The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index; 12 of the 34 sources its claims cite were checked for support.
BRI2 (ITM2b) Inhibits A Deposition In Vivo
Open accessAbstract
Analyses of the biologic effects of mutations in the BRI2 (ITM2b) and the amyloid beta precursor protein (APP) genes support the hypothesis that cerebral accumulation of amyloidogenic peptides in familial British and familial Danish dementias and Alzheimer's disease (AD) is associated with neurodegeneration. We have used somatic brain transgenic technology to express the BRI2 and BRI2-Abeta1-40 transgenes in APP mouse models. Expression of BRI2-Abeta1-40 mimics the suppressive effect previously observed using conventional transgenic methods, further validating the somatic brain transgenic methodology. Unexpectedly, we also find that expression of wild-type human BRI2 reduces cerebral Abeta deposition in an AD mouse model. Additional data indicate that the 23 aa peptide, Bri23, released from BRI2 by normal processing, is present in human CSF, inhibits Abeta aggregation in vitro and mediates its anti-amyloidogenic effect in vivo. These studies demonstrate that BRI2 is a novel mediator of Abeta deposition in vivo.
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TL;DR
Using somatic brain transgenesis in APP mouse models, the authors show that wild-type BRI2, like BRI2-Aβ1-40, reduces cerebral Aβ deposition without altering APP processing or inducing anti-Aβ antibodies. The effect is mediated by the secreted Bri2-23 peptide, which is present in human CSF and inhibits Aβ1-42 aggregation in vitro.
Key findings
- rAAV1-delivered BRI2-Aβ1-40 suppressed parenchymal Aβ1-40 and Aβ1-42 accumulation in TgCRND8 mice, validating the somatic brain transgenic method; unexpectedly, wild-type human BRI2 also reduced Aβ deposition to an equivalent extent.
- BRI2del244-266, which lacks the Bri2-23 peptide, had no significant effect on Aβ loads, indicating the Bri2-23 sequence is required for the anti-amyloidogenic effect in vivo.
- Bri2-23 inhibited Aβ1-42 aggregation in vitro; after 120–200 h, it inhibited aggregation by 46 ± 9% (n = 6; p = 0.0004), and native gel/AFM assays supported a net inhibitory effect on amyloid formation.
- Bri2-23 was detected by HPLC/MS in conditioned media from BRI2-transfected cells and in human CSF from all samples tested, including three normal subjects shown.
Methods
- rAAV1 constructs expressing BRI2, BRI2-Aβ1-40, BRI2del244-266, eGFP, or nonspecific scFv were injected intracerebroventricularly into postnatal day 0 TgCRND8 or Tg2576 APP mice; controls totaled n = 20 (noninjection n = 4, PBS n = 4, eGFP n = 5, nonspecific scFv n = 7), and experimental groups were BRI2-Aβ1-40 (n = 11), BRI2 (n = 8), and BRI2del244-266 (n = 13).
- Aβ deposition was assessed by anti-total Aβ immunostaining, cortical plaque burden, Thio S-positive plaque counts, and Aβ end-specific ELISAs of SDS-soluble and formic acid-insoluble brain extracts; plasma Aβ and anti-Aβ IgG were also measured.
- In vitro aggregation was analyzed by native gel electrophoresis, thioflavin T fluorescence, and atomic force microscopy; Bri2-23 was detected by HPLC/mass spectrometry in cell media and human CSF.
Limitations
- The paper states it cannot completely rule out subtle effects on Aβ generation that could influence deposition, and that further study of BRI2/Bri2-23 and related peptides is required to fully understand their anti-amyloidogenic action and other functions.
- Evident from the text: in vivo evidence comes from APP transgenic mouse models with viral overexpression, not from endogenous BRI2 manipulation or human disease cohorts; human CSF evidence is limited to detection of Bri2-23 in normal CSF samples shown, and no cognitive or neurodegeneration outcomes are reported.
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Claims the paper makes
34 Own result · 17 Own interpretation · 7 No full text of the sources · 6 Partly supported · 4 Supported · 4 Sources not found · 4 Own method · 2 Not checked yet · 1 Supported so far · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Notably, synthetic ABri and ADan undergo rapid aggregation and fibrillization into amyloid, and they are neurotoxic (Gibson et al., 2005;Ghiso et al., 2006).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Introduction
What the sources say
- Not checked — no full text of the sourcecites Gibson et al., 2005 source
- Partly supportedcites Ghiso et al., 2006 sourceExperimental — accuracy not yet measured
The Abstract (page not provided) identifies ABri and ADan as amyloid peptides and reports that both form ion-channel-like structures in reconstituted membranes. The References name a study of ADan neurotoxicity, but the passages do not establish that synthetic ABri and ADan are both neurotoxic. (LLM, conf=0.68)
plain- Asserted: passes — The authors put it forward as true.
