Changes of the Primary Cilia in Alzheimer's Disease Pathogenesis
Open accessAbstract
Alzheimer's disease (AD), a neurodegenerative disorder intricately linked with aging, poses an escalating global health challenge. Currently, no effective treatment exists for AD. Although the pathological characteristics of AD predominantly emerge in older age, numerous structural and functional alterations in the nervous system may commence early in life or even during developmental stages. Primary cilia, organelles associated with age-related diseases, have not been extensively studied in the context of AD progression. This study initiated an examination of the common pathological features of AD and identified that amyloid-beta (Aβ) plaque deposition resulted in the shortening of primary cilia. In the hippocampus of familial AD mice, there was a significant upregulation of somatostatin receptor 3 (SSTR3) expression. To further elucidate the role of SSTR3 in AD pathology, we knocked out SSTR3 expression in 5 × FAD mice, which resulted in an exacerbation of AD-related pathological features. Our study offers novel insights into the pathological alterations associated with AD.
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Claims the paper makes
28 of 55 cited sources checked · 11 supported · 0 flagged · accuracy not yet measured
- Premisecitation
Destruction of primary cilia in the cortex and hippocampus can disrupt learning, memory, and recognition of novel objects, thereby impairing cognitive function.
“For instance, the destruction of primary cilia in the cortex and hippocampus can disrupt learning, memory, and recognition of novel objects, thereby impairing cognitive function (Rodríguez et al. 2008;Armato et al. 2013).”
Quote in the paperSubstantial claim1 of 2 sources checked- cites Rodríguez et al. 2008 source
The Discussion (page unavailable) links reduced hippocampal neurogenesis to certain learning and memory impairments. It does not address destruction of primary cilia in the cortex or hippocampus, or recognition of novel objects; searches for those terms found no supporting passage. The cognitive effect is thus supported only for a different proposed mechanism. (LLM, conf=0.84)
Experimental — accuracy not yet measured - cites Armato et al. 2013
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Interpretationcitation
Overexpression of SSTR3 in AD may act as a compensatory mechanism to counteract the deficiency of SST, potentially mitigating some pathophysiological effects of the disease.
“Therefore, overexpression of SSTR3 in AD may act as a compensatory mechanism to counteract the deficiency of SST, potentially mitigating some of the pathophysiological effects of the disease (Yeo et al. 2023).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Yeo et al. 2023 source
The Results and Discussion passages from our copy address microglial primary cilia, secretion, and amyloid pathology, not SSTR3 or SST. Searches for SSTR3, somatostatin, and a compensatory response to SST deficiency found no passage addressing the claim. (LLM, conf=0.76)
Experimental — accuracy not yet measured
- Rests on an assumption: SSTR3 is a unique GPCR localized to the primary cilia.
- Rests on an assumption: SST-expressing neurons form extensive neural connections and play a critical role in regulating hippocampal activity, learning, and memory.
- Premisecitation
SSTR3-induced signalling is associated with AC in the hippocampus.
“Previous research has demonstrated that SSTR3-induced signalling is associated with AC in the hippocampus (Einstein et al. 2010), and the genetic ablation of both AC3 and SSTR3 significantly impacts several region-related functions, including specific forms of memory (Wang, Phan, and Storm 2011;Chen et al. 2016;Wang et al. 2025).”
Quote in the paperSubstantial claim1 of 1 sources checked- cites Einstein et al. 2010 source
- Premisecitation
Primary cilia are of vital importance for neuronal synaptogenesis.
“Primary cilia are also of vital importance for neuronal synaptogenesis.Defects in primary cilia can lead to reduced neuronal dendrite length and prevent neurons from being properly integrated into neural circuits (Kumamoto et al. 2012).”
Quote in the paperSubstantial claim1 of 1 sources checked- cites Kumamoto et al. 2012 source
The Results report shorter dendrites and reduced synaptic input after cilia disruption in adult-born dentate granule cells; the Discussion describes severely disrupted integration with entorhinal projections. This supports an important role for cilia in that specific setting, but the unqualified claim about neuronal synaptogenesis generally extends beyond what the paper establishes. (LLM, conf=0.86)
Experimental — accuracy not yet measured
- Premisecitation
Genetic ablation of both AC3 and SSTR3 significantly impacts several region-related functions, including specific forms of memory.
