The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index; 15 of the 49 sources its claims cite were checked for support.
An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice
Open accessAbstract
The antidepressant drug citalopram decreased CSF amyloid-β in healthy humans, and in an aged transgenic mouse model of Alzheimer’s disease, it decreased ISF amyloid-β in a dose-dependent manner.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
In aged APP/PS1 mice, citalopram dose-dependently lowered brain interstitial fluid Aβ, blocked growth of existing plaques, and reduced new plaque appearance by 78%. In healthy human volunteers, acute citalopram reduced CSF Aβ production by 37% and total CSF Aβ concentrations by 38% without changing clearance.
Key findings
- In 12-month-old plaque-bearing APP/PS1 mice, citalopram reduced ISF Aβ at 5 mg/kg (12.4%) and 10 mg/kg (24.5%) versus baseline; 20 mg/kg gave no additional effect (27.5% reduction), while 2.5 mg/kg was not significant.
- Chronic citalopram (10 mg/kg daily for 28 days) prevented plaque growth: vehicle plaques grew 111.4 μm² on average, whereas citalopram plaques did not grow (−22.4 μm², p=0.26); new plaques were reduced from 10 (3.9) to 2.2 (1.1), p=0.01, a 78% reduction.
- In healthy human volunteers, citalopram lowered mean CSF Aβ production rate to 1.33 pg/hr (0.15) versus 2.11 pg/hr (0.20) for placebo, a 37% reduction (p=0.005), and lowered average CSF Aβ concentration by 38% over 37 hours (p=0.001).
- Aβ clearance rate was unchanged (−0.61 versus −0.96 per hour; p=0.115), and tracer/tracee ratio did not differ significantly between groups.
Methods
- Mouse studies used APP/PS1+/− mice: in vivo hippocampal microdialysis to measure ISF Aβ after acute citalopram doses (2.5, 5, 10, 20 mg/kg) and longitudinal multiphoton microscopy with thinned-skull cranial windows to track individual plaque growth over 28 days of citalopram (10 mg/kg) or vehicle.
- Human study was a randomized, double-blind, placebo-controlled trial in healthy volunteers receiving 60 mg citalopram in divided oral doses; CSF and blood were sampled hourly during stable-isotope labeling kinetics (SILK) with 13C6-leucine, and labeled/unlabeled Aβ was measured by mass spectrometry.
- Analyses used repeated-measures ANOVA with treatment, time, and treatment-by-time effects, mixed models, post-hoc approximate t-tests, and non-proportional odds cumulative logit models for plaque outcomes.
Limitations
- The paper states that human data were not collected during the first 8 hours after drug/placebo administration, so the timing of when CSF concentration differences arose is unknown.
- The paper states that human studies were conducted in young individuals presumably before plaque formation, so it is unknown whether the same effect occurs in older individuals with plaque deposition.
- The paper notes that production and clearance were modeled as independent phenomena even though they occur simultaneously; evident additional constraints include the small human sample (23 analyzed), acute dosing rather than long-term prevention outcomes, and adverse events including post-lumbar puncture headaches and nausea/vomiting.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
24 Own result · 13 Own method · 13 Own interpretation · 10 Not checked yet · 8 No full text of the sources · 5 Supported · 3 Supported so far · 1 Partly supported · 1 Mixed support · 1 Not supported · 1 No basis given · accuracy not yet measured
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“Serotonin signaling suppresses generation of amyloid-β (Aβ) in vitro and in animal models of Alzheimer’s disease (AD).”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Abstract
What the sources say
- Not checked — no full text of the sourcecites [10] Arjona AA Pooler AM Lee RK Wurtman RJ Effect of a 5-HT(2C) serotonin agonist, dexnorfenfluramine, on amyloid precursor protein metabolism in guinea pigs Brain Res 951 135 9 27 2002 12231467 source
- Partly supportedcites [11] Nitsch RM Deng M Growdon JH Wurtman RJ Serotonin 5-HT2a and 5-HT2c receptors stimulate amyloid precursor protein ectodomain secretion J Biol Chem 271 4188 2 23 1996 8626761 sourceExperimental — accuracy not yet measured
The Discussion (page not provided) reports that serotonin increased non-amyloidogenic APP ectodomain secretion in cultured cells, which could reduce amyloidogenic products. But the authors say they could not measure Aβ in those experiments and that an effect on Aβ secretion remained to be investigated. The cited paper also does not report experiments in animal models of AD. (LLM, conf=0.87)
- Disputedcites [12] Robert SJ Zugaza JL Fischmeister R Gardier AM Lezoualc’h F The human serotonin 5-HT4 receptor regulates secretion of non-amyloidogenic precursor protein J Biol Chem 276 44881 11 30 2001 11584021 sourceExperimental — accuracy not yet measured
In “Effect of 5-HT4 Receptor Activation on Aβ Production,” the authors report no effect of serotonin on Aβ production in CHO cells compared with untreated controls, contrary to the claimed in vitro suppression. The provided passages do not report Aβ suppression in animal models of AD. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
- Supportedcites [13] Cirrito JR Serotonin signaling is associated with lower amyloid-beta levels and plaques in transgenic mice and humans Proc Natl Acad Sci U S A 108 14968 9 6 2011 21873225 PMC3169155 source
The introductory passage (section labelled Abstract; page unavailable) reports that activation of select serotonin receptors increases nonamyloidogenic APP processing in vitro, which prevents Aβ formation. The Abstract and Results report reduced Aβ production following serotonin signaling in mouse models of AD. The in vitro finding is reported from earlier studies, not presented as this paper’s own experiment. (LLM, conf=0.90)
- Partly supportedcites [14] Nelson RL Prophylactic treatment with paroxetine ameliorates behavioral deficits and retards the development of amyloid and tau pathologies in 3xTgAD mice Exp Neurol 205 166 5 2007 17368447 PMC1979096 sourceExperimental — accuracy not yet measured
The Results (page not provided) show that paroxetine treatment lowered Aβ1−40 levels in 3xTgAD mice, but did not significantly affect Aβ1−42. The Discussion says serotonergic signaling might mediate this effect, while also allowing a mechanism independent of serotonin signaling. The paper does not establish that serotonin signaling suppresses Aβ generation, and it reports no in vitro experiment of its own. (LLM, conf=0.88)
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.
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“Activation of serotonin receptors has been shown to reduce Aβ production in vitro; treatment with serotonin or receptor agonists activates intracellular signaling cascades and increases levels of the α-secretase product sAPP-α (10–12).”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Introduction
What the sources say
- Not checked — no full text of the sourcecites [10] Arjona AA Pooler AM Lee RK Wurtman RJ Effect of a 5-HT(2C) serotonin agonist, dexnorfenfluramine, on amyloid precursor protein metabolism in guinea pigs Brain Res 951 135 9 27 2002 12231467 source
- Disputedcites [11] Nitsch RM Deng M Growdon JH Wurtman RJ Serotonin 5-HT2a and 5-HT2c receptors stimulate amyloid precursor protein ectodomain secretion J Biol Chem 271 4188 2 23 1996 8626761 sourceExperimental — accuracy not yet measured
The Discussion says the authors could not measure Aβ secretion in the serotonin-treated 3T3 cells and that whether serotonin receptor stimulation changes Aβ secretion remains to be investigated. The Results show increased APPs secretion, but not the claimed reduction in Aβ production. (LLM, conf=0.86)
Checked by a reasoning model — may be wrong.
