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Synthetic amyloid-β oligomers impair long-term memory independently of cellular prion protein
Open accessAbstract
Inability to form new memories is an early clinical sign of Alzheimer’s disease (AD). There is ample evidence that the amyloid-β (Aβ) peptide plays a key role in the pathogenesis of this disorder. Soluble, bio-derived oligomers of Aβ are proposed as the key mediators of synaptic and cognitive dysfunction, but more tractable models of Aβ−mediated cognitive impairment are needed. Here we report that, in mice, acute intracerebroventricular injections of synthetic Aβ 1–42 oligomers impaired consolidation of the long-term recognition memory, whereas mature Aβ 1–42 fibrils and freshly dissolved peptide did not. The deficit induced by oligomers was reversible and was prevented by an anti-Aβ antibody. It has been suggested that the cellular prion protein (PrP C ) mediates the impairment of synaptic plasticity induced by Aβ. We confirmed that Aβ 1–42 oligomers interact with PrP C , with nanomolar affinity. However, PrP-expressing and PrP knock-out mice were equally susceptible to this impairment. These data suggest that Aβ 1–42 oligomers are responsible for cognitive impairment in AD and that PrP C is not required.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
Acute intracerebroventricular injection of synthetic Aβ1–42 oligomers impaired consolidation of long-term object-recognition memory in mice, whereas fibrils and freshly dissolved peptide did not. Although Aβ oligomers bound cellular prion protein (PrPC) with high affinity, PrP-expressing and PrP knockout mice were equally susceptible, indicating PrPC is not required for this memory impairment.
Key findings
- Synthetic Aβ1–42 oligomers (estimated 10–50 nM) impaired long-term recognition memory; mature fibrils and freshly dissolved Aβ did not.
- The oligomer-induced deficit was reversible: memory had fully recovered 10 days after injection without further Aβ, and was completely prevented by i.c.v. pretreatment with 0.25 μg/2 μL of the anti-Aβ antibody 4G8.
- Aβ oligomers bound PrPC with high affinity (Kd ≤20 nM monomer equivalent), but Prnp 0/0 mice were as susceptible as Prnp +/+ mice to oligomer-induced memory impairment; oligomers were also toxic to both Prnp +/+ and Prnp 0/0 hippocampal neurons in vitro.
- Oligomers disrupted memory encoding/consolidation but not retrieval: injection before familiarization prevented memory, whereas injection before the test phase did not.
Methods
- Male C57BL/6 mice, 7–8 weeks old, received acute i.c.v. injections of synthetic Aβ1–42 preparations and were tested in the novel-object recognition task; Prnp 0/0 and Prnp +/+ mice were compared.
- Aβ1–42 oligomers, fibrils, and initial-state peptide were characterized by atomic force microscopy and size exclusion chromatography before behavioral testing.
- Binding to PrPC was measured by surface plasmon resonance using brain homogenates and anti-PrP antibodies; primary hippocampal neuron cultures were treated with 1–3 μM oligomers for 72 h and survival measured by MTT assay. Statistical analysis used ANOVA with post hoc tests.
Limitations
- The paper states that one limitation is the use of oligomeric Aβ preparations not proven identical to those found in AD patient brains.
- Evident from the text: object recognition memory is associated more with perirhinal cortex than hippocampus, so the behavioral model may not fully align with hippocampal LTP studies.
- Evident from the text: the study used only male C57BL/6 mice and a single behavioral task, and it does not establish the mechanism linking Aβ oligomer binding to PrPC with memory impairment.
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Claims the paper makes
20 Own result · 18 Not checked yet · 11 Own interpretation · 2 No basis given · 1 Own method
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 deficit induced by oligomers was reversible and was prevented by an anti-Aβ antibody.”
- Also stated in: § Results · plain
“After 10 days, with no further Aβ injection, the memory deficit had fully recovered (Fig. 3A).”
plaindirect- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Results · 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
“However, PrP-expressing and PrP knock-out mice were equally susceptible to this impairment.”