“Previous research has demonstrated that SSTR3-induced signalling is associated with AC in the hippocampus (Einstein et al. 2010), and the genetic ablation of both AC3 and SSTR3 significantly impacts several region-related functions, including specific forms of memory (Wang, Phan, and Storm 2011;Chen et al. 2016;Wang et al. 2025).”
Quote in the paperNot a substantial claim3 of 3 sources checked- cites Wang, Phan, and Storm 2011 source
The Discussion reports that separate AC3−/− and SSTR3−/− mice are both deficient in novel-object memory. It also reports several learning and memory deficits in AC3−/− mice, but does not establish that SSTR3 ablation affects several functions or that both genes were ablated together. (LLM, conf=0.84)
Experimental — accuracy not yet measured - cites Chen et al. 2016 source
The Results section reports that AC3 knockout mice had impaired hippocampus-dependent spatial navigation and reduced long-lasting potentiation, supporting the AC3 and memory portion of the claim. The passages do not report SSTR3 ablation or its effects, so this source does not support that portion. (LLM, conf=0.87)
Experimental — accuracy not yet measured - cites Wang et al. 2025 source
The Results section, “Altered Spatial Memory and Synaptic Function” (page unavailable), reports significantly impaired spatial learning and memory in SSTR3-knockout mice, while working memory was not significantly affected. The cited paper therefore supports the SSTR3 and specific-memory portion, but our copy does not establish an effect of AC3 ablation; a search for AC3 found no such result. (LLM, conf=0.88)
Experimental — accuracy not yet measured
- Premisecitation
Liao et al. showed that N9 microglia possess primary cilium marked by acetylated α-tubulin.
“However, Liao et al. showed that N9 microglia possess primary cilium marked by acetylated α-tubulin (Liao et al. 2023).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Liao et al. 2023 source
- Findingown data
Primary hippocampal neurons demonstrated greater sensitivity to Aβ1-42 treatment compared to HEK293T cells.
“Notably, primary hippocampal neurons demonstrated greater sensitivity to Aβ 1-42 treatment compared to HEK293T cells.”
Quote in the paperNot a substantial claim - Findingown data
No significant alterations in Aβ42 secretion were observed in the supernatant from the culture medium of 5xFAD neurons.
“Likewise, when the supernatant from the culture medium was used in the ELISA experiment, no significant alterations in Aβ 42 secretion were observed (Figure S1E).”
Quote in the paperNot a substantial claim - Findingown data
Exogenous Aβ1-42 reduced primary cilia length in primary cultured mouse hippocampal neurons.
“These experiments confirmed that exogenous Aβ 1-42 similarly reduced ciliary length without altering the proportion of ciliated cells (Figure 1C,D).”
Quote in the paperSubstantial claim - Findingown data
Aβ1-42 treatment did not change the proportion of ciliated HEK293T cells.
“However, the proportion of cells bearing primary cilia remained unaffected by Aβ treatment, as determined by cell counting (Figure 1B).”
Quote in the paperSubstantial claim - Findingown data
Treatment of HEK293T cells with Aβ1-42 at concentrations of 1 μM or higher for 24 h significantly reduced primary cilia length.
“we observed that treatment with Aβ 1-42 at concentrations of 1 μM or higher for 24 h significantly reduced ciliary length (Figure 1A,B).”
Quote in the paperSubstantial claim - Findingown data
On the seventh day of in vitro culture, Aβ immunostaining on neurons from 5xFAD mice did not reveal significant Aβ deposits.
“On the seventh day of in vitro culture, Aβ immunostaining on neurons from 5 × FAD mice did not reveal significant Aβ deposits (Figure S1D).”
Quote in the paperSubstantial claim - Findingown data
Exogenous Aβ1-42 did not alter the proportion of ciliated primary cultured mouse hippocampal neurons.
“These experiments confirmed that exogenous Aβ 1-42 similarly reduced ciliary length without altering the proportion of ciliated cells (Figure 1C,D).”
Quote in the paperSubstantial claim - Findingown data
Tau treatment did not change the proportion of ciliated hippocampal neurons.