- Disputedcites [12] Robert SJ Zugaza JL Fischmeister R Gardier AM Lezoualc’h F The human serotonin 5-HT4 receptor regulates secretion of non-amyloidogenic precursor protein J Biol Chem 276 44881 11 30 2001 11584021 sourceExperimental — accuracy not yet measured
In “Effect of 5-HT4 Receptor Activation on Aβ Production” (page not supplied), the authors report no effect of serotonin on Aβ production in their CHO-cell experiment. The Discussion likewise says that receptor stimulation did not change secreted Aβ levels, although it increased sAPPα secretion. (LLM, conf=0.93)
Checked by a reasoning model — may be wrong.
boosteddirect- 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.
Every source the paper cites for this claim was checked and supports it.
In the paper
“Modulating serotonin levels in vivo shows consistent effects: single-dose treatment of SSRIs in young APP/PS1 mice reduced Aβ levels in the brain interstitial fluid (ISF) by 25% (13).”
- Also stated in: § Citalopram dose-response in aged APP/PS1 mice · boosted
“Previous studies demonstrated in 3 month old APP/PS1+/− mice, an age prior to Aβ pathology, that 10mg/kg citalopram reduces brain ISF Aβ concentrations by 25% (13).”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Introduction
What the sources say
- Supportedcites [13] Cirrito JR Serotonin signaling is associated with lower amyloid-beta levels and plaques in transgenic mice and humans Proc Natl Acad Sci U S A 108 14968 9 6 2011 21873225 PMC3169155 source
The Results report that a single administration of several SSRIs to 2- to 3-month-old PS1APP mice reduced brain ISF Aβ, with levels remaining 25% lower at 24 hours. The Discussion also summarizes acute SSRI treatment as reducing ISF Aβ by 25%. (LLM, conf=0.94)
boosteddirect- 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: § Citalopram dose-response in aged APP/PS1 mice · boosted
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In animal models, a 12–25% reduction in Aβ concentrations was sufficient to dramatically decrease plaque formation (32).”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Discussion
What the sources say
- Partly supportedcites [32] Yan P Characterizing the appearance and growth of amyloid plaques in APP/PS1 mice J Neurosci 29 10706 8 26 2009 19710322 PMC2756291 sourceExperimental — accuracy not yet measured
The Results report that Compound E dramatically attenuated new plaque appearance in APP/PS1 mice, while a separate Results passage reports 24-hour reductions of 22% and 25% in interstitial-fluid Aβ. Our copy does not report a 12% reduction, and the Discussion describes the reduction in Aβ as associated with—not definitively sufficient to cause—the reduction in plaque formation. No page numbers are available in our copy. (LLM, conf=0.88)
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.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Chronic SSRI treatment over the course of four months reduced Aβ plaque load by 50% in mice (13).”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Introduction
What the sources say
- Supportedcites [13] Cirrito JR Serotonin signaling is associated with lower amyloid-beta levels and plaques in transgenic mice and humans Proc Natl Acad Sci U S A 108 14968 9 6 2011 21873225 PMC3169155 source
The Results report that PS1APP mice received the SSRI citalopram for four months and had significantly less plaque burden than water-treated controls. Hippocampal plaque load fell by 50% (and cortical plaque load by 62%), supporting the citing sentence's 50% figure. (LLM, conf=0.95)
plaindirect- 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.
- Supported
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
“In humans, CSF Aβ concentrations begin changing before tau levels; amyloid deposition occurs in the brain decades before the onset of clinical symptoms (3–5).”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Introduction
What the sources say
- Not checked — no full text of the sourcecites [3] Price JL Morris JC Tangles and plaques in nondemented aging and “preclinical” Alzheimer’s disease Ann Neurol 45 358 3 1999 10072051 source
- Not checked — no full text of the sourcecites [4] Hardy J Selkoe DJ The amyloid hypothesis of Alzheimer’s disease: progress and problems on the road to therapeutics Science 297 353 7 19 2002 12130773 source
- Supportedcites [5] Bateman RJ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease N Engl J Med 7 11 2012 PMC3474597 22784036 source
The Results (Combined Model) report that CSF Aβ42 appeared to decline about 25 years before expected symptom onset in human mutation carriers, while CSF tau increases were detected about 15 years before onset. This supports the attributed ordering of the changes. (LLM, conf=0.93)
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.
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
“Stimulation of serotonin receptors activates the ERK signaling cascade in as little as 5 minutes (27–29).”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Discussion
What the sources say
- Not checked — no full text of the sourcecites [27] Lione A Errico M Lin S Cowen D Activation of extracellular signal-regulated kinase (ERK) and Akt by human serotonin 5-HT1B receptors in transfected BE(2)-C neuroblastoma cells is inhibited by RGS4 J Neurochem 2000 9 75 3 934 8 10936173 source
- Supportedcites [28] Johnson-Farley N Kertesy S Dubyak G Cowen D Enhanced activation of Akt and extracellular-regulated kinase pathways by simultaneous occupancy of Gq-coupled 5-HT2A receptors and Gs-coupled 5-HT7A receptors in PC12 cells J Neurochem 2005 1 92 1 72 82 15606897 source
The figure captions reproduced in the Discussion (Figs. 2–3) describe ERK activation after five-minute treatments with 5-HT or a serotonin-receptor agonist in PC12 cells. This supports the stated timing in the cell models studied. (LLM, conf=0.92)
- Not checked — no full text of the sourcecites [29] Norum J Hart K Levy F Ras-dependent ERK activation by the human Gs-coupled serotonin receptors 5-HT4(b) and 5-HT7(a) J Biol Chem 2003 1 31 278 5 3098 104 12446729 source
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.
Every source the paper cites for this claim was checked and supports it.
In the paper
“In those studies, serotonin signaling did not alter the rate of Aβ clearance, suggesting that reduced Aβ production was responsible for lower Aβ concentrations.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Introduction
What the sources say
- Supportedcites [13] Cirrito JR Serotonin signaling is associated with lower amyloid-beta levels and plaques in transgenic mice and humans Proc Natl Acad Sci U S A 108 14968 9 6 2011 21873225 PMC3169155 source
In the Results section, serotonin-treated and vehicle-treated mice had the same ISF Aβ elimination half-life, approximately one hour. The authors conclude that altered elimination did not explain the lower Aβ levels and report reduced Aβ production instead. (LLM, conf=0.94)
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Our previous studies demonstrated that ERK activation was required for serotonin-dependent suppression of Aβ (13).”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Discussion
What the sources say
- Supportedcites [13] Cirrito JR Serotonin signaling is associated with lower amyloid-beta levels and plaques in transgenic mice and humans Proc Natl Acad Sci U S A 108 14968 9 6 2011 21873225 PMC3169155 source
The Results section, under “ERK Is Required for Serotonin-Dependent Depression of ISF Aβ,” reports that inhibiting MEK or ERK completely blocked citalopram’s effect on interstitial-fluid Aβ levels in mice. The Discussion likewise states that the ERK cascade is required for serotonin-receptor-mediated changes in Aβ generation. (LLM, conf=0.94)
boosteddirect- 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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“SSRI treatment in the 3xTg AD mouse model showed similar reductions in Aβ (14).”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Introduction
What the sources say
- Supportedcites [14] Nelson RL Prophylactic treatment with paroxetine ameliorates behavioral deficits and retards the development of amyloid and tau pathologies in 3xTgAD mice Exp Neurol 205 166 5 2007 17368447 PMC1979096 source
The Results report that paroxetine-treated 3xTgAD mice had significantly lower cortical Aβ1−40 levels than saline-treated mice, with reductions exceeding 50% in both sexes. They also report fewer hippocampal neurons with Aβ accumulations. Paroxetine is the SSRI treatment described in the claim. (LLM, conf=0.92)
plaindirect- 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.