- Also stated in: § Results · plain
“We found that Prnp 0/0 mice were as susceptible as Prnp +/+ mice to oligomer-induced memory impairment (Figs. 2B and 4A).”
plain- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Results · 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
“Here we report that, in mice, acute intracerebroventricular injections of synthetic Aβ1–42 oligomers impaired consolidation of the long-term recognition memory, whereas mature Aβ1–42 fibrils and freshly dissolved peptide did not.”
- Also stated in: § Results · plain
“Aβ oligomer–injected mice were unable to distinguish the new object, with no significant difference in the percentage of time spent investigating the two (Fig. 2A), and a discrimination index significantly lower than vehicle-injected mice (Fig. 2B).”
plaindirect- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Results · 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 confirmed that Aβ1–42 oligomers interact with PrPC, with nanomolar affinity.”
- Also stated in: § Results · plain
“The binding was dose dependent, with a dissociation constant (K d) of ≤20 nM monomer equivalent (Fig. 7 B and D).”
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Results · 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 deficit induced by oligomers was reversible and was prevented by an anti-Aβ antibody.”
- Also stated in: § Results · plain
“An i.c.v. injection of 0.25 μg/2 μL of 4G8, 5 min before the Aβ oligomers, completely prevented the memory impairment (Fig. 3B).”
plaindirect- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Results · plain
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In the paper
“but found no evidence that the two events are related.”
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“An i.c.v. injection of 4G8 alone did not affect memory.”
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
“On the basis of SEC, we estimated the actual oligomer concentration in this sample as 10–50 nM.”
- Also stated in: § Discussion · plain
“The effect was detectable at a nanomolar concentration of Aβ oligomers (10–50 nM).”
plain- 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
“A single i.c.v. injection of a nanomolar concentration of synthetic Aβ1–42 oligomers impairs memory consolidation within 24 h, suggesting that oligomers rapidly interfere with the synaptic activity necessary for the stabilization of new memories.”
plaindirect- 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
“Heat-denatured antibody, unable to bind Aβ, could not antagonize the effect of Aβ oligomers.”
hedged- Asserted: passes — The authors put it forward as true.
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In the paper
“The performance of vehicle-treated Prnp 0/0 and vehicle-treated Prnp +/+ mice was similar (Figs. 2B and 4 A), indicating that lack of PrPC did not affect recognition memory per se.”
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
“Using this model we demonstrated that Aβ oligomers induce in vivo memory impairment and bind PrPC with high affinity, but found no evidence that the two events are related.”
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“The 22 °C-Aβ oligomers impaired recognition memory in both Prnp +/+ and Prnp 0/0 mice (Fig. 4C).”
What the sources say
- Not checked yetcites [17] Laurén J, Gimbel DA, Nygaard HB, Gilbert JW, Strittmatter SM. Cellular prion protein mediates impairment of synaptic plasticity by amyloid-beta oligomers. Nature. 2009;457:1128–1132. doi: 10.1038/nature07761. [DOI] [PMC free article] [PubMed] [Google Scholar] source
plaindirect- 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
“Oligomers were toxic to both Prnp +/+ and Prnp 0/0 hippocampal cells, consistent with the conclusion that their adverse effects are independent of PrPC (Fig. 5).”
plaindirect- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Using this model we demonstrated that Aβ oligomers induce in vivo memory impairment and bind PrPC with high affinity, but found no evidence that the two events are related.”
boosteddirect- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Only a few small Aβ particles were detected in the initial state, whereas the oligomer preparation contained spherical particles of 2–3 nm diameter (Fig. 1A) appearing in the SEC void volume (>75 kDa; Fig. 1B).”
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Moreover, PrPC captured by both 94B4 and 3F4 maintains the ability to bind 6D11, an anti-PrP antibody directed against the epitope 93–109, i.e., the region suggested to be involved in the interaction with Aβ oligomers.”
plain- 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 data suggest that Aβ1–42 oligomers are responsible for cognitive impairment in AD and that PrPC is not required.”
