,500.
Reported 34500 · recomputed 36846
“Section sampling fraction (ssf) 1/30 1/30 1/30 1/30 1/30 Area sampling fraction (asf) 1/545 1/66 1/79 1/534 1/133 Thickness sampling fraction (tsf) 1/2.3 1/2.3 1/2.3 1/2.3 1/2.3Total fraction 1/37674 1/4554 1/5451 1/34500 1/9177”
Only four AD cases exceed the stated MMSE threshold
MinorThe 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.
“5 out of 14 cases were of mild to moderate severity, i.e., with MMSE > 16.”
“| 20 | 74 | M | 23 | B | IV | AD | | 21 | 83 | M | 24 | C | III | AD | | 22 | 81 | M | 19 | C | V | AD | | 23 | 73 | F | 18 | C | V | AD | | 24 | 92 | F | 16 | C | IV | AD |”
Male-only table includes all 11 controls
MinorTable 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.
“Table 4 Total number of neurons in hippocampal subdivisions of male cases and controls Subregion Controls, N = 11”
“| 03 | 73 | F | 30 | 0 | II | Control/infarct remote |”
Section sampling fraction has two incompatible definitions
MinorTable 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.
“Section sampling fraction (ssf) 1/30 1/30 1/30 1/30 1/30”
“ssf: 30 (sections taken at 30 section intervals, after a random start within the first 30 sections)”
Citations
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Neuropathological stageing of Alzheimer-related changes.
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Self-citationConsortium to Establish a Registry for Alzheimer's Disease (CERAD)
Fillenbaum, G., & Heyman, A. (2002) · doi:10.1002/0470846410.ch42(iii · Cited by 2,859
Gundersen, H. J. G., Bagger, P. V., Bendtsen, T. F., Evans, S. M., Korbo, L., Marcussen, N., Møller, A., Nielsen, K. N., Nyengaard, J. R., Pakkenberg, B., et al. (1988) · Apmis · doi:10.1111/j.1699-0463.1988.tb00954.x · Cited by 2,480
Self-citationProfound Loss of Layer II Entorhinal Cortex Neurons Occurs in Very Mild Alzheimer’s Disease
Gómez-Isla, T., Price, J. L., McKeel Jr., D. W., Morris, J. C., Growdon, J. H., & Hyman, B. T. (1996) · The Journal of Neuroscience · doi:10.1523/jneurosci.16-14-04491.1996 · Cited by 1,796 · cited 1×
“In demented subjects with AD, the pathological hallmarks are A amyloid deposits, senile plaques (SP), neurofibrillary tangles (NFT), degeneration of synapses [34], and loss of neurons[10,26,39] .”
Background
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Research works printed but not linked: 3
- 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.
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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
“1996), and they do not seem to have significant neuronal loss, not even in vulnerable regions such as the entorhinal cortex and the hippocampus (Price et al. 2001; West et al. 2004).”
BackgroundMultimodal classification of Alzheimer's disease and mild cognitive impairment
Zhang, D., Wang, Y., Zhou, L., Yuan, H., & Shen, D. G. (2011) · NeuroImage · doi:10.1016/j.neuroimage.2011.01.008 · Cited by 1,340
“, 2009), and 3) hippocampal volumes (Gerardin et al., 2009; West et al., 2004).”
BackgroundSynaptic alterations in CA1 in mild Alzheimer disease and mild cognitive impairment
Scheff, S. W., Price, D. A., Schmitt, F. A., DeKosky, S. T., & Mufson, E. J. (2007) · Neurology · doi:10.1212/01.wnl.0000260698.46517.8f · Cited by 824
Yushkevich, P. A., Pluta, J. B., Wang, H., Xie, L., Ding, S., Gertje, E. C., Mancuso, L., Kliot, D., Das, S. R., & Wolk, D. A. (2014) · Human Brain Mapping · doi:10.1002/hbm.22627 · Cited by 587
“An additional motivation for more granular measurement of MTL cortical subregions is that the PRC and ERC are amongst the earliest sites of neurodegeneration in AD [Braak and Braak, 1995; Bobinski et al., 1997; Simić et al., 1997; West et al., 2004].”
BackgroundNeuropathology of nondemented aging: presumptive evidence for preclinical Alzheimer disease
Price, J. L., McKeel, D. W., Buckles, V. D., Roe, C. M., Xiong, C., Grundman, M., Hansen, L. A., Petersen, R. C., Parisi, J. E., Dickson, D. W., et al. (2009) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2009.04.002 · Cited by 661
Sultana, R., Perluigi, M., & Butterfield, D. A. (2013) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2012.09.027 · Cited by 478
“Some patients showed a presymptomatic phase before MCI, namely preclinical Alzheimer disease (PCAD), characterized by the absence of memory deficits and normal activities of daily living but pronounced AD neuropathology (Braak scores are III or higher) [65,66].”
Changes in the structural complexity of the aged brain
Dickstein, D. L., Kabaso, D., Rocher, A. B., Luebke, J. I., Wearne, S. L., & Hof, P. R. (2007) · Aging Cell · doi:10.1111/j.1474-9726.2007.00289.x · Cited by 460
“The neuronal degeneration observed in AD is reflected by significant neuron and synapse loss in specific brain regions (West et al., 1994, 2004; Morrison & Hof, 1997, 2002; Price et al., 2001; Hof et al., 2003; Hof & Morrison, 2004).”