- Supported
- Probably not a substantial claim. 21
- It may state two separate claims as one. 11
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
“Nonetheless, the efficacy of the current proposed prevention strategy depends critically on the validity of the amyloid hypothesis of Alzheimer’s disease.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Discussion
plainconditional- 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: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
In the paper
“Citalopram is one of the most selective SSRIs for serotonin re-uptake and has among the most favorable side effect profiles compared with other antidepressants (17).”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Results > Citalopram dose-response in aged APP/PS1 mice
What the sources say
- Not checked yetcites [17] Cipriani A Furukawa T Salanti G Geddes J Higgins J Churchill R Watanabe N Nakagawa A Omori I McGuire H Tansella M Barbui C Comparative efficacy and acceptability of 12 new-generation antidepressants: a multiple-treatments meta-analysis Lancet 373 746 758 2009 19185342
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.
None of the sources cited for this claim have been checked yet.
In the paper
“Current theories for SSRI- mediated treatment of depression include increased production of BDNF (22), increased hippocampal neurogenesis (23–25) and reduced expression of serotonin autoreceptors (26).”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Discussion
What the sources say
- Not checked yetcites [22] Sen S Duman R Sanacora G Serum brain-derived neurotrophic factor, depression, and antidepressant medications: meta-analyses and implications Biol Psychiatry 2008 9 15 64 6 527 32 18571629 PMC2597158
- Not checked yetcites [23] Malberg J Eisch A Nestler E Duman R Chronic antidepressant treatment increases neurogenesis in adult rat hippocampus J Neurosci 2000 12 15 20 24 9104 10 11124987 PMC6773038
- Not checked yetcites [24] Kempermann G Kronenberg G Depressed new neurons--adult hippocampal neurogenesis and a cellular plasticity hypothesis of major depression Biol Psychiatry 2003 9 1 54 5 499 503 12946878
- Not checked yetcites [25] Eisch AJ Petrik D Depression and hippocampal neurogenesis: a road to remission? Science 2012 10 5 338 72 5 23042885 PMC3756889
- Not checked yetcites [26] Hamon M Blier P Monoamine neurocircuitry in depression and strategies for new treatments Prog Neuropsychopharmacol Biol Psychiatry 2013 8 1 45 54 63 23602950
plaindirect- 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.
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
“For newly generated Aβ, the power of time by treatment group interaction was also > 99.99% while the power of the main effect of treatment was 66.18%.”
- Also stated in: § Study Design · plain
“For newly generated Aβ, the power of time by treatment group interaction was also > 99.99% while the power of the main effect of treatment was 66.18%.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Materials and Methods > Study Design
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.
- Also stated in: § Study Design · plain
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
“In order to account for the within-subject dependencies in the outcome variables, these models incorporated a random intercept at the subject level and, for plaque growth, also a random intercept at the plaque level.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Materials and Methods > Study Design
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.
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 concentrations over the time course were such that steady-state kinetics applied reasonably well after the first 12 hours and the rate of change of concentration appeared similar in both groups.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Discussion
hedged- 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
“Based on the power analysis of the data, for Aβ concentration with alpha=0.05, the power of the time by treatment group interaction was > 99.99% and the power of the main effect of treatment was 95.03%.”
- Also stated in: § Study Design · plain
“Based on a repeated measures ANOVA, with a compound symmetry covariance structure and alpha=0.05, for Aβ concentration the power of the time by treatment group interaction was > 99.99% and the power of the main effect of treatment was 95.03%.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Materials and Methods > Study Design
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.
- Also stated in: § Study Design · 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
“Interestingly, the tracer/tracee ratio (labeled Aβ/unlabeled Aβ) (TTR) over the 37 hours of CSF sampling was overlapping for both groups (Fig. S2 suggesting that the fractional turnover of Aβ was unchanged at the time of the SILK study and that Aβ metabolism had reached a new steady state.”
- Also stated in: § Discussion · hedged
“Tracer kinetics established that the fractional turnover rate in the two groups was very similar suggesting that Aβ metabolism had reached a new steady state at the time when the SILK study was carried out.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Results > Citalopram reduces CSF Aβ production and concentrations in humans
hedged- 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.
- Also stated in: § Discussion · hedged
None of the sources cited for this claim have been checked yet.
In the paper
“In humans, CSF Aβ concentrations begin changing before tau levels; amyloid deposition occurs in the brain decades before the onset of clinical symptoms (3–5).”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Introduction
What the sources say
- Not checked yetcites [3] Price JL Morris JC Tangles and plaques in nondemented aging and “preclinical” Alzheimer’s disease Ann Neurol 45 358 3 1999 10072051
- Not checked yetcites [4] Hardy J Selkoe DJ The amyloid hypothesis of Alzheimer’s disease: progress and problems on the road to therapeutics Science 297 353 7 19 2002 12130773
- Not checked yetcites [5] Bateman RJ Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease N Engl J Med 7 11 2012 PMC3474597 22784036
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.
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
“A randomized double-blind placebo controlled study was performed to determine the central nervous system effect of 60 mg of the SSRI antidepressant citalopram, given in divided oral doses (2 doses of 30 mg each).”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Materials and Methods > Study Design
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.
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
“These data suggest that citalopram reduced CSF Aβ concentrations by suppressing Aβ production while having a negligible effect on Aβ clearance mechanisms.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Results > Citalopram reduces CSF Aβ production and concentrations in humans
hedgeddirect- 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
“For newly generated Aβ, the power of time by treatment group interaction was also > 99.99% while the power of the main effect of treatment was 66.18%.”
- Also stated in: § Study Design · plain
“For newly generated Aβ, the power of time by treatment group interaction was also > 99.99% while the power of the main effect of treatment was 66.18%.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Materials and Methods > Study Design
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.
- Also stated in: § Study Design · 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
“Phosphorylation of either of these secretase enzymes by activated ERK could occur within minutes of SSRI treatment, thus accounting for the rapid changes in Aβ levels.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > 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.
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
“Taken together, these results suggest that citalopram reduces plaque appearance and growth, but has no effect on plaque regression.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Results > Chronic citalopram treatment blocks plaque-growth in APP/PS1 mice
hedgeddirect- 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 models also incorporated a Toeplitz covariance structure for the model errors in basal ISF Aβ, first-order autoregressive process heterogeneous variance covariance structure for the model errors in newly-generated Aβ and the same covariance structure but with homogeneous variance for CSF concentrations of total Aβ and TTR, as these provided the best measures on Akaike’s information criterion (”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Materials and Methods > Study Design
What the sources say
- Not checked yetcites [39] Akaike H A new look at the statistical model identification IEEE Transactions on Automatic Control 19 716 1974
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
“After citalopram treatment in mice, we also found increased α-secretase activity, which appears to be downstream of ERK signaling (30).”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Discussion
What the sources say
- Not checked yetcites [30] Cisse M Duplan E Guillot-Sestier MV Rumigny J Bauer C Pages G Orzechowski HD Slack B Checler F Vincent B The extracellular regulated kinase-1 (ERK1) controls regulated alpha-secretase-mediated processing, promoter transactivation, and mRNA levels of the cellular prion protein J Biol Chem 2011 8 19 286 33 29192 206 21586567 PMC3190726
hedgeddirect- 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
“Another limitation is that our human studies were conducted in young individuals, presumably prior to plaque formation.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Discussion
hedged- 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
“Citalopram is one of the most selective SSRIs for serotonin re-uptake and has among the most favorable side effect profiles compared with other antidepressants (17).”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Results > Citalopram dose-response in aged APP/PS1 mice
What the sources say
- Not checked yetcites [17] Cipriani A Furukawa T Salanti G Geddes J Higgins J Churchill R Watanabe N Nakagawa A Omori I McGuire H Tansella M Barbui C Comparative efficacy and acceptability of 12 new-generation antidepressants: a multiple-treatments meta-analysis Lancet 373 746 758 2009 19185342
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.