- Also stated in: § Results · hedged
“This suggests that PrPC is not required for the oligomer-mediated memory impairment.”
- Also stated in: § Discussion · plain
“We confirmed that Aβ oligomers bind to PrPC with high affinity, but also found that PrPC is not required for oligomer-induced memory impairment and cytotoxicity.”
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § Results · hedged
None of the sources cited for this claim have been checked yet.
In the paper
“In vitro and in vivo studies have now indicated that soluble Aβ oligomers impair synaptic plasticity, inhibiting hippocampal long-term potentiation (LTP), the electrophysiological correlate of learning and memory (3 –6).”
What the sources say
- Not checked yetcites [3] Lambert MP, et al. Diffusible, nonfibrillar ligands derived from Abeta1-42 are potent central nervous system neurotoxins. Proc Natl Acad Sci USA. 1998;95:6448–6453. doi: 10.1073/pnas.95.11.6448. [DOI] [PMC free article] [PubMed] [Google Scholar] source
- Not checked yetcites [4] Shankar GM, et al. Amyloid-beta protein dimers isolated directly from Alzheimer’s brains impair synaptic plasticity and memory. Nat Med. 2008;14:837–842. doi: 10.1038/nm1782. [DOI] [PMC free article] [PubMed] [Google Scholar] source
- Not checked yetcites [5] Townsend M, Shankar GM, Mehta T, Walsh DM, Selkoe DJ. Effects of secreted oligomers of amyloid beta-protein on hippocampal synaptic plasticity: A potent role for trimers. J Physiol. 2006;572:477–492. doi: 10.1113/jphysiol.2005.103754. [DOI] [PMC free article] [PubMed] [Google Scholar] source
- Not checked yetcites [6] Wang HW, et al. Soluble oligomers of beta amyloid (1-42) inhibit long-term potentiation but not long-term depression in rat dentate gyrus. Brain Res. 2002;924:133–140. doi: 10.1016/s0006-8993(01)03058-x. [DOI] [PubMed] [Google Scholar] source
hedgeddirect- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
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 Aβ1–42 oligomers are responsible for cognitive impairment in AD and that PrPC is not required.”
- Also stated in: § Discussion · boosted
“Here we demonstrated that well-characterized synthetic Aβ oligomers were responsible for an immediate memory impairment in mice injected i.c.v. and tested in the novel-object recognition task.”
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.
- Rests on an assumption: Synthetic Aβ1–42 oligomers injected intracerebroventricularly in mice reproduce the relevant actions of endogenous Aβ oligomers in Alzheimer’s disease.
- Also stated in: § Discussion · boosted
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 performance of vehicle-treated Prnp 0/0 and vehicle-treated Prnp +/+ mice was similar (Figs. 2B and 4 A), indicating that lack of PrPC did not affect recognition memory per se.”
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.
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 do not support the contention that PrPC is involved in the toxic effects of Aβ.”
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“This suggests that the memory deficit in our murine model mimics the situation in early-stage AD patients who are unable to store newly acquired information but preserve old memories (22).”
What the sources say
- Not checked yetcites [22] Greene JD, Baddeley AD, Hodges JR. Analysis of the episodic memory deficit in early Alzheimer’s disease: Evidence from the doors and people test. Neuropsychologia. 1996;34:537–551. doi: 10.1016/0028-3932(95)00151-4. [DOI] [PubMed] [Google Scholar] source
hedgedcorrelational- 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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- Rests on an assumption: Synthetic Aβ1–42 oligomers injected intracerebroventricularly in mice reproduce the relevant actions of endogenous Aβ oligomers in Alzheimer’s disease.
In the paper
“This indicates that Aβ oligomer-mediated memory impairment does not depend on a persistent neurodegenerative phenomenon and can be rescued, suggesting that targeting Aβ oligomers might lead to recovery of cognitive functions (10).”