BackgroundCacciottolo, M., Wang, X., Driscoll, I. F., Woodward, N., Saffari, A., Reyes, J. M., Serre, M. L., Vizuete, W., Sioutas, C., Morgan, T. E., et al. (2017) · Translational Psychiatry · doi:10.1038/tp.2016.280 · Cited by 441
Model‐guided microarray implicates the retromer complex in Alzheimer's disease
Small, S. A., Kent, K., Pierce, A., Leung, C., Kang, M. S., Okada, H., Honig, L., Vonsattel, J., & Kim, T. (2005) · Annals of Neurology · doi:10.1002/ana.20667 · Cited by 440
Detection of prodromal Alzheimer's disease via pattern classification of magnetic resonance imaging
Davatzikos, C., Fan, Y., Wu, X., Shen, D., & Resnick, S. M. (2008) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2006.11.010 · Cited by 385
“( West et al., 2004 ), albeit the resolution of current 1.5 T MR images does not allow us to specifically define hippocampal subfields.”
BackgroundInfluentialLipid peroxidation and neurodegenerative disease
Reed, T. T. (2011) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2011.06.027 · Cited by 385
“Typically, these persons possess no significant brain cell loss or neuronal atrophy but have Braak scores of III or higher due to the neuritic plaque count postmortem [100,101].”
BackgroundYushkevich, P. A., Amaral, R. S. C., Augustinack, J. C., Bender, A. R., Bernstein, J. D., Boccardi, M., Bocchetta, M., Burggren, A. C., Carr, V. A., Chakravarty, M. M., et al. (2015) · NeuroImage · doi:10.1016/j.neuroimage.2015.01.004 · Cited by 342
“Different psychiatric and neurological disorders are known to affect hippocampal subfields and MTL cortical subregions differently, selectively, and in a complex progression (Braak & Braak, 1995; Arnold et al., 1995; Simić et al., 1997; de Lanerolle et al., 2003; West et al., 2004; Lucassen et al., 2006; Small et al.,…”
BackgroundStructural imaging of hippocampal subfields in healthy aging and Alzheimer’s disease
de Florès, R., Joie, R. L., & Chételat, G. (2015) · Neuroscience · doi:10.1016/j.neuroscience.2015.08.033 · Cited by 387
Hippocampal atrophy patterns in mild cognitive impairment and Alzheimer's disease
Mueller, S. G., Schuff, N., Yaffe, K., Madison, C., Miller, B., & Weiner, M. W. (2010) · Human Brain Mapping · doi:10.1002/hbm.20934 · Cited by 361
“There is also evidence from animal models and histopathological studies that different disease processes affect subfields differently, e.g. stress affects predominantly the dentate gyrus while AD typically shows the most prominent neuron loss in CA1 [Lucassen et al., 2006; West et al., 1994, 2004].”
ResultAgrawal, M., Ajazuddin, Tripathi, D. K., Saraf, S., Saraf, S., Antimisiaris, S. G., Mourtas, S., Hammarlund-Udenaes, M., & Alexander, A. (2017) · Journal of Controlled Release · doi:10.1016/j.jconrel.2017.05.019 · Cited by 356
“These fragments have a tendency to normally get dissolved and eliminated from the brain but in elderly peoples or person with some abnormalities, this peptide gets accumulated and forms a large aggregate that causes nerve degeneration and may lead to Alzheimer disease [15].”
BackgroundTramutola, A., Triplett, J. C., Di Domenico, F., Niedowicz, D. M., Murphy, M. P., Coccia, R., Perluigi, M., & Butterfield, D. A. (2015) · Journal of Neurochemistry · doi:10.1111/jnc.13037 · Cited by 347
Decreased cerebrospinal fluid Aβ 42 correlates with brain atrophy in cognitively normal elderly
Fagan, A. M., Head, D., Shah, A. R., Marcus, D., Mintun, M., Morris, J. C., & Holtzman, D. M. (2009) · Annals of Neurology · doi:10.1002/ana.21559 · Cited by 327
Brain aging, Alzheimer's disease, and mitochondria
Swerdlow, R. H. (2011) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2011.08.012 · Cited by 306
“In brains from cognitively intact subjects, hippocampal CA1 neuron counts do not correlate with age [47–49].”
BackgroundNeural reserve, neuronal density in the locus ceruleus, and cognitive decline
Wilson, R. S., Nag, S., Boyle, P. A., Hizel, L. P., Yu, L., Buchman, A. S., Schneider, J. A., & Bennett, D. A. (2013) · Neurology · doi:10.1212/wnl.0b013e3182897103 · Cited by 283
“Similar findings have been reported for the entorhinal cortex and hippocampus.(29,30) The present results are consistent with this research and extend it in important ways.”
BackgroundResultMeasurement of hippocampal subfields and age-related changes with high resolution MRI at 4T
Mueller, S. G., Stables, L. A., Du, A., Schuff, N. W., Truran, D., Cashdollar, N. M., & Weiner, M. W. (2006) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2006.03.007 · Cited by 272
Altered Machinery of Protein Synthesis in Alzheimer's: From the Nucleolus to the Ribosome
Hernández‐Ortega, K., Garcia‐Esparcia, P., Gil, L., Lucas, J. J., & Ferrer, I. (2016) · Brain Pathology · doi:10.1111/bpa.12335 · Cited by 245
“As a working hypothesis, it can be suggested that it is not the accumulation of cytoplasmic hyper-phosphorylated tau which disassembles chromatin but rather it is the decrease in nuclear tau that is responsible for DNA disassembly.”