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The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“By crossing BRI2-A1-40 or BRI-A1-42 transgenic mice with Tg2576 mice, we previously demonstrated that A1-40 and A42 have opposing effects on amyloid deposition (McGowan et al., 2005;Kim et al., 2007).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Introduction
What the sources say
- Partly supportedcites McGowan et al., 2005 sourceExperimental — accuracy not yet measured
The Results report that crossing BRI-Aβ42 mice with Tg2576 mice markedly increased amyloid deposition. The Discussion reports that BRI-Aβ40 mice did not develop deposits on their own, but our copy does not report a BRI-Aβ40/Tg2576 cross or show that Aβ40 had an opposing effect on deposition in crossed mice. (LLM, conf=0.88)
- Partly supportedcites Kim et al., 2007 sourceExperimental — accuracy not yet measured
The Results section reports 60–90% less amyloid deposition in BRI-Aβ40/Tg2576 mice than in Tg2576 littermates. The Abstract states that Aβ42 promotes deposition while Aβ40 inhibits it, and the Generation of mice section says both BRI lines were crossed with Tg2576. But the passages do not establish the opposing effects on deposition by comparing both types of Tg2576 cross; the Aβ42 deposition evidence described in the Introduction concerns BRI-Aβ42 mice. (LLM, conf=0.84)
boosteddirect- Asserted: passes — The authors put it forward as true.
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- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Notably, synthetic ABri and ADan undergo rapid aggregation and fibrillization into amyloid, and they are neurotoxic (Gibson et al., 2005;Ghiso et al., 2006).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Introduction
What the sources say
- Not checked — no full text of the sourcecites Gibson et al., 2005 source
- Partly supportedcites Ghiso et al., 2006 sourceExperimental — accuracy not yet measured
The Abstract identifies ABri and ADan as the main components of amyloid fibrils in familial British and Danish dementias. It does not establish that synthetic versions of both peptides aggregate or fibrillize rapidly; searches for “synthetic,” “aggregation,” and “fibrillization” found no passage reporting that behavior. (LLM, conf=0.82)
plaindirect- Asserted: passes — The authors put it forward as true.
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Every source the paper cites for this claim was checked and supports it.
In the paper
“Analyses of the biologic effects of mutations in the BRI2 (ITM2b) and the amyloid  precursor protein (APP) genes support the hypothesis that cerebral accumulation of amyloidogenic peptides in familial British and familial Danish dementias and Alzheimer's disease (AD) is associated with neurodegeneration.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Abstract
What the sources say
- Supportedcites Golde, 2003 source
In “Toward a complete understanding of AD pathogenesis,” the paper describes British familial dementia and familial Danish dementia as disorders with amyloidogenic peptide accumulation, tangles, and neuronal loss, and links that accumulation to dementia. The same section describes APP mutations that increase or alter Aβ and evidence connecting Aβ to neurotoxicity in Alzheimer’s disease. (LLM, conf=0.91)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The reduction in A deposition observed in the mice expressing the rAAV1 BRI2-A1-40 transgene was consistent with our previous transgenic mice studies (Kim et al., 2007), whereas the reduction of A deposition observed in the mice expressing BRI2 was unexpected.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > BRI2 and BRI2-A1-40 suppress amyloid deposition in APP transgenic mice
What the sources say
- Supportedcites Kim et al., 2007 source
The section on bitransgenic BRI-Aβ40/Tg2576 mice reports substantially reduced Aβ deposition compared with Tg2576 littermates. That transgenic finding supports the citing sentence’s claim that the later rAAV1 BRI2-Aβ1-40 result was consistent with the previous mouse studies; the cited paper need not have studied the rAAV1 mice themselves. (LLM, conf=0.92)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- 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
“The studies with BRI2-A1-40 confirmed previous studies obtained using conventional transgenic mice expressing BRI2-A1-40 (McGowan et al., 2005;Kim et al., 2007).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
What the sources say
- Not checked yetcites McGowan et al., 2005 source
Checked before — its earlier verdict is held back until a new check runs.
- Supportedcites Kim et al., 2007 source
The Generation of mice section describes conventional transgenic mice expressing BRI-Aβ40. The results section reports that crossing these mice with Tg2576 mice markedly reduced amyloid deposition, making this paper an example of the earlier conventional-transgenic work identified by the citation. (LLM, conf=0.90)
plain- Asserted: passes — The authors put it forward as true.
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- Not checked yet
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
“BRI2-A1-40 expression slightly increased plasma A40 levels, attributable to brain to plasma efflux of A1-40; plasma A1-42 levels were not significantly changed by BRI2 expression (Fig. 2 D).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > BRI2 and BRI2-A1-40 suppress amyloid deposition in APP transgenic mice
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
“There was no evidence for an anti-A titer in any of the rAAV1injected mice (Fig. 2 F).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > BRI2 and BRI2-A1-40 suppress amyloid deposition in APP transgenic mice
plain- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Additional data indicate that the 23 aa peptide, Bri23, released from BRI2 by normal processing, is present in human CSF, inhibits A aggregation in vitro and mediates its anti-amyloidogenic effect in vivo.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Abstract
hedged- Asserted: passes — The authors put it forward as true.