- Also stated in: § Discussion · hedged
“This suggests that the oligomer-mediated memory impairment might be therapeutically rescued.”
What the sources say
- Not checked yetcites [10] Lesné S, et al. A specific amyloid-beta protein assembly in the brain impairs memory. Nature. 2006;440:352–357. doi: 10.1038/nature04533. [DOI] [PubMed] [Google Scholar] source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
- Also stated in: § Discussion · hedged
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
“suggesting that oligomers rapidly interfere with the synaptic activity necessary for the stabilization of new memories.”
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.
In the paper
“This indicates that Aβ oligomer-mediated memory impairment does not depend on a persistent neurodegenerative phenomenon and can be rescued, suggesting that targeting Aβ oligomers might lead to recovery of cognitive functions (10).”
What the sources say
- Not checked yetcites [10] Lesné S, et al. A specific amyloid-beta protein assembly in the brain impairs memory. Nature. 2006;440:352–357. doi: 10.1038/nature04533. [DOI] [PubMed] [Google Scholar] source
hedged- Asserted: passes — The authors put it forward as true.
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In the paper
“4G8 abrogates the disruption of synaptic plasticity induced by cell-derived Aβ oligomers (24).”
What the sources say
- Not checked yetcites [24] Klyubin I, et al. Amyloid beta protein immunotherapy neutralizes Abeta oligomers that disrupt synaptic plasticity in vivo. Nat Med. 2005;11:556–561. doi: 10.1038/nm1234. [DOI] [PubMed] [Google Scholar] source
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
“We confirmed that Aβ oligomers bind to PrPC with high affinity, but also found that PrPC is not required for oligomer-induced memory impairment and cytotoxicity.”
plain- 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
“In conclusion, we describe a simple and reliable mouse model of Aβ-induced memory dysfunction.”
plain- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 14
- Probably not a substantial claim. 15
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“whereas mature Aβ1–42 fibrils and freshly dissolved peptide did not.”
- Also stated in: § Results · plain
“Neither Aβ in the initial state nor the fibrils affected memory (Fig. 2 A and B).”
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Also stated in: § Results · 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 Aβ initial state, oligomers or fibrils were assayed for their binding to PrPC, only Aβ oligomers bound PrPC specifically, and Aβ initial state and fibrils did not (Fig. 7 A and C).”
plaincorrelational- 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
“Mice injected 2 h before familiarization were unable to remember the object previously investigated, whereas mice injected 2 h before the test phase recalled the familiar object investigated the day before (Fig. 8).”
plaindirect- 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
“Preliminary data confirmed that the captured protein is actually PrPC, as no capture was detected when flowing brain homogenate from Prnp 0/0 mice (Fig. 6).”
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“PrPC binds synthetic Aβ oligomers with high affinity and plays a role in the oligomer-mediated inhibition of LTP (17).”
What the sources say
- Not checked yetcites [17] Laurén J, Gimbel DA, Nygaard HB, Gilbert JW, Strittmatter SM. Cellular prion protein mediates impairment of synaptic plasticity by amyloid-beta oligomers. Nature. 2009;457:1128–1132. doi: 10.1038/nature07761. [DOI] [PMC free article] [PubMed] [Google Scholar] 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.
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Probably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“All of these processes are affected by Aβ oligomers in vitro, using primary neuronal cultures (12, 15, 36, 37).”
What the sources say
- Not checked yetcites [12] Shankar GM, et al. Natural oligomers of the Alzheimer amyloid-beta protein induce reversible synapse loss by modulating an NMDA-type glutamate receptor-dependent signaling pathway. J Neurosci. 2007;27:2866–2875. doi: 10.1523/JNEUROSCI.4970-06.2007. [DOI] [PMC free article] [PubMed] [Google Scholar] source
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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.
None of the sources cited for this claim have been checked yet.
In the paper
“Several neuronal receptors have been proposed as mediating the effect of Aβ on synaptic plasticity and memory, including the α-7-nicotinic (16), glutamatergic (39–40), and insulin (14) receptors.”