BackgroundInfluentialSelective effect of age, Apo e4, and Alzheimer's disease on hippocampal subfields
Mueller, S. G., & Weiner, M. W. (2009) · Hippocampus · doi:10.1002/hipo.20614 · Cited by 248
“The mild, nonsignificant volume loss in SUB, CA1, CA3&DG is in good agreement with the mild, nonsignificant neuronal cell described in a histopathological study of MCI by West et al. (2004).”
BackgroundResultInfluentialNearly automatic segmentation of hippocampal subfields in in vivo focal T2-weighted MRI
Yushkevich, P. A., Wang, H., Pluta, J. B., Das, S. R., Craige, C. P., Avants, B., Weiner, M. W., & Mueller, S. G. (2010) · NeuroImage · doi:10.1016/j.neuroimage.2010.06.040 · Cited by 240
“Given the extensive pathological evidence of heterogeneity in the way AD and other diseases affect the HF (Braak and Braak, 1991; Arnold et al., 1995; Bobinski et al., 1997; West et al., 2004; Duvernoy, 2005; Amaral and Lavenex, 2007), there is great interest in a robust HF subfield segmentation method that could be u…”
Integrating new findings and examining clinical applications of pattern separation
Leal, S. L., & Yassa, M. A. (2018) · Nature Neuroscience · doi:10.1038/s41593-017-0065-1 · Cited by 228
Perluigi, M., Coccia, R., & Butterfield, D. A. (2012) · Antioxidants & Redox Signaling · doi:10.1089/ars.2011.4406 · Cited by 229
“The identification of PCAD is a very recent finding and describes individuals who do not show memory deficits but have pronounced AD neuropathology (208).”
Cell number changes in Alzheimer's disease relate to dementia, not to plaques and tangles
Andrade-Moraes, C. H., de Oliveira-Pinto, A. V., Castro-Fonseca, E., da Silva, C. G., Guimarães, D. M., Szczupak, D., Parente-Bruno, D. R., Carvalho, L. R. B., Polichiso, L., Valério‐Gomes, B., et al. (2013) · Brain · doi:10.1093/brain/awt273 · Cited by 223
“Our results are in agreement with these histopathological findings, and support previous stereological (Kril et al., 2004; West et al., 2004) and neuroimaging studies (Apostolova et al.”
ResultRamos, B., Baglietto‐Vargas, D., del Río, J. C., Moreno‐González, I., Santa‐María, C., Jiménez, S., Caballero, C., Lopez-Tellez, J. F., Khan, Z. U., Ruano, D., et al. (2005) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2005.09.022 · Cited by 219
“The pathological hallmarks of AD are beta amyloid (Abeta) deposits and plaques, hyperphosphorylation of tau and formation of neurofibrillary tangles, degeneration of synapses and loss of neuronal cells [52] [53] [39] [44].”
BackgroundAdler, D. H., Wisse, L. E. M., Ittyerah, R., Pluta, J. B., Ding, S., Xie, L., Wang, J., Kadivar, S., Robinson, J. L., Schuck, T., et al. (2018) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1801093115 · Cited by 193
“15 and 16), but they provide limited reference information for MRI research because of the 2D nature of histology, difficulty of extrapolating quantitative measures such as neuronal counts to 3D, and inconsistencies between studies.”
BackgroundBehavioral assays with mouse models of Alzheimer's disease: Practical considerations and guidelines
Puzzo, D., Lee, L. S., Palmeri, A., Calabrese, G., & Arancio, O. (2014) · Biochemical Pharmacology · doi:10.1016/j.bcp.2014.01.011 · Cited by 226
Hippocampal Subfield Volumes: Age, Vascular Risk, and Correlation with Associative Memory
Shing, Y. L., Rodrigue, K. M., Kennedy, K. M., Fandakova, Y., Bodammer, N., Werkle‐Bergner, M., Lindenberger, U., & Raz, N. (2011) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2011.00002 · Cited by 200
“In some (but not all) samples, CA1 appears as the focal point of neuronal loss in AD (West et al., 2004; but see Simic et al., 1997).”
BackgroundFreeman, S. H., Kandel, R., Cruz, L., Rozkalne, A., Newell, K. L., Frosch, M. P., Hedley‐Whyte, E. T., Locascio, J. J., Lipsitz, L. A., & Hyman, B. T. (2008) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0b013e31818fc72f · Cited by 212
Aging, stress and the hippocampus
Miller, D. B., & O’Callaghan, J. P. (2005) · Ageing Research Reviews · doi:10.1016/j.arr.2005.03.002 · Cited by 206
Neuronal Hypertrophy in Asymptomatic Alzheimer Disease
Iacono, D., O'Brien, R., Resnick, S. M., Zonderman, A. B., Pletnikova, O., Rudow, G., An, Y., West, M. J., Crain, B., & Troncoso, J. C. (2008) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0b013e3181772794 · Cited by 188
“Using the StereoInvestigator Optical Disector software from MicroBrightField, Inc. Biosciences (Williston, VT) (45), we outlined a contour of cortical gray matter and selected sampling sites with a 700 700-Km grid for the ACG, PCG and PVC, and a 250 250-Km grid for the CA1.”