None of the sources cited for this claim have been checked yet.
In the paper
“Serotonin receptor levels are reduced in human AD brains (8,9).”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Introduction
What the sources say
- Not checked yetcites [8] Arai H Kosaka K Iizuka R Changes of biogenic amines and their metabolites in postmortem brains from patients with Alzheimer-type dementia J Neurochem 43 388 8 1984 6204013
- Not checked yetcites [9] Reynolds GP 5-Hydroxytryptamine (5-HT)4 receptors in post mortem human brain tissue: distribution, pharmacology and effects of neurodegenerative diseases British journal of pharmacology 114 993 3 1995 7780656 PMC1510307
plaincorrelational- 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.
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
“Admittedly, this model is limited by presuming that production and clearance rates are independent phenomena in the analysis, while practically production and clearance occur simultaneously.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Materials and Methods > Study Design
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.
- The authors state this as an assumption: The model presumes that production and clearance rates are independent phenomena in the analysis.
In the paper
“The accumulation of amyloid-β (Aβ) peptide in the brain and its aggregation into amyloid plaques is currently considered the pathological trigger for AD (2).”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Introduction
What the sources say
- Not checked yetcites [2] Holtzman DM Morris JC Goate AM Alzheimer’s disease: the challenge of the second century Science translational medicine 3 77sr1 4 6 2011 21471435 PMC3130546
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.
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
“Placebo and citalopram treated volunteers were first matched on gender and then as closely as possible in age, always within 5 years.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Results > Citalopram reduces CSF Aβ production and concentrations in humans
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.
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
“Importantly, this effect was seen in the production phase of Aβ with no significant group differences initially, but with subsequent differences that remained throughout the production phase and with no effect on clearance.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > 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.
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
“In addition, since the groups were not explicitly matched on race, at study mid-point the groups were checked by an unblinded research assistant to ensure that they were balanced in racial composition.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Results > Citalopram reduces CSF Aβ production and concentrations in humans
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.
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
“Based on the power analysis of the data, for Aβ concentration with alpha=0.05, the power of the time by treatment group interaction was > 99.99% and the power of the main effect of treatment was 95.03%.”
- Also stated in: § Study Design · plain
“Based on a repeated measures ANOVA, with a compound symmetry covariance structure and alpha=0.05, for Aβ concentration the power of the time by treatment group interaction was > 99.99% and the power of the main effect of treatment was 95.03%.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Materials and Methods > Study Design
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.
- Also stated in: § Study Design · 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
“However, these trials were conducted after the onset of clinical symptoms and thus may have been too late to prevent further disease progression.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > 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.
Probably not a substantial claim.
- Rests on an assumption: There have been many clinical trials using Aβ lowering drugs in AD and MCI that were unsuccessful.
None of the sources cited for this claim have been checked yet.
In the paper
“Activation of serotonin receptors has been shown to reduce Aβ production in vitro; treatment with serotonin or receptor agonists activates intracellular signaling cascades and increases levels of the α-secretase product sAPP-α (10–12).”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Introduction
What the sources say
- Not checked yetcites [10] Arjona AA Pooler AM Lee RK Wurtman RJ Effect of a 5-HT(2C) serotonin agonist, dexnorfenfluramine, on amyloid precursor protein metabolism in guinea pigs Brain Res 951 135 9 27 2002 12231467
- Not checked yetcites [11] Nitsch RM Deng M Growdon JH Wurtman RJ Serotonin 5-HT2a and 5-HT2c receptors stimulate amyloid precursor protein ectodomain secretion J Biol Chem 271 4188 2 23 1996 8626761
- Not checked yetcites [12] Robert SJ Zugaza JL Fischmeister R Gardier AM Lezoualc’h F The human serotonin 5-HT4 receptor regulates secretion of non-amyloidogenic precursor protein J Biol Chem 276 44881 11 30 2001 11584021
boosteddirect- 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
“A limitation of the study is that data were not collected during the eight hours following drug/placebo administration.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Discussion
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.
The paper relies on this without support.
To date, there have not been drugs with both an established safety profile and a mechanism-based rationale that have been tested in primary or secondary prevention trials of AD.
“To date, there have not been drugs with both an established safety profile and a mechanism-based rationale that have been tested in primary or secondary prevention trials of AD.”
The paper relies on this without support.
Early in disease pathogenesis, soluble Aβ monomers aggregate into soluble Aβ oligomers and insoluble Aβ plaques, both of which can alter synaptic transmission and be toxic to neurons under certain conditions.
“Early in disease pathogenesis, soluble Aβ monomers aggregate into soluble Aβ oligomers and insoluble Aβ plaques, both of which can alter synaptic transmission and be toxic to neurons under certain conditions.”
The paper relies on this without support.
Individuals with autosomal dominant AD or Down’s syndrome have only 20–50% higher CSF Aβ42 concentrations than normal but manifest disease 20–30 years before AD patients with the sporadic form of the disease.
“Individuals with autosomal dominant AD or Down’s syndrome have only 20–50% higher CSF Aβ42 concentrations than normal but manifest disease 20–30 years before AD patients with the sporadic form of the disease.”
The paper relies on this without support.
There have been many clinical trials using Aβ lowering drugs in AD and MCI that were unsuccessful.
“A caveat is that there have been many clinical trials using Aβ lowering drugs in AD and MCI that were unsuccessful.”
The paper relies on this without support.
Citalopram has a long half-life.
“Citalopram has a long half-life, meaning there was likely a sustained effect on Aβ throughout CSF sampling despite the single administration at the beginning of the study.”
The authors state this as an assumption.
The model presumes that production and clearance rates are independent phenomena in the analysis.
“Admittedly, this model is limited by presuming that production and clearance rates are independent phenomena in the analysis, while practically production and clearance occur simultaneously.”
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
“Sheline et al. proposed that Citalopram, an SSRI, decreased cerebrospinal fluid (CSF) amyloid beta protein production in a dose-dependent manner in both animal and human studies”
From Risk analysis of use of different classes of antidepressants on subsequent dementia: A nationwide cohort study in Taiwan (2017) · cites this paper as [56]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“and this ability may be a potential preventive strategy for AD [56].”
From Risk analysis of use of different classes of antidepressants on subsequent dementia: A nationwide cohort study in Taiwan (2017) · cites this paper as [56]
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
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Results > Citalopram reduces CSF Aβ production and concentrations in humans
“Healthy subjects age 18–50, without medical disease, electrocardiogram (ECG) or laboratory abnormalities and with no prior history of antidepressant treatment, were enrolled in a double-blind study.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Materials and Methods > Study Design
“Healthy 21–50 year old male and female volunteers were invited to participate, screened, and enrolled.”