What the sources say
- Not checked yetcites [16] Snyder EM, et al. Regulation of NMDA receptor trafficking by amyloid-beta. Nat Neurosci. 2005;8:1051–1058. doi: 10.1038/nn1503. [DOI] [PubMed] [Google Scholar] source
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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.
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 indicate that Aβ oligomers acutely disrupt anterograde memory storage but do not interfere with its retrieval when the information has been properly stored.”
- Also stated in: § Discussion · plain
“Aβ oligomers inhibited the encoding/consolidation of information, without affecting its retrieval if properly stored.”
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.
- Also stated in: § Discussion · plain
In the paper
“In an elegant study Lauren et al. (17) reported that PrPC mediates the Aβ oligomer-induced hippocampal synaptic plasticity impairment.”
What the sources say
- Not checked yetcites [17] Laurén J, Gimbel DA, Nygaard HB, Gilbert JW, Strittmatter SM. Cellular prion protein mediates impairment of synaptic plasticity by amyloid-beta oligomers. Nature. 2009;457:1128–1132. doi: 10.1038/nature07761. [DOI] [PMC free article] [PubMed] [Google Scholar] source
plaindirect- Asserted: fails — The authors may not 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 authors may not put it forward as true. The paper’s conclusions may not depend on it.
In the paper
“Because recognition memory is dependent on the medial temporal lobe including the hippocampus (25), we examined whether oligomer-mediated memory impairment was also related to PrPC expression.”
What the sources say
- Not checked yetcites [25] Squire LR, Wixted JT, Clark RE. Recognition memory and the medial temporal lobe: A new perspective. Nat Rev Neurosci. 2007;8:872–883. doi: 10.1038/nrn2154. [DOI] [PMC free article] [PubMed] [Google Scholar]
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.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Unlike Aβ aggregates purified from biological sources, synthetic Aβ oligomers are chemically defined, and can be easily produced and biophysically characterized.”
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. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“However, some human and primate studies have shown that hippocampal lesions result in impaired object recognition (41, 42)”
What the sources say
- Not checked yetcites [41] Reed JM, Squire LR. Impaired recognition memory in patients with lesions limited to the hippocampal formation. Behav Neurosci. 1997;111:667–675. doi: 10.1037//0735-7044.111.4.667. [DOI] [PubMed] [Google Scholar]
- Not checked yetcites [42] Zola SM, et al. Impaired recognition memory in monkeys after damage limited to the hippocampal region. J Neurosci. 2000;20:451–463. doi: 10.1523/JNEUROSCI.20-01-00451.2000. [DOI] [PMC free article] [PubMed] [Google Scholar]
hedgeddirect- 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
“These preparations, and freshly dissolved Aβ1−42 (hereafter referred to as “initial state”), were characterized by atomic force microscopy (AFM) and size exclusion chromatography (SEC) before behavioral investigation.”
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.
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, although Aβ oligomers interact with PrPC with high affinity, they do not act together to induce memory derangement.”
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“PrPC has been involved in neurotrophic signaling (44, 45), and in the regulation of Aβ-production (46), suggesting that PrPC and Aβ may be part of a common molecular pathway governing neuronal differentiation.”
What the sources say
- Not checked yetcites [44] Kanaani J, Prusiner SB, Diacovo J, Baekkeskov S, Legname G. Recombinant prion protein induces rapid polarization and development of synapses in embryonic rat hippocampal neurons in vitro. J Neurochem. 2005;95:1373–1386. doi: 10.1111/j.1471-4159.2005.03469.x. [DOI] [PubMed] [Google Scholar]
- Not checked yetcites [45] Santuccione A, Sytnyk V, Leshchyns’ka I, Schachner M. Prion protein recruits its neuronal receptor NCAM to lipid rafts to activate p59fyn and to enhance neurite outgrowth. J Cell Biol. 2005;169:341–354. doi: 10.1083/jcb.200409127. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Not checked yetcites [46] Parkin ET, et al. Cellular prion protein regulates beta-secretase cleavage of the Alzheimer’s amyloid precursor protein. Proc Natl Acad Sci USA. 2007;104:11062–11067. doi: 10.1073/pnas.0609621104. [DOI] [PMC free article] [PubMed] [Google Scholar]
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. It may state two separate claims as one.