“Similarly, no significant differences were observed when counting the proportion of cells with primary cilia (Figure 1F).”
Quote in the paperSubstantial claim - Findingown data
In the brains of 4-month-old SSTR3-/-*5xFAD mice, numerous swollen axonal structures were observed around Aβ plaques.
“Immunofluorescence staining revealed that, in the brains of 4-month-old SSTR3 -/-*5 × FAD mice, numerous swollen axonal structures were observed around Aβ plaques (Figure 4C), indicating that these axons had begun to degenerate.”
Quote in the paperSubstantial claim - Findingown data
Primary cilia length in hippocampal neurons on the 7th day in vitro from APP/PS1, 5xFAD, and 3xTg mice was significantly longer compared to control wild-type mice.
“The results showed that the primary cilia length in hippocampal neurons on 7th day in vitro from APP/PS1, 5 × FAD, and 3*Tg mice in was significantly longer compared to control wild-type (WT) mice (Figure 3A,B).”
Quote in the paperSubstantial claim - Findingown data
Exogenous Tau treatment did not significantly change primary cilia length in cultured hippocampal neurons.
“Cultured hippocampal neurons treated with varying concentrations of exogenous Tau protein exhibited no significant changes in primary cilia length (Figure 1E,F).”
Quote in the paperSubstantial claim - Findingown data
Loss of SSTR3 in 5xFAD mice led to a significant increase in Aβ accumulation in the hippocampus as early as 2 months of age.
“Immunohistochemical staining demonstrated that the loss of SSTR3 in 5 × FAD mice led to a significant increase in Aβ accumulation in the hippocampus as early as 2 months of age (Figure 4A,B).”
Quote in the paperSubstantial claim - Findingown data
Treatment with a mixture of Aβ1-42 and Tau did not significantly differ in primary cilia length from treatment with Aβ1-42 alone.
“Statistical analysis showed no significant difference in primary cilia length between neurons treated with the Aβ 1-42 and Tau mixture and those treated with Aβ 1-42 alone (Figure S1C).”
Quote in the paperSubstantial claim - Findingown data
In APP/PS1 and 5xFAD mice, primary cilia length gradually increased with age.
“The results showed that the length of primary cilia in both APP/PS1 and 5 × FAD mice gradually increased with age.”
Quote in the paperSubstantial claim - Findingown data
Tau overexpression in primary cultured hippocampal neurons did not significantly alter ciliary length.
“Statistical analysis revealed that Tau overexpression in primary cultured hippocampal neurons did not significantly alter ciliary length (Figure 1H).”
Quote in the paperSubstantial claim - Findingown data
In SSTR3-/-*5xFAD mice, the number of microglia in the CA1 region of the hippocampus was not significantly different from 5xFAD mice.
“Immunohistochemical analysis revealed no significant difference in the number of microglia in the CA1 region of the hippocampus between SSTR3 -/-*5 × FAD and 5 × FAD mice (Figure 5A,B).”
Quote in the paperSubstantial claim - Findingown data
Aβ deposition is associated with significant changes in the morphology of primary cilia, particularly their shortening.
“We found that the deposition of Aβ is associated with significant changes in the morphology of primary cilia, particularly their shortening.”
- Also stated in: § 5 | Conclusion · plain
“The length of primary cilia was correlated with Aβ deposition in AD model mice.”
Quote in the paperSubstantial claim - Also stated in: § 5 | Conclusion · plain
- Findingown data
In SSTR3-/-*5xFAD mice, the number of Aβ-associated microglia was significantly reduced compared to 5xFAD mice.
“While Aβ plaques still attracted microglia in SSTR3 -/-*5 × FAD mice, the number of Aβ-associated microglia was significantly reduced compared to 5 × FAD mice (Figure 5D,E).”
- Also stated in: § 5 | Conclusion · plain
“A significant reduction in microglial numbers was observed in SSTR3 -/-* 5 × FAD mice compared to 5 × FAD mice.p = 0.0107.”
Quote in the paperSubstantial claim - Also stated in: § 5 | Conclusion · plain
- Findingown data
There was a significant increase in cell death in the CA1 region of the hippocampus of SSTR3-/-*5xFAD mice compared to 5xFAD controls.