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
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Materials and Methods > Study Design
“This technique samples soluble molecules within the extracellular fluid that are smaller than 38-kilodaltons, the molecular-weight cut off of the probe membrane.”
§ An Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice > Materials and Methods > Study Design
“Two millimeter microdialysis probes were inserted through the guides so the membrane was contained entirely within the hippocampus (BR-2, 30-kilodalton MWCO membrane, Bioanalytical Systems).”
Citations
Cites
A new look at the statistical model identification
Akaike, H. (1974) · IEEE Transactions on Automatic Control · doi:10.1109/tac.1974.1100705 · Cited by 51,879
The Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics
Hardy, J., & Selkoe, D. J. (2002) · Science · doi:10.1126/science.1072994 · Cited by 13,864
Amyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
Selenica, M.-L. B., Brownlow, M., Jimenez, J. P., Lee, D. C., Pena, G., Dickey, C. A., Gordon, M. N., & Morgan, D. (2013) · Neurodegenerative Diseases · doi:10.1159/000337230 · Cited by 10,359
Molecular Mechanisms of Depression: Perspectives on New Treatment Strategies
Lang, U. E., & Borgwardt, S. (2013) · Cellular Physiology and Biochemistry · doi:10.1159/000350094 · Cited by 8,526
Everitt, B. S. (2001) · Psychology Press eBooks · doi:10.4324/9781410605542-11 · Cited by 6,877
Dose translation from animal to human studies revisited.
Reagan‐Shaw, S., Nihal, M., & Ahmad, N. (2008) · The FASEB Journal · doi:10.1096/fj.07-9574lsf · Cited by 6,524
Small sample inference for fixed effects from restricted maximum likelihood
Kenward, M. G., & Roger, J. H. (1997) · Biometrics · doi:10.2307/2533558 · Cited by 4,552
Clinical and biomarker changes in dominantly inherited Alzheimer's disease
Bateman, R. J., Xiong, C., Benzinger, T. L. S., Fagan, A. M., Goate, A., Fox, N. C., Marcus, D. S., Cairns, N. J., Xie, X., Blazey, T. M., et al. (2012) · New England Journal of Medicine · doi:10.1056/nejmoa1202753 · Cited by 3,814
Self-citationDiggle, P. J., Heagerty, P. J., Liang, K., & Zeger, S. L. (2002) · doi:10.1093/oso/9780198524847.001.0001 · Cited by 3,388
Chronic antidepressant treatment increases neurogenesis in adult rat hippocampus
Malberg, J. E., Eisch, A. J., Nestler, E. J., & Duman, R. S. (2000) · The Journal of Neuroscience · doi:10.1523/jneurosci.20-24-09104.2000 · Cited by 3,111
Cited by
Sorted by citations
Items 101–200 of 224
Converged avenues: depression and Alzheimer’s disease– shared pathophysiology and novel therapeutics
Bajaj, S., & Mahesh, R. (2024) · Molecular Biology Reports · doi:10.1007/s11033-023-09170-1 · Cited by 25
Escitalopram Ameliorates Forskolin-Induced Tau Hyperphosphorylation in HEK239/tau441 Cells
Ren, Q., Wang, Y., Gong, W.-G., Zhou, Q.-D., Xu, L., & Zhang, Z. (2015) · Journal of Molecular Neuroscience · doi:10.1007/s12031-015-0519-4 · Cited by 24
Preclinical Evidence Supporting Early Initiation of Citalopram Treatment in Machado-Joseph Disease
Esteves, S., Oliveira, S., Duarte‐Silva, S., Cunha‐Garcia, D., Teixeira‐Castro, A., & Maciel, P. (2018) · Molecular Neurobiology · doi:10.1007/s12035-018-1332-1 · Cited by 23
Iatrou, A., Kenis, G., Rutten, B. P. F., Lunnon, K., & van den Hove, D. (2016) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-016-2361-4 · Cited by 22
Joshi, A., Wang, D., Watterson, S., McClean, P. L., Behera, C. K., Sharp, T., & Wong‐Lin, K. (2020) · Neuropharmacology · doi:10.1016/j.neuropharm.2020.108118 · Cited by 22
Serotonergic Regulation in Alzheimer’s Disease
Долгачева, Л. П., Зинченко, В. П., Nadeev, A. D., & Goncharov, N. V. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26115218 · Cited by 21
Johnson, N. R., Wang, A. C.-J., Coughlan, C. M., Sillau, S., Lucero, E., Viltz, L., Markham, N. E., Allen, C., Dhanasekaran, A. R., Chial, H. J., et al. (2022) · Alzheimer s Research & Therapy · doi:10.1186/s13195-022-01020-9 · Cited by 24
Sawant, N. A., Kshirsagar, S., Reddy, P. H., & Reddy, A. P. (2023) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2023.166942 · Cited by 21
Severino, M., Sivasaravanaparan, M., Olesen, L. Ø., von Linstow, C. U., Metaxas, A., Bouzinova, E. V., Khan, A. M., Lambertsen, K. L., Babcock, A. A., Gramsbergen, J. B., et al. (2018) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1016/j.trci.2018.04.005 · Cited by 21
Niotis, K., Saperia, C., Saif, N., Carlton, C., & Isaacson, R. (2024) · Nature Mental Health · doi:10.1038/s44220-023-00191-0 · Cited by 20
Genetics of Aggression in Alzheimer’s Disease (AD)
Lukiw, W. J., & Rogaev, E. I. (2017) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2017.00087 · Cited by 20
Locus coeruleus catecholamines link neuroticism and vulnerability to tau pathology in aging
Parent, J. H., Ciampa, C. J., Harrison, T. M., Adams, J. N., Zhuang, K., Betts, M. J., Maaß, A., Winer, J. R., Jagust, W. J., & Berry, A. S. (2022) · NeuroImage · doi:10.1016/j.neuroimage.2022.119658 · Cited by 20
Galasko, D., Farlow, M. R., Lucey, B. P., Honig, L. S., Elbert, D. L., Bateman, R. J., Momper, J. D., Thomas, R. G., Rissman, R. A., Pa, J., et al. (2024) · Alzheimer s Research & Therapy · doi:10.1186/s13195-024-01490-z · Cited by 19
Self-citationFrameworking memory and serotonergic markers
Meneses, A. (2017) · Reviews in the Neurosciences · doi:10.1515/revneuro-2016-0079 · Cited by 19
Bouter, Y., & Bouter, C. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.883256 · Cited by 18
Serotonergic drugs for the treatment of neuropsychiatric symptoms in dementia
Magierski, R., & Sobów, T. (2016) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.2016.1155453 · Cited by 18
Li, X., Wang, Q., Hu, T., Wang, Y., Zhao, J., Lu, J. N., & Pei, G. (2017) · Scientific Reports · doi:10.1038/s41598-017-04144-3 · Cited by 18
Current Drug Targets in Alzheimer’s Associated Memory Impairment: A Comprehensive Review
Chandrashekar, K. S., Mathew, A., Vignesh Balaji, E., Pai, K. S. R., Kishore, A., Pai, V., & Pemmireddy, R. (2022) · CNS & Neurological Disorders - Drug Targets · doi:10.2174/1871527321666220401124719 · Cited by 18
Mitochondrial Interaction with Serotonin in Neurobiology and Its Implication in Alzheimer’s Disease
Tian, J., Du, E. Y., & Guo, L. (2023) · Journal of Alzheimer s Disease Reports · doi:10.3233/adr-230070 · Cited by 17
Olesen, L. Ø., Sivasaravanaparan, M., Severino, M., Babcock, A. A., Bouzinova, E. V., West, M. J., Wiborg, O., & Finsen, B. R. (2017) · Neurobiology of Disease · doi:10.1016/j.nbd.2017.04.021 · Cited by 17
Dementia: Psychosocial/Mental Health Risk Factors
Nasisi, C. R. (2020) · The Journal for Nurse Practitioners · doi:10.1016/j.nurpra.2020.03.013 · Cited by 17