In the paper
“However, some human and primate studies have shown that hippocampal lesions result in impaired object recognition (41, 42) and that, for the 24 h intertrial interval from familiarization to test phase used in our study, hippocampal activity is required (43).”
What the sources say
- Not checked yetcites [43] Hammond RS, Tull LE, Stackman RW. On the delay-dependent involvement of the hippocampus in object recognition memory. Neurobiol Learn Mem. 2004;82:26–34. doi: 10.1016/j.nlm.2004.03.005. [DOI] [PubMed] [Google Scholar] source
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.
None of the sources cited for this claim have been checked yet.
In the paper
“Memory processing requires NMDA receptor activation and intracellular signaling leading to AMPA receptor trafficking, synthesis of new proteins, and formation of dendritic spines (34, 35).”
What the sources say
- Not checked yetcites [34] Collingridge GL, Isaac JT, Wang YT. Receptor trafficking and synaptic plasticity. Nat Rev Neurosci. 2004;5:952–962. doi: 10.1038/nrn1556. [DOI] [PubMed] [Google Scholar]
- Not checked yetcites [35] Lüscher C, Nicoll RA, Malenka RC, Muller D. Synaptic plasticity and dynamic modulation of the postsynaptic membrane. Nat Neurosci. 2000;3:545–550. doi: 10.1038/75714. [DOI] [PubMed] [Google Scholar]
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.
In the paper
“The novel-object recognition task is simple and reproducible, it measures recognition memory, which is heavily impaired in AD, and relies on spontaneous animal behavior without the need for stressor elements such as food or water deprivation, electric foot-shock, or aversive environments like water (25).”
What the sources say
- Not checked yetcites [25] Squire LR, Wixted JT, Clark RE. Recognition memory and the medial temporal lobe: A new perspective. Nat Rev Neurosci. 2007;8:872–883. doi: 10.1038/nrn2154. [DOI] [PMC free article] [PubMed] [Google Scholar]
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Proof that Aβ oligomers are the active amyloid-β species was the lack of effect of either the freshly solubilized Aβ (initial state) or fibrils.”
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.
In the paper
“The novel-object recognition task is simple and reproducible, it measures recognition memory, which is heavily impaired in AD, and relies on spontaneous animal behavior without the need for stressor elements such as food or water deprivation, electric foot-shock, or aversive environments like water (25).”
What the sources say
- Not checked yetcites [25] Squire LR, Wixted JT, Clark RE. Recognition memory and the medial temporal lobe: A new perspective. Nat Rev Neurosci. 2007;8:872–883. doi: 10.1038/nrn2154. [DOI] [PMC free article] [PubMed] [Google Scholar]
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. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“At variance with the native peptide, the depsi-peptide is highly soluble and it has a much lower propensity to aggregate, thus preventing the spontaneous formation of seeds in the solution (49, 50).”
What the sources say
- Not checked yetcites [49] Taniguchi A, et al. “Click peptide”: pH-triggered in situ production and aggregation of monomer Abeta1-42. ChemBioChem. 2009;10:710–715. doi: 10.1002/cbic.200800765. [DOI] [PubMed] [Google Scholar]
- Not checked yetcites [50] Taniguchi A, et al. ‘O-Acyl isopeptide method’ for peptide synthesis: Solvent effects in the synthesis of Abeta1-42 isopeptide using ‘O-acyl isodipeptide unit’. J Pept Sci. 2007;13:868–874. doi: 10.1002/psc.905. [DOI] [PubMed] [Google Scholar]
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.