“The results showed a significant increase in cell death in the CA1 region of SSTR3 -/-*5 × FAD mice compared to 5 × FAD controls (Figure 4E,F).”
Quote in the paperSubstantial claim - Findingown data
In the study, AD pathogenesis was accompanied by changes in primary cilia.
“In our study, we found that the pathogenesis of AD was accompanied by changes in primary cilia.”
Quote in the paperSubstantial claim - Findingown data
In SSTR3-/-*5xFAD mice, the Iba1-positive area in the hippocampal CA1 region was significantly increased compared to 5xFAD mice.
“However, the Iba1-positive area, reflecting microglial activation, was significantly increased in SSTR3 -/-*5 × FAD mice (Figure 5C).”
- Also stated in: § 5 | Conclusion · plain
“A significant increase in microglial activation was observed in SSTR3 -/-* 5 × FAD mice compared to 5 × FAD mice.p < 0.001.”
Quote in the paperSubstantial claim - Also stated in: § 5 | Conclusion · plain
- Findingown data
Compared to age-matched 5xFAD mice, axonal swelling was more pronounced in SSTR3-/-*5xFAD mice.
“Compared to age-matched 5 × FAD mice, the axonal swelling was more pronounced in SSTR3 -/-*5 × FAD mice (Figure 4D).”
Quote in the paperSubstantial claim - Findingown data
In APP/PS1 mice, neuronal ciliary length differed significantly with distance from Aβ deposition.
“Statistical analysis of ciliary length in neurons at different distances from Aβ deposition.One-way ANOVA followed by Tukey's post hoc test.F (3, 225) = 23.06;40 μm vs. 80 μm, p = 0.0861; 40 μm vs. 120 μm, p < 0.001; 40 μm vs. 160 μm, p < 0.001; 80 μm vs. 120 μm, p < 0.001; 80 μm vs. 160 μm, p < 0.001.”
Quote in the paperSubstantial claim - Findingown data
In SSTR3-/-*5xFAD mice, the area occupied by axonal swelling within a 30 μm radius around Aβ deposition was significantly increased compared to 5xFAD mice.
“A significant increase was observed in SSTR3 -/-* 5 × FAD mice compared to 5 × FAD mice.p = 0.0013.”
Quote in the paperSubstantial claim - Findingown data
In vitro, ciliary length of neurons from AD model mice on day 7 differed significantly from WT neurons.
“Statistical data of ciliary length of neurons in vitro on 7the day in AD model neuron and WT neuron.p < 0.001; One-way ANOVA followed by Šídák post hoc test.F (3, 287) = 25.63;WT, n = 101; APP/PS1, n = 60; 5 × FAD, n = 78; 3*Tg, n = 52.”
Quote in the paperSubstantial claim - Findingown data
In this study, SSTR3 expression was significantly increased in the hippocampal tissue of AD model mice.
“In this study, we observed a significant increase in SSTR3 expression in the hippocampal tissue of AD model mice.”
Quote in the paperSubstantial claim - Findingown data
In SSTR3-/-*5xFAD mice, Aβ deposition in the hippocampal region was significantly increased compared to 5xFAD mice.
“A significant increase in deposition was observed in SSTR3 -/-* 5 × FAD mice compared to 5 × FAD mice.p < 0.001.”
Quote in the paperSubstantial claim - Findingown data
In SSTR3-/-*5xFAD mice, the TUNEL-stained area in the hippocampus was significantly increased compared to 5xFAD mice.
“A significant increase in apoptotic signals was observed in SSTR3 -/-* 5 × FAD mice compared to 5 × FAD mice.p = 0.0041.”
Quote in the paperSubstantial claim - Findingown data
Knockout of SSTR3 increased the area of Aβ plaques.
“Additionally, knockout of SSTR3 accelerated the progression of AD pathology, increased the area of Aβ plaques, and impaired microglial phagocytosis.”
- Also stated in: § 5 | Conclusion · plain
“A significant increase in deposition was observed in SSTR3 -/-* 5 × FAD mice compared to 5 × FAD mice.p < 0.001.”