Park, D. I., Novak, B., Yan, Y., Kaya, M. E., & Turck, C. W. (2020) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2020.05.033 · Cited by 17
Dosing, collection, and quality control issues in cerebrospinal fluid research using animal models
Barten, D. M., Cadelina, G. W., & Weed, M. R. (2017) · Handbook of clinical neurology · doi:10.1016/b978-0-12-804279-3.00004-6 · Cited by 17
Role of Citalopram in the Treatment of Agitation in Alzheimer’s Disease
Porsteinsson, A. P., Keltz, M., & Smith, J. S. (2014) · Neurodegenerative Disease Management · doi:10.2217/nmt.14.35 · Cited by 17
Wang, H., Li, S., Zhang, J., Peng, W., Li, T., & Zhang, J. (2024) · European journal of medical research · doi:10.1186/s40001-024-02006-z · Cited by 16
Khoury, R., & Grossberg, G. T. (2018) · CNS Drugs · doi:10.1007/s40263-018-0590-9 · Cited by 16
Javaherian, K., Newman, B. M., Weng, H., Hassenstab, J. J., Xiong, C., Coble, D. W., Fagan, A. M., Benzinger, T. L. S., & Morris, J. C. (2018) · Alzheimer Disease & Associated Disorders · doi:10.1097/wad.0000000000000284 · Cited by 16
Self-citationAngelopoulou, E., Bougea, A. M., Hatzimanolis, A., Scarmeas, N., & Papageorgiou, S. G. (2024) · Cells · doi:10.3390/cells13131164 · Cited by 15
Repurposing Sigma-1 Receptor-Targeting Drugs for Therapeutic Advances in Neurodegenerative Disorders
Eskandari, K., Bélanger, S.-M., Lachance, V., & Kourrich, S. (2025) · Pharmaceuticals · doi:10.3390/ph18050700 · Cited by 15
Systems biology of Alzheimer’s Disease: a scoping review of key pathways and mechanisms
Bice, P. J., Nho, K. T., Ertekin‐Taner, N., & Saykin, A. J. (2026) · Molecular Neurodegeneration · doi:10.1186/s13024-026-00934-4 · Cited by 14
Putative pathological mechanisms of late-life depression and Alzheimer’s disease
Hasan, S. M. N., Clarke, C., Strand, T., & Bambico, F. R. (2023) · Brain Research · doi:10.1016/j.brainres.2023.148423 · Cited by 13
Brüge, A., Ponimaskin, E. G., & Labus, J. (2025) · Pharmacological Reviews · doi:10.1016/j.pharmr.2025.100071 · Cited by 13
Tian, J., Stucky, C. S., Wang, T., Muma, N. A., Johnson, M. A., & Du, H. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230072 · Cited by 13
Khavinson, V. K., Linkova, N. S., Kozhevnikova, E. O., & Trofimova, S. (2020) · Molecules · doi:10.3390/molecules26010159 · Cited by 13
Cortes-Flores, H., Torrandell-Haro, G., & Brinton, R. D. (2024) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2024.1358568 · Cited by 12
Yang, J., Zhou, J., Zhou, J. L., Wang, H., Sun, Z., Zhu, X., He, Y., Wong, A. H. C., Liu, F., & Wang, G. (2021) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2021.12.051 · Cited by 12
CYP2C19 variant mitigates Alzheimer disease pathophysiology in vivo and postmortem
Benedet, A. L., Yu, L., Labbe, A., Mathotaarachchi, S. S., Pascoal, T. A., Shin, M., Kang, M.-S., Gauthier, S. G., Rouleau, G. A., Poirier, J., et al. (2018) · Neurology Genetics · doi:10.1212/nxg.0000000000000216 · Cited by 12
Self-citationSerotonin and amyloid deposition: A link between depression and Alzheimer’s disease?
Gründer, G., & Cumming, P. D. (2021) · Journal of Neurochemistry · doi:10.1111/jnc.15269 · Cited by 12
Ramos‐Cejudo, J., Corrigan, J. K., Zheng, C., Swinnerton, K. N., Jacobson, S. R., La, J., Betensky, R. A., Osorio, R. S., Madanes, S., Pomara, N., et al. (2024) · Alzheimer's & Dementia · doi:10.1002/alz.13853 · Cited by 11
Zippo, A. G., Castiglioni, I., Borsa, V. M., & Biella, G. E. M. (2015) · Frontiers in Computational Neuroscience · doi:10.3389/fncom.2015.00148 · Cited by 11
Zhang, X., Hatoum, L., Ying, J., & Huang, C. (2025) · Psychoradiology · doi:10.1093/psyrad/kkaf031 · Cited by 11
Poorer aging trajectories are associated with elevated serotonin synthesis capacity
Markova, T. Z., Ciampa, C. J., Parent, J. H., LaPoint, M. R., D’Esposito, M., Jagust, W. J., & Berry, A. S. (2023) · Molecular Psychiatry · doi:10.1038/s41380-023-02177-x · Cited by 10
The impact of Alzheimer’s disease risk factors on the pupillary light response
Sparks, S., Pinto, J., Hayes, G., Spitschan, M., & Bulte, D. P. (2023) · Frontiers in Neuroscience · doi:10.3389/fnins.2023.1248640 · Cited by 10
Sivasaravanaparan, M., Olesen, L. Ø., Severino, M., von Linstow, C. U., Lambertsen, K. L., Gramsbergen, J. B., Hasselstrøm, J. B., Metaxas, A., Wiborg, O., & Finsen, B. R. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220019 · Cited by 10
Shared Mechanisms in Dementia and Depression: The Modulatory Role of Physical Exercise
de Souza, P. B., Rodrigues, A. L. S., & Felice, F. G. D. (2025) · Journal of Neurochemistry · doi:10.1111/jnc.70185 · Cited by 9
Kim, K., Jang, Y. J., Shin, J., Park, M. J., Kim, H., Seong, J., & Jeon, H. J. (2024) · Alzheimer s Research & Therapy · doi:10.1186/s13195-024-01562-0 · Cited by 9
von Linstow, C. U., Waider, J., Bergh, M. S., Anzalone, M., Madsen, C., Nicolau, A. B., Wirenfeldt, M., Lesch, K., & Finsen, B. R. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210581 · Cited by 9
Emilsson, J. F., Andréasson, U., Blennow, K., Eriksson, E., & Zetterberg, H. (2014) · Science Translational Medicine · doi:10.1126/scitranslmed.3010053 · Cited by 9
Khan, N. S., Isaza, J. U., Rouhi, N., Jamani, N. F., Jabeen, S., Gill, A. K., Tsutsui, M., Visser, F., & Sargin, D. (2024) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.3c00626 · Cited by 8
Anxious–depressive symptoms and sleep disturbances across the Alzheimer disease spectrum
Chai, Y., Kojori, E. S., Saykin, A. J., & Yu, M. (2025) · Nature Mental Health · doi:10.1038/s44220-025-00416-4 · Cited by 8
Sheline, Y. I., West, T., Yarasheski, K. E., Jasielec, M. S., Hettinger, J. C., Tripoli, D. L., Xiong, C., Frederiksen, C., Grzelak, M. V., Bateman, R. J., et al. (2014) · Science Translational Medicine · doi:10.1126/scitranslmed.3010609 · Cited by 8
Self-citationChronic Stress, Depression, and Alzheimer’s Disease: The Triangle of Oblivion
Dioli, C., Papadimitriou, G., Megalokonomou, A., Campos‐Marques, C., Sousa, N., & Sotiropoulos, I. (2023) · Advances in experimental medicine and biology · doi:10.1007/978-3-031-31978-5_31 · Cited by 7
Exploring the Complex Relationship Between Antidepressants, Depression and Neurocognitive Disorders
Neațu, M., Ioniță, I., Jugurt, A., Davidescu, E. I., & Popescu, B. O. (2024) · Biomedicines · doi:10.3390/biomedicines12122747 · Cited by 7
Clinical Biomarkers and Novel Drug Targets to Cut Gordian Knots of Alzheimer's Disease
Mir, R. H., Masoodi, M. H., Shah, A. J., Mohi-ud-din, R., Sabreen, S., Wani, T. U., Jan, R., Javed, M. N., & Mir, P. A. (2022) · Current Molecular Pharmacology · doi:10.2174/1874467215666220903095837 · Cited by 6
Aβ mediates Sigma receptor degradation via CaN/NFAT pathway.