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In the paper
“Expression of BRI2-A1-40 mimics the suppressive effect previously observed using conventional transgenic methods, further validating the somatic brain transgenic methodology.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Abstract
plaindirect- 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
“Moreover, levels of endogenous rodent A levels in the brains of the nontransgenic littermates of the TgCRND8 mice expressing the BRI2 transgene were not altered (Fig. 2C).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > BRI2 and BRI2-A1-40 suppress amyloid deposition in APP transgenic mice
plain- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Unexpectedly, we also find that expression of wild-type human BRI2 reduces cerebral A deposition in an AD mouse model.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Abstract
plaindirect- 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
“BRI2-A1-40 expression slightly increased plasma A40 levels, attributable to brain to plasma efflux of A1-40; plasma A1-42 levels were not significantly changed by BRI2 expression (Fig. 2 D).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > BRI2 and BRI2-A1-40 suppress amyloid deposition in APP transgenic mice
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.
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In the paper
“As in the studies of BRI2-A transgenic mice crossed into Tg2576 mice (McGowan et al., 2005;Kim et al., 2007), we found no evidence for alterations in the steady-state levels of APP or APP CTF in TgCRND8 mice expressing the virally delivered BRI2-A1-40 or BRI2 transgenes (Fig. 2 A, B).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > BRI2 and BRI2-A1-40 suppress amyloid deposition in APP transgenic mice
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Addition of Bri2-23 or A1-40 to the reaction resulted in retention of the monomeric A1-42 signal, suggesting direct inhibition of aggregation (Fig. 3A, compare lane 10 with lanes 4, 6, and 8).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Bri2-23 inhibits A1-42 aggregation in vitro
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“rAAV1-mediated delivery of BRI2 to P0 Tg2576 did not lower steady-state A levels in brains of 2-month-old mice.(Fig. 2 E).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > BRI2 and BRI2-A1-40 suppress amyloid deposition in APP transgenic mice
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.
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- Rests on an assumption: Because of the rapid onset of Aβ deposition in TgCRND8 mice, it is not possible to measure steady-state Aβ levels.
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
“These analyses revealed a dramatic suppressive effect of both the BRI2-A1-40 and BRI2 transgenes on parenchymal A1-40 and A1-42 accumulation as measured by biochemical and histochemical assessments of A levels (Fig. 1C-E).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > BRI2 and BRI2-A1-40 suppress amyloid deposition in APP transgenic mice
boosteddirect- 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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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
“Additional data indicate that the 23 aa peptide, Bri23, released from BRI2 by normal processing, is present in human CSF, inhibits A aggregation in vitro and mediates its anti-amyloidogenic effect in vivo.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Abstract
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The Bri2-23 peptide is present in human CSF”
- Also stated in: § The Bri2-23 sequence is required to suppress A deposition in vivo · plain
“We then tested normal human CSF and were able to detect the endogenously secreted Bri2-23 peptide in all samples tested (Fig. 4G).”
- Also stated in: § Discussion · plain
“Spectra from the CSF of three normal subjects each yielded a peak absent from the blank with an assessed mass-to-charge ratio nearly identical to the Bri2-23 peptide standard.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > The Bri2-23 sequence is required to suppress A deposition in vivo
plainn = 3- Asserted: passes — The authors put it forward as true.
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- Also stated in: § The Bri2-23 sequence is required to suppress A deposition in vivo · 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
“We demonstrate that expression of the BRI2del244 -266 construct that lacks a secreted peptide sequence has no effect on A deposition after expression in vivo.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
boosted- Asserted: passes — The authors put it forward as true.
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In the paper
“The novel result from these studies was the finding that BRI2 suppresses A deposition in APP CRND8 transgenic mice to an extent equivalent to A1-40.”
- Also stated in: § Discussion · plain
“BRI2 expression inhibits A deposition in vivo.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
plaindirect- Asserted: passes — The authors put it forward as true.
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- Also stated in: § 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 expression of BRI2 did not lower the steady-state A levels compared with control group.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Atomic force microscopy (AFM) imaging confirmed the inhibitory effects of Bri2-23 on A1-42 aggregation in these assays (Fig. 3D).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Bri2-23 inhibits A1-42 aggregation in vitro
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“B, Quantification of APP and CTF protein level after normalization to -actin level showed no change in the relative levels of both proteins in all groups.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Prolonged incubations of Bri2-23, by itself, did not result in aggregation or -sheet formation as assessed by ThT fluorescence assay, change in circular dichroism spectra, or insolubility (data not shown) (Gibson et al., 2005).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Bri2-23 inhibits A1-42 aggregation in vitro
What the sources say
- Not checked — no full text of the sourcecites Gibson et al., 2005 source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Analyses of A loads showed no significant difference between BRI2del244 -266 and the control groups (Fig. 4 B-D).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > The Bri2-23 sequence is required to suppress A deposition in vivo
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
“Quantification by an ELISA capable of only recognizing monomeric A confirmed that the Bri2-23 peptide retained A1-42 in its monomeric state, and this effect was more robust with increasing concentrations of Bri2-23 (Fig. 3B).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Bri2-23 inhibits A1-42 aggregation in vitro
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“C, The steady-state endogenous mouse A levels in nontransgenic littermates of TgCNRD8 mice, measured by rodent A-specific ELISA, were comparable between PBS injection control and rAAV1-BRI2 group.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
plain- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Bri2-23 peptide inhibits A aggregation in vitro.”