InfluentialSelf-citationYushkevich, P. A., Avants, B., Pluta, J. B., Das, S. R., Minkoff, D. L., Mechanic-Hamilton, D. J., Glynn, S. M., Pickup, S., LIU, W., & Gee, J. C. (2008) · NeuroImage · doi:10.1016/j.neuroimage.2008.08.042 · Cited by 178
“Non-uniform neuron loss across the hippocampal subfields has been reported in neurodegenerative disorders (West et al., 2004; Bobinski et al., 1997; Braak and Braak, 1991), as has a non-uniform rate of neuroplasticity (Eriksson et al., 1998; Kuhn et al., 1996; van Praag et al., 2002).”
Aβ Toxicity in Alzheimer's Disease
Cavallucci, V., D’Amelio, M., & Cecconi, F. (2012) · Molecular Neurobiology · doi:10.1007/s12035-012-8251-3 · Cited by 179
“In this preclinical phase, no or minimal neuronal death can be detected, although a deficit in the communication between neurons occurs [7].”
Familial risk for Alzheimer's disease alters fMRI activation patterns
Bassett, S. S., Yousem, D. M., Cristinzio, C., Kusevic, I., Yassa, M. A., Caffo, B. S., & Zeger, S. L. (2006) · Brain · doi:10.1093/brain/awl089 · Cited by 174
“Indeed, neuropathology studies of individuals showing significant amyloid deposits in the context of normal cognition do not find neuronal loss in temporal lobe structures (Price et al., 2001; West et al., 2004).”
BackgroundHippocampal plasticity during the progression of Alzheimer’s disease
Mufson, E. J., Mahady, L. J., Waters, D., Counts, S., Perez, S. E., DeKosky, S. T., Ginsberg, S. D., Ikonomović, M. D., Scheff, S. W., & Binder, L. I. (2015) · Neuroscience · doi:10.1016/j.neuroscience.2015.03.006 · Cited by 184
Carlesimo, G. A., Piras, F., Orfei, M. D., Iorio, M., Caltagirone, C., & Spalletta, G. (2015) · Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring · doi:10.1016/j.dadm.2014.12.001 · Cited by 159
“[11,12] found the most striking AD-related neuronal loss at the level of the CA1 subfield, whereas Simic et al.”
Schumacher, M., Guennoun, R., Ghoumari, A. M., Massaad, C., Robert, F., El‐Etr, M., Akwa, Y., Rajkowski, K. M., & Baulieu, É.-É. (2007) · Endocrine Reviews · doi:10.1210/er.2006-0050 · Cited by 170
Fernando, W. M. A. D. B., Martins, I. J., Morici, M., Bharadwaj, P., Rainey-Smith, S. R., Lim, W. L. F., & Martins, R. N. (2020) · Journal of Alzheimer's Disease · doi:10.3233/jad-190120 · Cited by 164
Maruszak, A., & Thuret, S. (2014) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2014.00095 · Cited by 147
“…neurogenesis (Yang et al., 2011; Dean et al., 2014), there are also studies that do not find positive association of APOE4 allele with hippocampal volume changes (Reitz et al., 2009; Wang et al., 2012) or that APOE4 influences not the hippocampal volume but the rate of volume loss over time…”
BackgroundAlpha-2 macroglobulin in Alzheimer’s disease: a marker of neuronal injury through the RCAN1 pathway
Varma, V. R., Varma, S., An, Y., Hohman, T. J., Seddighi, S., Casanova, R., Beri, A., Dammer, E. B., Seyfried, N. T., Pletniková, O., et al. (2016) · Molecular Psychiatry · doi:10.1038/mp.2016.206 · Cited by 146
Self-citationWęgiel, J., Flory, M. J., Kuchna, I., Nowicki, K., Ma, S. Y., Imaki, H., Wegiel, J., Cohen, I. L., London, E., Wısnıewskı, T., et al. (2014) · Acta Neuropathologica Communications · doi:10.1186/s40478-014-0141-7 · Cited by 153
“7 million, respectively [108].”
Tang, X., Holland, D., Dale, A. M., Laurent Younes, B., Miller, M. I., & Initiative, A. D. N. (2014) · Human Brain Mapping · doi:10.1002/hbm.22431 · Cited by 148
“13 and 14) suggested that the most pronounced atrophy occurred in the subregion CA1, which has been reported to be associated with memory and learning [Lepage et al., 1998; Markesbery et al., 2006; Price et al., 2001; West et al., 2004].”
BackgroundPattern separation in the dentate gyrus: A role for the CA3 backprojection
Myers, C. E., & Scharfman, H. E. (2010) · Hippocampus · doi:10.1002/hipo.20828 · Cited by 140
“In Alzheimer’s disease, hilar cell loss also occurs (West et al., 2004), and may contribute to memory deficits for the same reason, although there is additional pathology besides hilar cell loss that is considered to be very important.”
BackgroundChételat, G., Fouquet, M., Kalpouzos, G., Denghien, I., De la Sayette, V., Viader, F., Mézenge, F., Landeau, B., Baron, J. C., Eustache, F., et al. (2008) · Neuropsychologia · doi:10.1016/j.neuropsychologia.2007.11.037 · Cited by 143
“Since the hippocampal subfields were found to be differentially affected by neurofibrillary tangles and neuronal loss (West et al., 1994; 2004; Rössler et al, 2002; Bobinski et al., 1998; Schönheit et al., 2004), with highest involvement of the CA1 region (and subiculum in some studies), it seems…”
Is aging part of Alzheimer's disease, or is Alzheimer's disease part of aging?