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
“One limitation of this study worth to be mentioned may be the use of oligomeric Aβ preparations which haven’t been proven to be identical to those found in the brain of AD patients.”
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.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The novel-object recognition task is simple and reproducible”
plain- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check 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. It may be too vague to check against evidence. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper relies on this without support.
Synthetic Aβ1–42 oligomers injected intracerebroventricularly in mice reproduce the relevant actions of endogenous Aβ oligomers in Alzheimer’s disease.
“These data suggest that Aβ1–42 oligomers are responsible for cognitive impairment in AD and that PrPC is not required.”
“Soluble, bio-derived oligomers of Aβ are proposed as the key mediators of synaptic and cognitive dysfunction, but more tractable models of Aβ−mediated cognitive impairment are needed.”
The paper relies on this without support.
There is no consensus as to which brain-derived oligomeric species mediate cognitive deficits in AD.
“since there remains no consensus as to which brain-derived oligomeric species mediate cognitive deficits in AD”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source says what the claim attributes to it.
In the citing paper
“Atomic Force Microscopy (AFM) was used to verify the actual and correct formation of the Aβ1-42 fibrils ([36]) [68,69].”
From PCSK9 affects astrocyte cholesterol metabolism and reduces neuron cholesterol supplying in vitro: potential implications in Alzheimer’s disease (2022) · cites this paper as [69]
In the citing paper
“other studies have shown that PrP-expressing and PrP-knockout mice are equally susceptible to long-term memory impairment induced by Aβ oligomers (Balducci et al., 2010; Calella et al., 2010)”
From The Aβ oligomer hypothesis for synapse failure and memory loss in Alzheimer’s disease (2011) · cites this paper as Balducci et al., 2010
Citations
Cites
1 retracted
RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
Lesné, S., Koh, M. T., Kotilinek, L., Kayed, R., Glabe, C. G., Yang, A., Gallagher, M., & Ashe, K. H. (2006) · Nature · doi:10.1038/nature04533 · Cited by 2,769
RetractedMemory - A century of consolidation
McGaugh, J. L. (2000) · Science · doi:10.1126/science.287.5451.248 · Cited by 4,250
Shankar, G. M., Li, S., Mehta, T. H., Garcia-Munoz, A., Shepardson, N. E., Smith, I., Brett, F. M., Farrell, M. A., Rowan, M. J., Lemere, C. A., et al. (2008) · Nature Medicine · doi:10.1038/nm1782 · Cited by 3,685
Diffusible, nonfibrillar ligands derived from Aβ 1–42 are potent central nervous system neurotoxins
Lambert, M. P., Barlow, A. K., Chromy, B. A., Edwards, C., Freed, R., Liosatos, M., Morgan, T. E., Rozovsky, I., Trommer, B., Viola, K. L., et al. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.11.6448 · Cited by 3,506
Mice devoid of PrP are resistant to scrapie
Büeler, H., Aguzzi, A., Sailer, A. W., Greiner, R., Autenried, P., Aguet, M., & Weissmann, C. (1993) · Cell · doi:10.1016/0092-8674(93)90360-3 · Cited by 2,107
Mucke, L., Masliah, E., Yu, G.-Q., Mallory, M., Rockenstein, E. M., Tatsuno, G., Hu, K., Kholodenko, D., Johnson-Wood, K., & McConlogue, L. (2000) · The Journal of Neuroscience · doi:10.1523/jneurosci.20-11-04050.2000 · Cited by 1,856
Natural oligomers of the amyloid-β protein specifically disrupt cognitive function
Cleary, J. P., Walsh, D. M., Hofmeister, J. J., Shankar, G. M., Kuskowski, M. A., Selkoe, D. J., & Ashe, K. H. (2004) · Nature Neuroscience · doi:10.1038/nn1372 · Cited by 1,722
Shankar, G. M., Bloodgood, B. L., Townsend, M., Walsh, D. M., Selkoe, D. J., & Sabatini, B. L. (2007) · The Journal of Neuroscience · doi:10.1523/jneurosci.4970-06.2007 · Cited by 1,592
Regulation of NMDA receptor trafficking by amyloid-β
Snyder, E. M., Nong, Y., Almeida, C. G., Paul, S., Moran, T., Choi, E. Y., Nairn, A. C., Salter, M. W., Lombroso, P. J., Gouras, G. K., et al. (2005) · Nature Neuroscience · doi:10.1038/nn1503 · Cited by 1,561 · cited 5×
“Almeida CG, et al. (2005) Beta-amyloid accumulation in APP mutant neurons reduces PSD-95 and GluR1 in synapses.”