Fang, M., Zhang, P., Zhao, Y., Jin, A., & Liu, X. (2016) · Europe PMC (PubMed Central) · Cited by 6
Serotonin and the CNS - New Developments in Pharmacology and Therapeutics
Olivier, B. (2021) · IntechOpen eBooks · doi:10.5772/intechopen.90962 · Cited by 6
Can antidepressant medication relieve agitation in Alzheimer’s disease?
Porsteinsson, A. P., Smith, J. S., Keltz, M., & Antonsdottir, I. M. (2014) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.2014.947964 · Cited by 6
Eroli, F., Johnell, K., Acararicin, Z., Tsagkogianni, C., Zerial, S., Lancia, S., Latorre‐Leal, M., Alanko, V., Hilmer, S. N., Matton, A., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70081 · Cited by 5
Ok, L., Ohlund, L. B., Inkster, A. M., Campbell, K. S. J., Peñaherrera, M. S., Brain, U. M., Sleno, L., Robinson, W. P., Barry, A., Oberlander, T. F., et al. (2025) · PLoS ONE · doi:10.1371/journal.pone.0322090 · Cited by 5
Zhang, X.-H., Tan, C., Zheng, Y.-W., Ma, X., Gong, J.-N., Tan, L., & Xu, W. (2024) · Journal of Affective Disorders · doi:10.1016/j.jad.2024.08.235 · Cited by 5
Intensive control of hypertension and risk of Alzheimer's dementia in older adults with depression
Yeung, A., Kiss, A., & Gallagher, D. (2020) · International Journal of Geriatric Psychiatry · doi:10.1002/gps.5309 · Cited by 5
Do Antidepressants Increase the Risk of Dementia?
Solomonov, N., & Alexopoulos, G. S. (2019) · The American Journal of Geriatric Psychiatry · doi:10.1016/j.jagp.2019.06.004 · Cited by 5
A bibliometric analysis of research on dementia comorbid with depression from 2005 to 2024
Li, X., Su, W., & Cai, L. (2025) · Frontiers in Neuroscience · doi:10.3389/fnins.2025.1508662 · Cited by 4
Identifying synergistic combinations of repurposed treatments for Alzheimer’s Disease
Ballard, C. G., Sultana, J., Doherty, P., Williams, G. H., & Corbett, A. (2025) · The Journal of Prevention of Alzheimer s Disease · doi:10.1016/j.tjpad.2025.100329 · Cited by 5
Booth, S., & Ko, J. H. (2024) · Nuclear Medicine and Molecular Imaging · doi:10.1007/s13139-024-00842-9 · Cited by 4
Psychiatry for People of African Descent in the USA
Bell, C. C., & McBride, D. F. (2013) · Springer eBooks · doi:10.1007/978-1-4614-8918-4_6 · Cited by 4
Kim, J., Ha, T. H., Kim, K., Lee, E.-M., Kim, H., Kim, D. K., Won, H., Lewis, M., Lee, H., & Myung, W. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-200994 · Cited by 4
Liao, M.-H., Lin, Y., Gau, F.-Y., Tseng, C., Wu, D.-C., Hsu, C.-Y., Chung, K., Li, R., Hu, C., Then, C. K., et al. (2024) · Frontiers in Pharmacology · doi:10.3389/fphar.2023.1260838 · Cited by 4
Serotonergic Modulators in Alzheimer's Disease: A Hope in the Hopeless Condition
Almohmadi, N. H., Al‐Kuraishy, H. M., Al‐Gareeb, A. I., Albuhadily, A. K., Fakhry, M., Alexiou, A. T., Papadakis, M., & Batiha, G. E. (2025) · Chemistry & Biodiversity · doi:10.1002/cbdv.202403401 · Cited by 3
Use of Common Psychiatric Medications and Risk and Prognosis of Amyotrophic Lateral Sclerosis
Chourpiliadis, C. P., Lovik, A., Ingre, C., Press, R., Samuelsson, K., Valdimarsdóttir, U. A., & Fang, F. (2025) · JAMA Network Open · doi:10.1001/jamanetworkopen.2025.14437 · Cited by 3
Stress and the risk of Alzheimer dementia: Can deconstructed engrams be rebuilt?
Jeanneteau, F. D. (2023) · Journal of Neuroendocrinology · doi:10.1111/jne.13235 · Cited by 3
Keegan, A. P., Stough, C. K. K., Paris, D., Luis, C. A., Abdullah, L. I., Ait‐Ghezala, G., Chaykin, J., Crawford, F., & MULLAN, M. J. (2023) · Neurological Research · doi:10.1080/01616412.2023.2294581 · Cited by 3
Sex-Related Differences in Alzheimer’s Disease
Acar, D., & King, C. J. (2019) · Springer eBooks · doi:10.1007/978-3-030-04245-5_25 · Cited by 3
Stable Isotope Labeling Kinetics in CNS Translational Medicine: Introduction to SILK Technology
Bateman, R. J., West, T., Yarasheski, K. E., Patterson, B. W., Lucey, B. P., Cirrito, J. R., Lehmann, S., Hirtz, C., Gabelle, A., Miller, T. M., et al. (2019) · Handbook of behavioral neuroscience · doi:10.1016/b978-0-12-803161-2.00011-4 · Cited by 3
Self-citationCould antidepressant drugs aid Alzheimer disease prevention?