Quote in the paperSubstantial claim - Also stated in: § 5 | Conclusion · plain
- Findingown data
In 5xFAD mice, neuronal ciliary length differed significantly with distance from Aβ deposition.
“Statistical analysis of ciliary length in neurons at different distances from Aβ deposition.One-way ANOVA followed by Tukey's post hoc test.F (3, 72) = 9.83; 40 μm vs. 120 μm, p < 0.001; 40 μm vs. 160 μm, p < 0.001; 80 μm vs. 160 μm, p = 0.013.”
Quote in the paperSubstantial claim - Interpretationown data
The effect on primary ciliary length was mediated by Aβ rather than Tau.
“These results indicated that the effect of primary ciliary length was mediated by Aβ rather than Tau.”
Quote in the paperSubstantial claim - Interpretationown data
Primary cilia abnormalities in AD pathology might emerge in the early stages of the disease.
“These findings suggested that primary cilia abnormalities in AD pathology might emerge in the early stages of the disease.”
Quote in the paperSubstantial claim - Interpretationown data
These axons had begun to degenerate.
“indicating that these axons had begun to degenerate.”
Quote in the paperSubstantial claim - Premisecitation
SSTR3 is unique among somatostatin receptor subtypes in containing a ciliary targeting sequence, allowing it to selectively target primary cilia of neurons in the brain.
“Among these, somatostatin receptor 3 (SSTR3) is unique that it contains a ciliary targeting sequence, allowing it to selectively target the primary cilia of neurons in the brain (Barbeito and Garcia-Gonzalo 2021).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Barbeito and Garcia-Gonzalo 2021 source
- Interpretationown data
SSTR3 knockout in AD pathology impaired microglial aggregation around Aβ plaques.
“These findings suggested that SSTR3 knockout in AD pathology impaired microglial aggregation around Aβ plaques, which might contribute to the increased Aβ plaque burden observed SSTR3 -/-*5 × FAD mice.”
Quote in the paperSubstantial claim - Premisecitation
Abnormalities in the primary cilia-mediated Hedgehog signalling pathway have been observed in AD patients.
“Abnormalities in the primary cilia-mediated Hedgehog (Hh) signalling pathway have been observed in AD patients (He et al. 2014).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites He et al. 2014
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Interpretationreasoning
SSTR3 expression in 5xFAD mice contributed to maintaining normal neuronal function.
“These findings suggested that SSTR3 expression in 5 × FAD mice contributed to maintaining normal neuronal function.”
Quote in the paperSubstantial claim - Interpretationreasoning
Shortened primary cilia may impair their ability to sense and regulate external signals, thereby promoting the progression of AD.
“Shortened cilia may impair their ability to sense and regulate external signals, thereby promoting the progression of AD.”
Quote in the paperSubstantial claim - Premisecitation
Primary cilia exhibit distinct regional specificity in length, density, and incidence across different brain regions.
“Quantitative analyses of ciliary length, density, and incidence have further revealed that primary cilia exhibit distinct regional specificity, with significant variations in these parameters across different brain regions (Sipos, Komoly, and Ács 2018).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Sipos, Komoly, and Ács 2018 source
- Interpretationreasoning
SSTR3 knockout may contribute to the increased Aβ plaque burden observed in SSTR3-/-*5xFAD mice.
“These findings suggested that SSTR3 knockout in AD pathology impaired microglial aggregation around Aβ plaques, which might contribute to the increased Aβ plaque burden observed SSTR3 -/-*5 × FAD mice.”
Quote in the paperSubstantial claim - Premisecitation
Primary cilia play a crucial role in the progression of cognitive impairment in AD by influencing the maturation of cholinergic neurons in the forebrain.
“Furthermore, primary cilia play a crucial role in the progression of cognitive impairment in AD by influencing the maturation of cholinergic neurons in the forebrain (Guadiana et al. 2013).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Guadiana et al. 2013 source
- Premisecitation
SST levels are persistently reduced in the brain and cerebrospinal fluid of AD patients.
“Research has also shown a persistent reduction in SST levels in the brain and cerebrospinal fluid of AD patients (Bissette et al. 1998;Nilsson et al. 2001)”
Quote in the paperNot a substantial claim0 of 2 sources checked - Premisecitation
This reduction in SST is strongly correlated with Aβ plaque formation.