InfluentialCellular prion protein mediates impairment of synaptic plasticity by amyloid-β oligomers
Laurén, J., Gimbel, D. A., Nygaard, H. B., Gilbert, J. W., & Strittmatter, S. M. (2009) · Nature · doi:10.1038/nature07761 · Cited by 1,560
Cited by
Sorted by citations
The Intersection of Amyloid Beta and Tau at Synapses in Alzheimer’s Disease
Spires-Jones, T. L., & Hyman, B. T. (2014) · Neuron · doi:10.1016/j.neuron.2014.05.004 · Cited by 1,201
Neurotoxicity of Amyloid -Protein: Synaptic and Network Dysfunction
Mucke, L., & Selkoe, D. J. (2012) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a006338 · Cited by 1,000
The Amyloid Beta Peptide: A Chemist’s Perspective. Role in Alzheimer’s and Fibrillization
Hamley, I. W. (2012) · Chemical Reviews · doi:10.1021/cr3000994 · Cited by 892
The Amyloid-β Oligomer Hypothesis: Beginning of the Third Decade
Cline, E. N., Bicca, M. A., Viola, K. L., & Klein, W. L. (2018) · Journal of Alzheimer's Disease · doi:10.3233/jad-179941 · Cited by 870
Busche, M. A., Chen, X., Henning, H. A., Reichwald, J., Staufenbiel, M., Sakmann, B., & Konnerth, A. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1206171109 · Cited by 715
“In addition, cerebroventricular injections of soluble Aβ rapidly and transiently induce memory deficits in wild-type mice (44), perhaps by causing transient neuronal hyperactivity.”
Background
Metadata
- Authors
- Balducci, C., Beeg, M., Stravalaci, M., Bastone, A., Sclip, A., Biasini, E., Tapella, L., Colombo, L., Manzoni, C., Borsello, T., Chiesa, R., Gobbi, M., Salmona, M., & Forloni, G.
- Affiliations
- Mario Negri Institute for Pharmacological Research (IT)
- Dulbecco Telethon Institute (IT)
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2010-01-19
- Volume
- 107
- Issue
- 5
- Pages
- 2295-2300
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2836680
- OpenAlex
- W2002280328
- Semantic Scholar
- 63625a2fc958c65a2cb276db617f403efa9be515
- Cited by
- 466
- References
- 57
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 14 · 2023: 19 · 2022: 20 · 2021: 24 · 2020: 31 · 2019: 25 · 2018: 32 · 2017: 40 · 2016: 31 · 2015: 35 · 2014: 27 · 2013: 47 · 2012: 36
- FWCI
- 33.78
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Iris (University of Trento) (submittedVersion)
- 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
- amyloid-beta oligomers, amyloid-beta 42, Alzheimer's disease, long-term memory, memory consolidation, recognition memory, cellular prion protein, anti-amyloid antibodies, cognitive impairment, intracerebroventricular administration, amyloid fibrils
- MeSH terms
- Prion Proteins, Alzheimer Disease, Animals, Cognition Disorders, Humans, Injections, Intraventricular, Male, Memory, Mice, Inbred C57BL, Neuronal Plasticity, Peptide Fragments, Prions, Protein Binding, Amyloid beta-Peptides, Mice, Knockout, PrPC Proteins, Surface Plasmon Resonance, 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 2026-10-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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