Wood, H. B. (2020) · Nature Reviews Neurology · doi:10.1038/s41582-020-00422-3 · Cited by 3
Jansen, C. U., & Qvortrup, K. M. (2021) · IntechOpen eBooks · doi:10.5772/intechopen.96381 · Cited by 3
Barnwal, M., Baksh, S. N., Ismail, Z., Shade, D. M., Moghekar, A., Ho, S. G., Rosenberg, P. B., Porsteinsson, A. P., & Lyketsos, C. G. (2026) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1002/trc2.70203 · Cited by 2
Han, Y., Liu, L., Li, C., Ge, X., Chen, Q., Li, Q., Li, H., Li, W., & Initiative, A. D. N. (2026) · Journal of Molecular Neuroscience · doi:10.1007/s12031-026-02497-x · Cited by 2
Trajectories of late-life depression: insights from molecular imaging
Holmes, S. E., & Smith, G. S. (2026) · Neuropsychopharmacology · doi:10.1038/s41386-026-02340-2 · Cited by 2
Neuroinflammation in Neurological Dysfunction and Degeneration
Chen, S., Oyarzabal, E. A., Santos, J. H., Wang, Q., Jiang, L., & Hong, J. (2015) · Elsevier eBooks · doi:10.1016/b978-0-12-800228-5.00018-2 · Cited by 2
Abdel-Rahman, M., Abdel-kader, S., Elmasry, H. A., & El‐Hennamy, R. E. (2020) · Egyptian Journal of Basic and Applied Sciences · doi:10.1080/2314808x.2020.1763033 · Cited by 2
Chapter 20. Psychopharmacology
Mulsant, B. H., & Pollock, B. G. (2022) · American Psychiatric Association Publishing eBooks · doi:10.1176/appi.books.9781615375196.ds20 · Cited by 1
(2024) · Frontiers research topics · doi:10.3389/978-2-8325-4734-2 · Cited by 1
Hernández‐Velázquez, E. D., Chávez‐Rivera, R., Ortíz‐Alvarado, R., & Solorio‐Alvarado, C. R. (2025) · Bioorganic Chemistry · doi:10.1016/j.bioorg.2025.109245 · Cited by 1
Desai, A., Agbomi, L. L., Imeh‐Nathaniel, A., Nathaniel, E. I., Roley, L. T., Goodwin, R. L., & Nathaniel, T. I. (2025) · Geriatric Nursing · doi:10.1016/j.gerinurse.2025.103769 · Cited by 1
Reconsidering Animal Models of Major Depressive Disorder in the Elderly
Toda, S., Iguchi, Y., Lin, Z., Nishikawa, H., Nagasawa, T., Watanabe, H., & Minabe, Y. (2016) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2016.00188 · Cited by 1
Ritsema, T. S. (2018) · JAAPA · doi:10.1097/01.jaa.0000547742.77686.2f · Cited by 1
Elderly patients with cognitive impairments on an ambulance care
Богданова, Т. А., Turusheva, A. V., Frolova, E. V., & Логунов, Д. Л. (2021) · Russian Family Doctor · doi:10.17816/rfd70198 · Cited by 1
Widespread Diseases of the Twenty-First Century
Gründer, G. (2022) · Springer eBooks · doi:10.1007/978-3-662-64225-2_5 · Cited by 1
The intricate connection between depression and dementia as a major challenge for clinicians
Ronchetto, F., & Ronchetto, M. (2022) · Journal of Gerontology and Geriatrics · doi:10.36150/2499-6564-n518 · Cited by 1
Chapter 14. Citalopram and Escitalopram
Shelton, R. C. (2024) · American Psychiatric Association Publishing eBooks · doi:10.1176/appi.books.9781615375523.as14 · Cited by 1
Depression in Alzheimer's disease : biomarkers and treatment
Enache, D. (2015) · Figshare · Cited by 1
Fišar, Z., Hroudová, J., Zvěřová, M., Jirák, R., Vaněčková, M., & Raboch, J. (2022) · Research Square · doi:10.21203/rs.3.rs-2402088/v1 · Cited by 1
Citalopram drives down amyloid-β
Harrison, C. (2014) · Nature Reviews Drug Discovery · doi:10.1038/nrd4378
Antidepressant Decreases Amyloid-Beta in AD Mice, Healthy People
Talan, J. (2014) · Neurology Today · doi:10.1097/01.nt.0000451830.73217.d1
Might SSRIs Reduce the Risk for Alzheimer Disease
Yager, J. (2014) · Journal watch · doi:10.1056/nejm-jw.na34689
Hettinger, J. C. (2017) · Open Scholarship Institutional Repository (Washington University in St. Louis) · doi:10.7936/k7jq10fn
Promoting Health Behaviors For Aging Persons
Alexopoulos, G. S. (2018) · American Journal of Geriatric Psychiatry · doi:10.1016/j.jagp.2018.12.024
Synthèse et évaluation biologique de ligands multi-cibles dirigés contre le système sérotoninergique
Hatat, B. (2019) · theses.fr (ABES) · doi:10.70675/50eb6d10z22edz4734za36bzc4a1894bd494
Identification de nouvelles molécules anti-prions et caractérisation de leurs modes d'action
Bamia, A. (2019) · theses.fr (ABES) · doi:10.70675/f788ba19zfa70z4533zabaaz843dc358343c
Metadata
- Authors
- Sheline, Y. I., West, T., Yarasheski, K., Swarm, R., Jasielec, M. S., Fisher, J. R., Ficker, W. D., Yan, P., Xiong, C., Frederiksen, C., Grzelak, M. V., Chott, R., Bateman, R. J., Morris, J. C., Mintun, M. A., Lee, J.-M., & Cirrito, J. R.
- Affiliations
- University of Pennsylvania (US)
- C2N Diagnostics (United States) (US)
- Washington University in St. Louis (US)
- Avid Radiopharmaceuticals (United States) (US)
- Corresponding author
- Sheline, Yvette I.
- ORCID
- Venue
- Science Translational Medicine
- Published
- 2014-05-14
- Volume
- 6
- Issue
- 236
- Pages
- 236re4-236re4
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC4269372
- OpenAlex
- W2163894029
- Semantic Scholar
- 60d1eff17ddf2e7b53b76651fafa944ed8ffb4f3
- Cited by
- 223
- References
- 43
- Citations by year
- 2026: 8 · 2025: 18 · 2024: 19 · 2023: 11 · 2022: 19 · 2021: 17 · 2020: 21 · 2019: 14 · 2018: 24 · 2017: 17 · 2016: 18 · 2015: 24 · 2014: 12
- FWCI
- 8.69
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5p60dk020579-35)
- National Institute on Aging (R01AG042513, R01AG041502, R21AG039690)
- National Institute of Mental Health (K24MH079510)
- National Institute of General Medical Sciences (R24GM136766, P41GM103422)
- National Institute of Diabetes and Digestive and Kidney Diseases (P60-DK-020579, P30DK056341, P30DK020579)
- National Institute of Neurological Disorders and Stroke (R21NS082529, R01NS067905)
- 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
- Health Sciences › Medicine › Pharmacology (medical) › Cholinesterase and Neurodegenerative Diseases
- Keywords
- citalopram, serotonin signaling, amyloid-beta, Alzheimer's disease, cerebrospinal fluid, amyloid plaques, APP/PS1 mice, selective serotonin reuptake inhibitors, amyloid-beta production, drug-target engagement, Alzheimer's disease prevention
- MeSH terms
- Adult, Alzheimer Disease, Animals, Antidepressive Agents, Brain, Dose-Response Relationship, Drug, Double-Blind Method, Enzyme-Linked Immunosorbent Assay, Female, Humans, Male, Mice, Inbred C3H, Mice, Transgenic, Middle Aged, Prospective Studies, Serotonin, Citalopram, Signal Transduction, Amyloid beta-Protein Precursor, Selective Serotonin Reuptake Inhibitors, Microdialysis, Mice, Young Adult, Plaque, Amyloid
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 2026-11-07, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-11-07 (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.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