Swerdlow, R. H. (2006) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2006.06.021 · Cited by 154
“This line of reasonng is supported by a fourth neuronal count study, which oncluded CA1 neuronal death in AD is a relatively late tage histopathologic feature [221], indicating it represents a ownstream consequence of more primary events.”
BackgroundResultLeandrou, S., Petroudi, S., Kyriacou, P. A., Reyes‐Aldasoro, C. C., & Pattichis, C. S. (2018) · IEEE Reviews in Biomedical Engineering · doi:10.1109/rbme.2018.2796598 · Cited by 142
“Histopathological studies [115] also agreed that there was a relatively higher de-”
Neuropathologic Studies of the Baltimore Longitudinal Study of Aging (BLSA)
O'Brien, R. J., Resnick, S. M., Zonderman, A. B., Ferrucci, L., Crain, B. J., Pletnikova, O., Rudow, G., Iacono, D., Riudavets, M. A., Driscoll, I., et al. (2009) · Journal of Alzheimer's Disease · doi:10.3233/jad-2009-1179 · Cited by 137
“Tau immunoreactivity appeared as the strongest morphological correlate of dementia [31].”
Self-citationRamírez-Rodríguez, G. B., Ortíz‐López, L., Domínguez-Alonso, A., Benítez‐King, G., & Kempermann, G. (2010) · Journal of Pineal Research · doi:10.1111/j.1600-079x.2010.00802.x · Cited by 142
“Therefore, the data presented here and data from other groups could suggest that melatonin might be important to prevent the impairment of adult neurogenesis, the loss of neuronal connectivity and neuronal loss present in some neuropsychiatric disorders [21, 45, 46].”
BackgroundAsymptomatic Alzheimers Disease: A Prodrome or a State of Resilience?
Driscoll, I., & Troncoso, J. (2011) · Current Alzheimer Research · doi:10.2174/156720511795745348 · Cited by 130
“The loss of neurons in the CA1 region of the hippocampus is characteristic of AD and distinctly separates this entity from normal aging [25, 26].”
BackgroundSelf-citationAccelerating drug discovery for Alzheimer's disease: best practices for preclinical animal studies
Shineman, D. W., Basi, G. S., Bizon, J. L., Colton, C. A., Greenberg, B., Hollister, B. A., Lincecum, J. M., Leblanc, G. G., Lee, L. H., Luo, F. R., et al. (2011) · Alzheimer s Research & Therapy · doi:10.1186/alzrt90 · Cited by 139
“Th e use of unbiased stereology and the optical fractionator method is critical to determining an accurate and statistically reliable neuronal count in brain sections [17].”
The human olfactory system in two proteinopathies: Alzheimer’s and Parkinson’s diseases
Úbeda‐Bañón, I., Saiz‐Sánchez, D., Flores‐Cuadrado, A., Corroto, E. R., González-Rodríguez, M., Villar‐Conde, S., Astillero‐Lopez, V., Cabello, J. P., Gallardo‐Alcañiz, M. J., Vaamonde‐Gamo, J., et al. (2020) · Translational Neurodegeneration · doi:10.1186/s40035-020-00200-7 · Cited by 131
“In fact, neuronal loss is detectable in mild Alzheimer’s disease but not in preclinical cases or those associated with normal aging [123, 124].”
BackgroundChristensen, D. Z., Kraus, S. L., Flohr, A., Cotel, M.-C., Wirths, O., & Bayer, T. A. (2008) · Acta Neuropathologica · doi:10.1007/s00401-008-0451-6 · Cited by 126
“This would correlate with the fact that neurons are not yet lost in pre-clinical AD [23] where intraneuronal accumulation of Ab42 would still be detectable; however, with the transition to AD, the intraneuronal immunoreactivity is strongly decreased or undetectable due to the loss of the respective neurons.”
BackgroundLactate deficit in an Alzheimer disease mouse model: the relationship with neuronal damage
Zhang, M., Cheng, X., Dang, R., Zhang, W., Zhang, J., & Yao, Z. (2018) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nly102 · Cited by 130
Rocha-Souto, B. D., Scotton, T. C., Coma, M., Serrano‐Pozo, A., Hashimoto, T., Serenó, L., Rodríguez, M., Sánchez, B., Hyman, B. T., & Gómez‐Isla, T. (2011) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0b013e318217a118 · Cited by 138
Alzheimer 100 – highlights in the history of Alzheimer research
Jellinger, K. A. (2006) · Journal of Neural Transmission · doi:10.1007/s00702-006-0578-3 · Cited by 133
“, 2006), whereas there may be no significant loss of hippocampal neurons in preclinical AD (West et al., 2004).”
BackgroundCellular, synaptic, and biochemical features of resilient cognition in Alzheimer’s disease
Arnold, S. E., Louneva, N., Cao, K., Wang, L.-S., Han, L.-Y., Wolk, D. A., Negash, S., Leurgans, S. E., Schneider, J. A., Buchman, A. S., et al. (2013) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2012.03.004 · Cited by 123
“In contrast to the aforementioned studies, which described similarities between resilient/preclinical AD and AD with dementia, Troncoso and colleagues have reported differences, including preserved numbers and larger neuronal sizes in the hippocampus and other brain regions in “asymptomatic AD” cases compared with nor…”
ResultWalton, J. R. (2014) · Journal of Alzheimer s Disease · doi:10.3233/jad-132204 · Cited by 126
“19A) or by stereological counts [383].”