- Also stated in: § Discussion · boosted
“Coupled with their inhibition of aggregation in vitro, we conclude that the A1-40 and Bri2-23 peptides are directly responsible for reduced A deposition in our experiments rather than any other part of the BRI2 protein scaffold on which they were delivered.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
boosteddirect- Asserted: passes — The authors put it forward as true.
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- Also stated in: § 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
“Although it is not possible to completely rule out subtle effects on A generation that could influence deposition, we found no evidence that the suppressive effect was mediated by alterations in APP processing or A production.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
hedged- Asserted: passes — The authors put it forward as true.
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In the paper
“Cerebral expression of BRI2 and BRI2-A1-40 in TgCRND8 mice did not trigger anti-A immune response in all groups, except in the positive control group immunized with fibrillar A42.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
plain- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“There was no change in A level in BRI2 group, compared with no injection control group.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > 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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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
“Quantification by an ELISA capable of only recognizing monomeric A confirmed that the Bri2-23 peptide retained A1-42 in its monomeric state, and this effect was more robust with increasing concentrations of Bri2-23 (Fig. 3B).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Bri2-23 inhibits A1-42 aggregation in vitro
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“BRI2-A1-40-injected TgCRND8 mice had significantly increased plasma A40 levels, compared with no injection and BRI2 injection groups (*p Ͻ 0.05).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
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In the paper
“A42 levels were comparable between all groups ( p Ͼ 0.05).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
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In the paper
“After 120 -200 h of incubation, Bri2-23 inhibited A1-42 aggregation by 46 Ϯ 9% (n ϭ 6; p ϭ 0.0004).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Bri2-23 inhibits A1-42 aggregation in vitro
plaindirectn = 6- Asserted: passes — The authors put it forward as true.
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In the paper
“This methodology of gene transfer, which we have termed somatic brain transgenesis, leads to consistent widespread and permanent expression of the transgene in forebrain and hippocampal neurons (Fig. 1 A) and enables one to rapidly and cost-effectively evaluate the effects of transgene expression on the amyloid deposition phenotype (Levites et al., 2006b).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Introduction
What the sources say
- Not matchedcites Levites et al., 2006b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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In the paper
“BRI2-A1-40 expression slightly increased plasma A40 levels, attributable to brain to plasma efflux of A1-40; plasma A1-42 levels were not significantly changed by BRI2 expression (Fig. 2 D).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > BRI2 and BRI2-A1-40 suppress amyloid deposition in APP transgenic mice
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In the paper
“Biochemical and histochemical A loads in the control groups were equivalent.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Materials and Methods
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In the paper
“It is expressed at high levels in the brain and cleaved by furin or furin-like proteases at its C terminus to produce a 23 aa peptide (Bri2-23) (Kim et al., 1999;Choi et al., 2004) (Fig. 1 B).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Introduction
What the sources say
- Not checked — no full text of the sourcecites Kim et al., 1999 source
- Not matchedcites Choi et al., 2004
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“This methodology of gene transfer, which we have termed somatic brain transgenesis, leads to consistent widespread and permanent expression of the transgene in forebrain and hippocampal neurons (Fig. 1 A) and enables one to rapidly and cost-effectively evaluate the effects of transgene expression on the amyloid deposition phenotype (Levites et al., 2006b).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Introduction
What the sources say
- Not matchedcites Levites et al., 2006b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- 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
“Collectively, these results in TgCRND8, wild-type TgCRND8 littermates, and Tg2576 mice demonstrate that the reduction of A accumulation by BRI2 and BRI2-A1-40 transgenes was not likely to be attributable to alterations in APP processing resulting from altered A production or induction of an anti-A immune response.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > BRI2 and BRI2-A1-40 suppress amyloid deposition in APP transgenic mice
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- Rests on an assumption: Anti-Aβ antibodies reduce Aβ deposition in mice.
- Rests on an assumption: Expression of virally encoded Aβ peptides in the periphery generates an anti-Aβ response.
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
“Thus, there are clear pathological and clinical similarities between FBD, FDD, and Alzheimer's disease (AD).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Introduction
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In the paper
“Additional data indicate that the 23 aa peptide, Bri23, released from BRI2 by normal processing, is present in human CSF, inhibits A aggregation in vitro and mediates its anti-amyloidogenic effect in vivo.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Abstract
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In the paper
“These studies demonstrate that BRI2 is a novel mediator of A deposition in vivo.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Abstract
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In the paper
“Together with the data demonstrating that Bri2-23 directly inhibits A aggre- gation in vitro, these data support an anti-amyloidogenic function for BRI2 mediated by the Bri2-23 peptide.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > The Bri2-23 sequence is required to suppress A deposition in vivo
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In the paper
“We validated this methodology by detecting untagged Bri2-23 peptide secretion from H4 cells transfected with BRI2 but not BRIdel244 -266 (Fig. 4 F).”
