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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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18 No full text of the sources · 16 Own result · 10 Own interpretation · 6 Own method · 2 No basis given · 1 Supported so far · 1 Partly supported · accuracy not yet measured
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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
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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- Also stated in: § 4. Discussion · plain
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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
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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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
boostedn = 8- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Abstract · plain
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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
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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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
boostedcorrelationaln = 7 ·- Asserted: passes — The authors put it forward as true.
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- 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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“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
boostedcorrelationaln = 7 ·- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- 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
plainn = 7- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- 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
boostedn = 11 ·- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § 4. Discussion · 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, 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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- 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
“but not in other subdivisions of the AD group (Table 3).”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 3. Results
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“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
boostedcorrelationaln = 7 ·- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- 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
“Subjects with preclinical AD had scores that were similar or even superior to the scores of the control subjects.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 2.1. Subjects
plain- Asserted: passes — The authors put it forward as true.
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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
“Many controls exhibited NFTs in hippocampus and entorhinal cortex.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 2.1. Subjects
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“The lack of change in hippocampal neuron number, at this stage, may then contribute to the preservation of normal cognitive function in preclinical AD.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“As such, we cannot state whether the process of cell death begins around the preclinical phase.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
plain- Asserted: passes — The authors put it forward as true.
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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
“Calculations indicate that a sample of 164 preclinical and 164 controls would be required to have 80% power to detect the difference we observed in this study.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
hedgedn = 164- Asserted: passes — The authors put it forward as true.
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In the paper
“In view of the early appearance of NFT in the hippocampus [4], the preservation of hippocampal neurons in preclinical AD is an unexpected observation.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
What the sources say
- Not checked — no full text of the sourcecites [4] Braak, 1991, Neuropathological stageing of Alzheimer-related changes, Acta Neuropathol. source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“It is also less sensitive than the N V V REF method to tissue deformation caused by changes in the thickness of the sections during staining and mounting.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“This most likely reflects the lack of inclusion of partial sections at the leading and trailing edges of the 1 cm thick blocks that contained hippocampal tissue.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“An important caveat to our observations, however, is that the preservation of hippocampal neurons does not necessarily mean that these neurons are not affected by the disease.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
hedged- Asserted: passes — The authors put it forward as true.
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In the paper
“According to this scenario, which is based on the idea that amyloid deposition is a primary event in the development of the disease [28], the disease first affects the neocortex (as evidenced by the presence of abundant amyloid) and then spreads to the hippocampus.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
What the sources say
- Not checked — no full text of the sourcecites [28] Selkoe, 1999, Translating cell biology into therapeutic advances in Alzheimer’s disease, Nature source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The existence of significant amyloid deposits and neuritic plaques in the neocortex, prior to the loss of hippocampal neurons, suggests that there is a hierarchical order of involvement of various brain regions during the development of AD.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Our results suggest that a majority of the decline in the CA1 cell count is likely to occur between the preclinical phase of the disease and the overt clinical phase.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
hedgedconditional- Asserted: passes — The authors put it forward as true.
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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 absence of differences in hippocampal neuronal counts in the preclinical stage of the disease, compared to controls, implies that the deposition of A and the development of neuritic plaques in the neocortex precedes significant neuronal death in the hippocampus.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
plaindirect- Asserted: passes — The authors put it forward as true.
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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
“We had only limited power (i.e., 12.6%) to detect a difference between controls and preclinical AD cases.”
- Also stated in: § 4. Discussion · plain
“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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § 4. Discussion · plain
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 suggests that in spite of severe amyloid pathology there may still be a large temporal window during which cognitive changes, perhaps resulting from hippocampal neuronal loss, can be prevented.”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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In the paper
“In view of the recent study [26] describing the sparing of neurons in entorhinal cortex in preclinical AD, this phenomenon does not appear to be unique to the hippocampus.”
§ 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
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“These results are in close agreement with those in a previous study [26], which was based on the examination of a segment of the hippocampus and also provided information on the entorhinal cortex.”
§ 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
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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In the paper
“Our observations are also consistent with a recent report which described substantial losses of neurons in CA1 both in mild and severe AD (46 and 65%, respectively) [26].”
§ 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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The inclusion of this relatively large number of cases of mild severity may have resulted in a smaller difference between the two groups than was observed in our first study [39].”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
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
hedgedconditionaln = 14- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- 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.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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)
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plainn = 7- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The 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
plainn = 14- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plainn = 14- Asserted: passes — The authors put it forward as true.
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It 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
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
plainn = 14- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
plainn = 8- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
plainn = 11- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
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]
The check wasn’t confident either way, so it gives no verdict — never disputed.
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]
Experimental — accuracy not yet measuredIn 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
“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]
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.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
“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”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
Reported 34500 · recomputed 36846
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
“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
“| 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 |”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 3. Results
“Table 4 Total number of neurons in hippocampal subdivisions of male cases and controls Subregion Controls, N = 11”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
“| 03 | 73 | F | 30 | 0 | II | Control/infarct remote |”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
“Section sampling fraction (ssf) 1/30 1/30 1/30 1/30 1/30”
§ Hippocampal neurons in pre-clinical Alzheimer's disease > 4. Discussion
“ssf: 30 (sections taken at 30 section intervals, after a random start within the first 30 sections)”
Citations
Cites
Folstein, M. F., Folstein, S. E., & McHugh, P. R. (1975) · Journal of Psychiatric Research · doi:10.1016/0022-3956(75)90026-6 · Cited by 88,282
McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D., & Stadlan, E. M. (1984) · Neurology · doi:10.1212/wnl.34.7.939 · Cited by 27,915
Neuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123
Mirra, S. S., Heyman, A., McKeel, D., Sumi, S. M., Crain, B. J., Brownlee, L. M., Vogel, F. S., Hughes, J. P., Belle, G. V., Berg, L., et al. (1991) · Neurology · doi:10.1212/wnl.41.4.479 · Cited by 4,961
Moms, J. C., Heyman, A., Mohs, R. C., Hughes, J. P., van Belle, G., Fillenbaum, G., Mellits, E. D., & Clark, C. (1989) · Neurology · doi:10.1212/wnl.39.9.1159 · Cited by 4,130
Blessed, G., Tomlinson, B. E., & Roth, M. (1968) · British Journal of Psychiatry · doi:10.1192/bjp.114.512.797 · Cited by 4,117
West, M. J., Slomianka, L., & Gundersen, H. J. G. (1991) · The Anatomical Record · doi:10.1002/ar.1092310411 · Cited by 2,994
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
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.
- 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.
- 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.
Cited by
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
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-11, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-11 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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