Hippocampal shape analysis in Alzheimer’s disease: A population-based study
Scher, I., Xu, Y., Korf, E. S. C., White, L. R., Scheltens, P., Toga, A. W., Thompson, P. M., Hartley, S. W., Witter, M. P., Valentino, D. J., et al. (2007) · NeuroImage · doi:10.1016/j.neuroimage.2006.12.036 · Cited by 117
Roles of hippocampal subfields in verbal and visual episodic memory
Zammit, A. R., Ezzati, A., Zimmerman, M. E., Lipton, R. B., Lipton, M. L., & Katz, M. J. (2016) · Behavioural Brain Research · doi:10.1016/j.bbr.2016.09.038 · Cited by 116
The Neurodegenerative Mitochondriopathies
Swerdlow, R. H. (2009) · Journal of Alzheimer s Disease · doi:10.3233/jad-2009-1095 · Cited by 115
“Hippocampal CA1 neuronal integrity may define a border between symptoms and no symptoms; aged individuals with CA1 neuron loss are much more likely to have clinical dementia than those who do not [46,47].”
Perturbations of neural circuitry in aging, mild cognitive impairment, and Alzheimer's disease
Leal, S. L., & Yassa, M. A. (2013) · Ageing Research Reviews · doi:10.1016/j.arr.2013.01.006 · Cited by 114
“Further, such work has even been able to show that cellular oss is correlated with the onset of disease symptoms (Price et al., 001; West et al., 2004).”
BackgroundNeuman, K. M., Molina-Campos, E., Musial, T. F., Price, A. L., Oh, K.-J., Wolke, M. L., Buss, E. W., Scheff, S. W., Mufson, E. J., & Nicholson, D. A. (2014) · Brain Structure and Function · doi:10.1007/s00429-014-0848-z · Cited by 104
MicroRNA in Alzheimer’s disease: an exploratory study in brain, cerebrospinal fluid and plasma
Bekris, L. M., Lutz, F., Montine, T. J., Yu, C. E., Tsuang, D., Peskind, E. R., & Leverenz, J. B. (2013) · Biomarkers · doi:10.3109/1354750x.2013.814073 · Cited by 97
“AD HP has been reported to contain less neurons relative to astroglial populations than cognitively normal controls (West et al., 2004).”
BackgroundAn Efficient Classifier for Alzheimer’s Disease Genes Identification
Xu, L., Liang, G., Liao, C., Chen, G.-D., & Chang, C.-C. (2018) · Molecules · doi:10.3390/molecules23123140 · Cited by 107
“The information obtained via structural MRI—for example, hippocampal volumes [21,22], cortical thickness [23,24], voxel-wise”
MethodDong, H., Yuede, C. M., Coughlan, C. A., Murphy, K. M., & Csernansky, J. G. (2009) · Brain Research · doi:10.1016/j.brainres.2009.09.097 · Cited by 106
“, 2001) and is a major site for Aβ deposition in both AD patients (Probst et al., 1983; West et al., 2004) and in several transgenic mouse models of AD (Su and Ni, 1998; Reilly et al.”
Liu, R., Gao, M., Qiang, G., Zhang, T.-T., Lan, X., Ying, J., & Du, G.-H. (2009) · Neuroscience · doi:10.1016/j.neuroscience.2009.05.009 · Cited by 107
“Besides, neuronal loss has been found predomnantly in AD compared to normal aging in humans and odents (West et al., 2004; Burke and Barnes, 2006; Rapp nd Gallagher, 1996; Rasmussen et al., 1996; Smith et al., 004).”
BackgroundResistance to Alzheimer's pathology is associated with nuclear hypertrophy in neurons
Riudavets, M. A., Iacono, D., Resnick, S. M., O’Brien, R., Zonderman, A. B., Martin, L. J., Rudow, G., Pletnikova, O., & Troncoso, J. C. (2007) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2007.05.005 · Cited by 106
“Previous studies of the neuropathology of asymptomatic AD (preclinical AD) have described and quantified Aβ plaques [32] and neurofibrillary tangles (NFT) [17] [31] [18] [8] and also have shown that the number of neurons remains stable in hippocampus and entorhinal cortex [59] [42].”
BackgroundMethodSelf-citationStereological estimation of the number of neurons in the human amygdaloid complex
Schumann, C. M., & Amaral, D. G. (2005) · The Journal of Comparative Neurology · doi:10.1002/cne.20704 · Cited by 100
“…techniques have been applied to other areas of the human brain to accurately measure absolute neuron numbers (Pakkenberg and Gundersen, 1988; West and Gundersen, 1990; Pakkenberg and Gundersen, 1997; West and Slomianka, 1998; Andersen et al., 2003, 2004; Korbo et al., 2004; West et al., 2004).”
MethodGulinello, M. E., Lebesgue, D., Jover‐Mengual, T., Zukin, R. S., & Etgen, A. M. (2005) · Hormones and Behavior · doi:10.1016/j.yhbeh.2005.07.010 · Cited by 102
“Quantitative estimates of neuronal loss are poor predictors of cognitive function in Alzheimer’s patients (von Gunten et al., 2005; West et al., 2004), for example.”