- Also stated in: § Discussion · plain
“Synthetic Bri2-23 yielded a peak that was in excellent agreement with its predicted mass-to-charge ratio (m/z) of 2630.”
- Also stated in: § Discussion · plain
“Spectra from the conditioned media of cells transiently transfected with pcDNA3-BRI2 yielded a peak absent from both the blank and conditioned media from cells transfected with pcDNA3 BRI2del-244 -266.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > The Bri2-23 sequence is required to suppress A deposition in vivo
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In the paper
“In support of our observations, Bri2-23 contains the sequence FENKF that is homologous to peptide-based A aggregation inhibitors incorporating a FxxxF motif (Sato et al., 2006).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
What the sources say
- Not checked — no full text of the sourcecites Sato et al., 2006 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“These later data and the lack of anti-amyloidogenic effect from BRI2del244 -266 demonstrate that the Bri2-23 peptide sequence is critical for the inhibitory effect of BRI2 in vivo.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > The Bri2-23 sequence is required to suppress A deposition in vivo
boosteddirect- 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
“These observations suggested that the anti-amyloidogenic effect of the BRI2 protein is mediated by an interaction between Bri2-23 and A.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > The Bri2-23 sequence is required to suppress A deposition in vivo
hedgeddirect- 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
“This finding strengthens the notion that the anti-aggregation effects of Bri2-23 peptide in our experiments may be physiologically relevant to human AD, FDD, and FBD.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > The Bri2-23 sequence is required to suppress A deposition in vivo
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In the paper
“Our mouse data suggested that endogenous BRI2 could function, at least in part, by secretion of the Bri2-23 peptide as an antiamyloidogenic binding partner of A.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > The Bri2-23 sequence is required to suppress A deposition in vivo
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“These data support a novel approach to AD therapy or prevention based on increasing levels of BRI2 and more specifically the Bri2-23 peptide in the brain.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
plaindirect- 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
“Coupled with their inhibition of aggregation in vitro, we conclude that the A1-40 and Bri2-23 peptides are directly responsible for reduced A deposition in our experiments rather than any other part of the BRI2 protein scaffold on which they were delivered.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
plaindirect- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: BRI2del244-266 encodes a protein containing the region of BRI2 previously shown to interact with APP and interfere with APP processing in cell culture.
- Rests on an assumption: BRI2 and BRI2-A1-40 are cleaved by furin and other kex2 proteases to release Bri2-23 and A1-40, respectively.
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 robust inhibitory effect of BRI2 on A deposition in vivo and aggregation in vitro BRI2 indicates that BRI2 is a novel factor that modulates A aggregation and deposition.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
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In the paper
“BRI2del244 -266 construct does not encode the Bri2-23 peptide.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“The Bri2-23 peptide is required for the anti-amyloidogenic effect of the BRI2 protein in vivo and is present in human CSF.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“These later findings suggest that the FDD-linked BRI2 mutation may corrupt a normally protective anti-amyloidogenic mechanism resulting in coaggregation of the mutant peptide with a normal binding partner.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
hedgedconditional- Asserted: passes — The authors put it forward as true.
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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
“Moreover, solid-state nuclear magnetic resonance analysis demonstrated direct binding of an 8 aa peptide containing the sequence FEGKF with the glycine zipper (G33xxxG37) segment of A1-40, a sequence proposed to be critical for formation and stability of -sheet structure (Liu et al., 2005;Sato et al., 2006).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
What the sources say
boostedcorrelational- 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
“Instead, we find that the suppressive effect of BRI2 is likely to be mediated by inhibition of A aggregation by the secreted peptide.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: BRI2 and BRI2-A1-40 are cleaved by furin and other kex2 proteases to release Bri2-23 and A1-40, respectively.
In the paper
“Thus, the somatic brain transgenic BRI2-A1-40 studies provide additional validation for this rapid cost-effective method of manipulating gene expression in the brain (Levites et al., 2006b).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
What the sources say
- Not matchedcites Levites et al., 2006b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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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- Not matched
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, Somatic brain transgenesis results in consistent transduction of forebrain and hippocampal neurons.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
plaindirectn = 3- Asserted: passes — The authors put it forward as true.
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- Probably not a substantial claim. 9
- It may state two separate claims as one. 10
Every source the paper cites for this claim was checked and supports it.