BackgroundZheng, K., Hu, F., Zhou, Y., Zhang, J., Zheng, J., Lai, C., Xiong, W., Cui, K., Hu, Y., Han, Z., et al. (2021) · Nature Communications · doi:10.1038/s41467-021-22196-y · Cited by 107
Hayakawa, N., Kato, H., & Araki, T. (2007) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2007.01.005 · Cited by 104
3D comparison of low, intermediate, and advanced hippocampal atrophy in MCI
Apostolova, L. G., Thompson, P. M., Green, A. E., Hwang, K., Zoumalan, C., Jack, C. R., Harvey, D. J., Petersen, R. C., Thal, L. J., Aisen, P. S. S., et al. (2010) · Human Brain Mapping · doi:10.1002/hbm.20905 · Cited by 100
“[Braak and Braak, 1991; Rossler et al., 2002; Schonheit et al., 2004; West et al., 2004].”
Malykhin, N. V., Huang, Y., Hrybouski, S., & Olsen, F. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.08.001 · Cited by 88
Silva, A. R. T., Santos, A. C. F., Farfel, J. M., Grinberg, L. T., Ferretti, R. E. L., Campos, A. H. J. F. M., Cunha, I. W., Begnami, M. D., Rocha, R. M., Carraro, D. M., et al. (2014) · PLoS ONE · doi:10.1371/journal.pone.0099897 · Cited by 99
“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].”
BackgroundMontero‐Crespo, M., Domínguez-Álvaro, M., Alonso‐Nanclares, L., DeFelipe, J., & Blázquez‐Llorca, L. (2020) · Brain · doi:10.1093/brain/awaa406 · Cited by 89
“neuronal loss and dendritic alterations in Alzheimer’s disease patients (Hyman et al., 1990; West et al., 2004; AndradeMoraes et al., 2013; Llorens-Martı́n et al., 2014; Furcila et al., 2019).”
BackgroundResultAluise, C. D., Robinson, R. A. S., Cai, J., Pierce, W. M., Markesbery, W. R., & Butterfield, D. A. (2011) · Journal of Alzheimer's Disease · doi:10.3233/jad-2010-101083 · Cited by 94
Initiative, T. A. D. N., Zu, C., Jie, B., Liu, M., Chen, S., Shen, D., & Zhang, D. (2016) · Brain Imaging and Behavior · doi:10.1007/s11682-015-9480-7 · Cited by 95
Deficits in memory and visuospatial learning correlate with regional hippocampal atrophy in MS
Longoni, G., Rocca, M. A., Pagani, E., Riccitelli, G. C., Colombo, B., Rodegher, M., Falini, A., Comı, G., & Filippi, M. (2013) · Brain Structure and Function · doi:10.1007/s00429-013-0665-9 · Cited by 93
The domestic cat as a natural animal model of Alzheimer’s disease
CHAMBERS, J. K., Tokuda, T., Uchida, K., Ishii, R., Tatebe, H., Takahashi, E., Tomiyama, T., Une, Y., & Nakayama, H. (2015) · Acta Neuropathologica Communications · doi:10.1186/s40478-015-0258-3 · Cited by 90
“Although neuronal loss in the entorhinal cortex and hippocampus is considered to be an early event in AD [22, 59], it has not been detected in combination with Aβ and tau pathologies in non-human species [50, 58].”
BackgroundKhan, W., Westman, E., Jones, N., Wahlund, L., Mecocci, P., Vellas, B. J., Tsolaki, M., Kłoszewska, I., Soininen, H. S., Spenger, C., et al. (2014) · Brain Topography · doi:10.1007/s10548-014-0415-1 · Cited by 88
“For classifying AD from HC, combined subfield volumes achieved comparable classification accuracy (81.7”
MethodInfluentialNeuropathological approaches to cerebral aging and neuroplasticity
Jellinger, K. A., & Attems, J. (2013) · Dialogues in Clinical Neuroscience · doi:10.31887/dcns.2013.15.1/kjellinger · Cited by 94
Negash, S., Wilson, R. S., Leurgans, S. E., Wolk, D. A., Schneider, J. S., Buchman, A. S., Bennett, D., & Arnold, S. E. (2013) · Current Alzheimer Research · doi:10.2174/15672050113109990157 · Cited by 88
Unbiased comparison of sample size estimates from longitudinal structural measures in ADNI
Holland, D., McEvoy, L. K., Dale, A. M., & Initiative, T. A. D. N. (2011) · Human Brain Mapping · doi:10.1002/hbm.21386 · Cited by 85
“, 2001] and hippocampal [West et al., 2004] neuron counts—even in CA1, the hippocampal sector most affected by neuron loss in the early stages of AD— between cognitively normal subjects essentially free of amyloid pathology and those exhibiting significant amounts of amyloid deposition, to a degree consistent with a n…”
ResultThe dentate gyrus in Alzheimer's disease
Ohm, T. G. (2007) · Progress in brain research · doi:10.1016/s0079-6123(07)63039-8 · Cited by 78
Bastide, M. F., Doveró, S., Charron, G., Porras, G., Gross, C. E., Fernagut, P., & Bézard, E. (2013) · Neurobiology of Disease · doi:10.1016/j.nbd.2013.09.020 · Cited by 82
Bonda, D., Evans, T. A., Santocanale, C., Llosá, J. C., Viña, J., Bajić, V., Castellani, R. J., Siedlak, S. L., Perry, G. L., Smith, M. A., et al. (2009) · Aging · doi:10.18632/aging.100044 · Cited by 82
Preclinical Alzheimer disease: Brain oxidative stress, Aβ peptide and proteomics
Aluise, C. D., Sowell, R. A., Beckett, T. L., Murphy, M. P., Cai, J., Pierce, W. M. J., Markesbery, W. R., & Butterfield, D. A. (2010) · Neurobiology of Disease · doi:10.1016/j.nbd.2010.04.011 · Cited by 83
“, 2009), no hippocampal cell loss (West et al., 2004), increased synaptic plasticity (O'Brien et al.”