In the paper
“Indeed, genetic analyses of FBD, FDD, and familial forms of AD support a unifying pathologic mechanism in which accumulation of amyloidogenic peptides triggers a complex pathological cascade leading to neurodegeneration (Golde, 2003).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Introduction
What the sources say
- Supportedcites Golde, 2003 source
In “Toward a complete understanding of AD pathogenesis,” the paper says evidence from familial British dementia (called BFD in the copy) and familial Danish dementia further supports the amyloid-accumulation hypothesis. The same section describes genetic evidence from familial AD and a modified amyloid cascade leading to neuronal death and dysfunction. No page numbers are provided in the supplied copy. (LLM, conf=0.90)
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Familial British and Danish dementias (FBD and FDD, respectively) are neurodegenerative dementias pathologically characterized by parenchymal preamyloid and amyloid deposits, cerebral amyloid angiopathy (CAA), neuronal loss, and neurofibrillary tangles (Ghiso et al., 2006).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Introduction
What the sources say
- Partly supportedcites Ghiso et al., 2006 sourceExperimental — accuracy not yet measured
The Abstract describes familial British and Danish dementias as having parenchymal pre-amyloid and amyloid deposits, cerebral amyloid angiopathy, and neurofibrillary tangles. It mentions neuronal loss specifically in relation to Alzheimer disease, not as an established pathological feature of both familial dementias, so that part of the citing sentence is not supported by our copy. (LLM, conf=0.84)
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Disease-causing mutations result in the production of C-terminally extended 277 aa mutant BRI2 proteins, which are cleaved at the normal furin processing site to generate distinct 34 aa peptides (ABri in FBD and ADan in FDD) that accumulate in the brains of affected patients (Vidal et al., 1999(Vidal et al., , 2000)).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Introduction
What the sources say
- Not checked — no full text of the sourcecites Vidal et al., 1999 source
- Partly supportedcites Vidal et al., 2000 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.
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Rests on an assumption: Two mutations in the ITM2b gene encoding the BRI2 protein cause familial British and familial Danish dementias.
Every source the paper cites for this claim was checked and supports it.
In the paper
“Several methods were used, including a native gel assay previously used to demonstrate that A1-40 inhibits A1-42 aggregation (Kim et al., 2007).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Bri2-23 inhibits A1-42 aggregation in vitro
What the sources say
- Supportedcites Kim et al., 2007 source
The ‘Aβ40 inhibits Aβ42 aggregation in vitro’ section reports that adding Aβ40 reduced Aβ42 high-molecular-weight complex formation. Figure 8 describes the nondenaturing gel assay used to demonstrate this effect. (LLM, conf=0.95)
boosteddirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Beyond the genetic link to FDD and FBD, little is known about the function of BRI2 and its homologues.”
- Also stated in: § Discussion · plain
“Nevertheless, other than the genetic link between BRI2 and FBD and FDD, almost nothing is known about the function of the BRI proteins (Ghiso et al., 2006).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
What the sources say
- Partly supportedcites Ghiso et al., 2006 sourceExperimental — accuracy not yet measured
The Abstract states that FBD and FDD are linked to mutations in BRI2. Neither the Abstract nor the retrieved passages on BRI2 and its homologues state that little is known about the proteins’ functions, so that central part of the claim is not supported by our copy. (LLM, conf=0.76)
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Also stated in: § 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
“When A1-42 aggregation was assessed using the native gel assay, we observed loss of the monomeric A1-42 signal and the appearance of high-molecular weight (HMW) aggregates (Fig. 3A, lane 10).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Bri2-23 inhibits A1-42 aggregation in vitro
plain- Asserted: passes — The authors put it forward as true.
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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
“Coaggregation of A42 and Bri2-23 demonstrates that Bri2-23 appears to initially increase the rate of aggregate formation during the first 12 h of incubation, but inhibits fibril formation at later time points (Fig. 3C).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Bri2-23 inhibits A1-42 aggregation in vitro
hedgeddirect- Asserted: passes — The authors put it forward as true.
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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
“Western blot analyses of brain lysates demonstrated that the somatic brain transgenic methodology produced approximately equivalent expression levels from the BRI2 and BRI2del244 -266 constructs and somewhat higher levels from BRI2-A1-40 (Fig. 4 E).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > The Bri2-23 sequence is required to suppress A deposition in vivo
boosted- Asserted: passes — The authors put it forward as true.
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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
“CAA was not increased by the BRI transgenes and was almost completely absent in the TgCRND8 mice at 3 months of age.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > 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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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
“Previous studies had demonstrated a potential interaction between BRI2 and APP and noted that BRI2 overexpression increased APP C-terminal fragment  (CTF) and reduced A secretion in cultured cells (Fotinopoulou et al., 2005;Matsuda et al., 2005).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > BRI2 and BRI2-A1-40 suppress amyloid deposition in APP transgenic mice
What the sources say
boosteddirect- 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
“Endogenous mouse A levels were measured using the previously validated rodent-specific A ELISA system as previously reported (Eckman et al., 2006).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > A sandwich ELISA.
What the sources say
- Not checked — no full text of the sourcecites Eckman et al., 2006 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
“Expression of BRI2 was intended to serve as a second control, because we had established that rAAV1-hGFP delivery and mock virus delivery did not alter A deposition in the CRND8 APP mouse model (Levites et al., 2006b).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > BRI2 and BRI2-A1-40 suppress amyloid deposition in APP transgenic mice
What the sources say
- Not matchedcites Levites et al., 2006b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
boosted- 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.
- Not matched
None of the sources cited for this claim have been checked yet.