BackgroundIn vivo MRI signatures of hippocampal subfield pathology in intractable epilepsy
Goubran, M., Bernhardt, B. C., Cantor‐Rivera, D., Lau, J. C., Blinston, C. A., Hammond, R. R., de Ribaupierre, S., Burneo, J. G., Mirsattari, S. M., Steven, D. A., et al. (2015) · Human Brain Mapping · doi:10.1002/hbm.23090 · Cited by 79
“…in vivo prediction of pathology might carry a broader impact, as associations between subfield-specific pathology and disease progression have been described in other neurological disorders, namely Alzheimer’s disease [West et al., 2004], stress [McEwen, 1999], and schizophrenia [Harrison, 2004].”
BackgroundInfluentialApostolova, L. G., Zarow, C., Biado, K., Hurtz, S., Boccardi, M., Somme, J. H., Honarpisheh, H., Blanken, A. E., Brook, J. K., Tung, S., et al. (2015) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2015.01.001 · Cited by 77
“Also, it is of interest to note that one of the studies examined the differences in neuronal counts in all hippocampal subfields between NC and AD subjects and found the exact same pattern as the one we report here, namely, significantly lower neuronal counts in subiculum and CA1 but not in CA2–4 in AD compared with N…”
Schoene‐Bake, J., Keller, S. S., Niehusmann, P., Volmering, E., Elger, C. E., Deppe, M., & Weber, B. (2014) · Human Brain Mapping · doi:10.1002/hbm.22506 · Cited by 78
“…one hand, the correlations of CA1 would seem particularly important for evaluation of patients with mTLE and Alzheimer’s disease, given that CA1 is most severely affected in these conditions (Blumcke et al., 2007; Bratz, 1899; Margerison and Corsellis, 1966; Sommer, 1880; West et al., 1994, 2004).”
BackgroundFilo, S., Shtangel, O., Salamon, N., Kol, A., Weisinger, B., Shifman, S., & Mezer, A. (2019) · Nature Communications · doi:10.1038/s41467-019-11319-1 · Cited by 76
Anti-dementia drugs and hippocampal-dependent memory in rodents
Yuede, C. M., Dong, H., & Csernansky, J. G. (2007) · Behavioural Pharmacology · doi:10.1097/fbp.0b013e3282da278d · Cited by 76
“In AD, the integrity of the hippocampus is compromised by plaques, tangles and, eventually, the loss of synapses and neuron cell bodies (Alzheimer, 1907; Probst et al., 1983; Bussiere et al., 2002; Rekart et al., 2004; West et al., 2004).”
BackgroundInvolvement of TRPV4 channels in Aβ40-induced hippocampal cell death and astrocytic Ca2+ signalling
Bai, J., & Lipski, J. (2014) · NeuroToxicology · doi:10.1016/j.neuro.2014.01.001 · Cited by 70
Hagihara, H., Murano, T., Ohira, K., Miwa, M., Nakamura, K., & Miyakawa, T. (2019) · Molecular Brain · doi:10.1186/s13041-019-0522-8 · Cited by 70
Marner, L., Frøkjær, V. G., Kalbitzer, J., Lehel, S., Madsen, K., Baaré, W. F. C., Knudsen, G. M., & Hasselbalch, S. G. (2010) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2010.03.023 · Cited by 73
Potential drug–drug interactions in Alzheimer patients with behavioral symptoms
Monzani, F., Pasqualetti, G., Tognini, S., Calsolaro, V., & Polini, A. (2015) · Clinical Interventions in Aging · doi:10.2147/cia.s87466 · Cited by 76
Region-Specific Genetic Alterations in the Aging Hippocampus: Implications For Cognitive Aging
Bürger, C. (2010) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2010.00140 · Cited by 75
“These reports suggest that the CA1 region is more susceptible to amyloid plaque deposits and ischemia relative to CA3(Gozal et al., 2002; West et al., 2004; Zarow et al., 2005; Wu et al., 2008).”
Hippocampal Deficits in Amyloid-β-Related Rodent Models of Alzheimer’s Disease
Vyas, Y., Montgomery, J. M., & Cheyne, J. E. (2020) · Frontiers in Neuroscience · doi:10.3389/fnins.2020.00266 · Cited by 66
Metadata
- 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
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2004-10
- Volume
- 25
- Issue
- 9
- Pages
- 1205-1212
- ISSN
- 0197-4580 (ISSN-L)
- 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
- bronze
- doi.org
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Funders
- National Institute on Aging (P50AG005146, AG 05146)
- 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
- 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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