In the paper
“It is expressed at high levels in the brain and cleaved by furin or furin-like proteases at its C terminus to produce a 23 aa peptide (Bri2-23) (Kim et al., 1999;Choi et al., 2004) (Fig. 1 B).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Introduction
What the sources say
- Not checked — no full text of the sourcecites Kim et al., 1999 source
- Not matchedcites Choi et al., 2004
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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 claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Previous studies had demonstrated a potential interaction between BRI2 and APP and noted that BRI2 overexpression increased APP C-terminal fragment  (CTF) and reduced A secretion in cultured cells (Fotinopoulou et al., 2005;Matsuda et al., 2005).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > BRI2 and BRI2-A1-40 suppress amyloid deposition in APP transgenic mice
What the sources say
hedgedcorrelational- 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
“These data show that Bri2-23 has a complex effect on aggregation of monomeric A1-42; however, both assays are consistent with a net inhibitory effect of Bri2-23 peptide on amyloid formation, presumably through inhibition of a later stage in fibril assembly.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Bri2-23 inhibits A1-42 aggregation in vitro
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
“Notably, in FDD brains, A and the ADan peptide are codeposited and bind to each other in vitro (Tomidokoro et al., 2005).”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
What the sources say
- Not checked — no full text of the sourcecites Tomidokoro et al., 2005 source
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.
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
“Note that the forebrain and hippocampus are routinely transduced, whereas hindbrain structures (e.g., cerebellum) are more variably transduced.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
plaincorrelationaln = 3- 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.
The paper relies on this without support.
Two mutations in the ITM2b gene encoding the BRI2 protein cause familial British and familial Danish dementias.
“Two mutations in the ITM2b gene encoding the BRI2 protein have been identified as the cause of FBD and FDD.”
The paper relies on this without support.
Anti-Aβ antibodies reduce Aβ deposition in mice.
“Because anti-A antibodies reduce A deposition in mice and expression of virally encoded A peptides in the periphery has been shown to generate an anti-A response, we examined whether CNS delivery of the transgene induced a humoral immune response to A.”
The paper relies on this without support.
Expression of virally encoded Aβ peptides in the periphery generates an anti-Aβ response.
“Because anti-A antibodies reduce A deposition in mice and expression of virally encoded A peptides in the periphery has been shown to generate an anti-A response, we examined whether CNS delivery of the transgene induced a humoral immune response to A.”
The paper relies on this without support.
Because of the rapid onset of Aβ deposition in TgCRND8 mice, it is not possible to measure steady-state Aβ levels.
“Because of the rapid onset of A deposition in TgCRND8 mice, it is not possible to measure steady-state A levels; therefore, we conducted additional experiments in Tg2576 mice to determine whether BRI2 altered steady-state A before plaque deposition.”
The paper relies on this without support.
First-generation antibodies were not sensitive enough to detect the Bri2-23 peptide in biological samples.
“First-generation antibodies were not sensitive enough to detect the Bri2-23 peptide in biological samples.”
The paper relies on this without support.
BRI2del244-266 encodes a protein containing the region of BRI2 previously shown to interact with APP and interfere with APP processing in cell culture.
“BRI2del244 -266 encodes a protein containing the region of BRI2 previously shown to interact with APP and interfere with APP processing in cell culture.”
The paper relies on this without support.
BRI2 and BRI2-A1-40 are cleaved by furin and other kex2 proteases to release Bri2-23 and A1-40, respectively.
“BRI2 and BRI2-A1-40 are cleaved by furin and other kex2 proteases to release Bri2-23 and A1-40, respectively.”
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
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Mouse anti-A IgG ELISA.
“Images are shown in amplitude mode, where increasing brightness indicates greater damping of cantilever oscillation.”
§ Neurobiology of Disease BRI2 (ITM2b) Inhibits A Deposition In Vivo > Discussion
“D, AFM analysis of aggregates at 72 h of incubation.Representative images, shown in height mode, are 10 ϫ 10 m.”
Citations
Cites
Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
Hsiao, K., Chapman, P., Nilsen, S., Eckman, C., Harigaya, Y., Younkin, S., Yang, F., & Cole, G. (1996) · Science · doi:10.1126/science.274.5284.99 · Cited by 4,210
Self-citationChishti, M. A., Yang, D.-S., Janus, C., Phinney, A. L., Horne, P., Pearson, J., Strome, R., Zuker, N., Loukides, J., French, J., et al. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m100710200 · Cited by 955
Aβ42 Is Essential for Parenchymal and Vascular Amyloid Deposition in Mice
McGowan, E., Pickford, F., Kim, J., Onstead, L., Eriksen, J., Yu, C., Skipper, L., Murphy, M. P., Beard, J., Das, P., et al. (2005) · Neuron · doi:10.1016/j.neuron.2005.06.030 · Cited by 565
Self-citationA stop-codon mutation in the BRI gene associated with familial British dementia
Vidal, R., Frangione, B., Rostagno, A., Mead, S., Révész, T., Plant, G., & Ghiso, J. (1999) · Nature · doi:10.1038/21637 · Cited by 466
Aβ40 Inhibits Amyloid Deposition In Vivo
Kim, J., Onstead, L., Randle, S., Price, R., Smithson, L., Zwizinski, C., Dickson, D. W., Golde, T., & McGowan, E. (2007) · The Journal of Neuroscience · doi:10.1523/jneurosci.4849-06.2007 · Cited by 359 · cited 10×
“4 m polyvinylidene fluoride membrane as previously described (Klug et al., 2003; Kim et al., 2007).”
BackgroundMethodResultInfluentialSelf-citationVidal, R., Révész, T., Rostagno, A., Kim, E., Holton, J. L., Bek, T., Bojsen-Møller, M., Braendgaard, H., Plant, G., Ghiso, J., et al. (2000) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.080076097 · Cited by 300
BRICHOS: a conserved domain in proteins associated with dementia, respiratory distress and cancer
Sánchez‐Pulido, L., Devos, D. P., & Valencia, A. (2002) · Trends in Biochemical Sciences · doi:10.1016/s0968-0004(02)02134-5 · Cited by 214
Passini, M. A., Watson, D. J., Vite, C. H., Landsburg, D. J., Feigenbaum, A. L., & Wolfe, J. H. N. (2003) · Journal of Virology · doi:10.1128/jvi.77.12.7034-7040.2003 · Cited by 213
Levites, Y. (2005) · Journal of Clinical Investigation · doi:10.1172/jci25410 · Cited by 209
Self-citationBroekman, M. L. D., Comer, L. A., Hyman, B. T., & Sena‐Esteves, M. (2006) · Neuroscience · doi:10.1016/j.neuroscience.2005.11.057 · Cited by 201
Cited by
Sorted by citations
A molecular chaperone breaks the catalytic cycle that generates toxic Aβ oligomers
Cohen, S. I. A., Arosio, P., Presto, J., Kurudenkandy, F. R., Biverstål, H., Dolfe, L., Dunning, C. J. R., Yang, X., Frohm, B., Vendruscolo, M., et al. (2015) · Nature Structural & Molecular Biology · doi:10.1038/nsmb.2971 · Cited by 413
Chakrabarty, P., Jansen‐West, K., Beccard, A., Ceballos‐Diaz, C., Levites, Y., Verbeeck, C., Zubair, A. C., Dickson, D., Golde, T. E., & Das, P. (2010) · The FASEB Journal · doi:10.1096/fj.09-141754 · Cited by 328
Self-citationCognitive deficits in single App knock-in mouse models
Masuda, A., Kobayashi, Y., Kogo, N., Saito, T., Saido, T. C., & Itohara, S. (2016) · Neurobiology of Learning and Memory · doi:10.1016/j.nlm.2016.07.001 · Cited by 248
Chakrabarty, P., Ceballos-Diaz, C., Beccard, A., Janus, C., Dickson, D., Golde, T. E., & Das, P. (2010) · The Journal of Immunology · doi:10.4049/jimmunol.0903382 · Cited by 206
Self-citationSingle cell molecular alterations reveal target cells and pathways of concussive brain injury
Arneson, D., Zhang, G., Ying, Z., Zhuang, Y., Byun, H. R., Ahn, I. S., Gomez-Pinilla, F., & Yang, X. (2018) · Nature Communications · doi:10.1038/s41467-018-06222-0 · Cited by 193
Metadata
- Authors
- Kim, J., Miller, V. M., Levites, Y., West, K. J., Zwizinski, C. W., Moore, B. D., Troendle, F. J., Bann, M., Verbeeck, C., Price, R. W., Smithson, L., Sonoda, L., Wagg, K., Rangachari, V., Zou, F., Younkin, S. G., Graff-Radford, N., Dickson, D., Rosenberry, T., & Golde, T. E.
- Affiliations
- Mayo Clinic (US)
- Mayo Clinic in Florida (US)
- ORCID
- Venue
- Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2008-06-04
- Volume
- 28
- Issue
- 23
- Pages
- 6030-6036
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC2586000
- OpenAlex
- W1992813803
- Semantic Scholar
- 6a6f30c6cabc6ff3434b78e2b58819c3fa74166a
- Cited by
- 113
- References
- 30
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 5 · 2023: 4 · 2022: 5 · 2021: 5 · 2020: 6 · 2019: 1 · 2018: 6 · 2017: 2 · 2016: 4 · 2015: 16 · 2014: 7 · 2013: 8 · 2012: 10
- FWCI
- 5.83
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (submittedVersion)
- Funders
- American Heart Association
- Mayo Foundation for Medical Education and Research (AG17216, AG03949)
- National Institutes of Health (5p01ag003949-40, AG03949, AG17216)
- National Institute on Aging (P01-AG003949, AG03949, P50AG025711, R01 AG18454, P01AG025531, R01AG018454, P01 AG 017216)
- 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
- BRI2, ITM2B, amyloid-beta deposition, Aβ40, Alzheimer's disease, familial British dementia, familial Danish dementia, cerebrospinal fluid, amyloid aggregation inhibition
- MeSH terms
- Dependovirus, Amyloid, Animals, Brain, Chickens, Female, Cricetinae, Humans, Male, Membrane Glycoproteins, Membrane Proteins, Mice, Transgenic, Peptide Fragments, Phenotype, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Gene Transfer Techniques, Adaptor Proteins, Signal Transducing, Mice
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 2026-10-17, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-17 (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 ›
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