“This reduction is strongly correlated with Aβ plaque formation (Morrison et al. 1985).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Morrison et al. 1985 source
- Premisecitation
In AD brains and cerebrospinal fluid, SST levels are significantly reduced.
“In AD brains and cerebrospinal fluid, SST levels are significantly reduced (Reinikainen et al. 1987).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Reinikainen et al. 1987 source
- Interpretationown data
Knockout of SSTR3 accelerated the progression of AD pathology.
“Additionally, knockout of SSTR3 accelerated the progression of AD pathology, increased the area of Aβ plaques, and impaired microglial phagocytosis.”
- Also stated in: § 5 | Conclusion · plain
“Knockout of SSTR3 expression in 5 × FAD mice accelerated the progression of AD pathology.”
Quote in the paperSubstantial claim - Also stated in: § 5 | Conclusion · plain
- Interpretationreasoning
The functions of primary cilia may be emphasized differently depending on the brain region.
“This regional specificity implies that the functions of primary cilia may be emphasized differently depending on the brain region.”
Quote in the paperNot a substantial claim - Interpretationown data
Knockout of SSTR3 impaired microglial phagocytosis.
“Additionally, knockout of SSTR3 accelerated the progression of AD pathology, increased the area of Aβ plaques, and impaired microglial phagocytosis.”
Quote in the paperSubstantial claim
- May combine two claims. 19
- Classified as probably not a substantial claim. 20
- The quote only partly states this claim. 2
May combine two claims.
PremisecitationIn 5xFAD mice, Aβ deposition occurs in the hippocampal substratum and deep cortex as early as 2 months, with substantial deposition observed by 6 months.
“In 5 × FAD mice, Aβ deposition occurs in the hippocampal substratum and deep cortex as early as 2 months, with substantial deposition observed by 6 months.”
Quote in the paperSubstantial claim1 of 2 sources checkedMay combine two claims.
PremisecitationThe presence of dystrophic neurites is associated with impairments in synaptic function, axonal transport, and neuroinflammation, serving as an early indicator of axonal damage prior to synaptic failure in the initial stages of AD.
“The presence of dystrophic neurites is associated with impairments in synaptic function, axonal transport, and neuroinflammation, thereby serving as an early indicator of axonal damage prior to synaptic failure in the initial stages of AD (Sanchez-Varo et al. 2012).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Sanchez-Varo et al. 2012 source
The Introduction (page unavailable) describes early dystrophic neurites as a possible sign of axonal damage preceding synaptic loss, and the Discussion reports defective axonal transport in dystrophic axons. The paper also describes altered presynaptic structures, but does not demonstrate impaired synaptic function or directly associate dystrophic neurites with neuroinflammation; its inflammatory-response statement concerns neuronal loss associated with amyloid in the mouse model. (LLM, conf=0.86)
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationThe formation and aggregation of Aβ fibrils are central to extracellular Aβ plaques, often accompanied by dystrophic neurites consisting of swollen axons and terminals.
“The formation and aggregation of Aβ fibrils are central to extracellular Aβ plaques, which are often accompanied by dystrophic neurites that consist of swollen axons and terminals (Sadleir et al. 2016;Tsering and Prokop 2024).”
Quote in the paperNot a substantial claim2 of 2 sources checked- cites Sadleir et al. 2016 source
- cites Tsering and Prokop 2024 source
The Introduction (Pathological Hallmarks of Alzheimer’s Disease; page unavailable) describes extracellular Aβ deposits and identifies neuritic plaques as Aβ plaques surrounded by swollen or dystrophic neurites. The Introduction (NP and Its Correlation with Network Dysfunction and Cognition; page unavailable) describes those neurites as swollen axonal structures. The paper discusses Aβ aggregation and a fibrillar plaque subtype, but does not establish that fibrils are central to all extracellular Aβ plaques or explicitly describe the neurites as swollen terminals. (LLM, conf=0.83)
Experimental — accuracy not yet measured
Classified as probably not a substantial claim.
PremisecitationAC3 is a commonly accepted neuronal primary cilia marker protein.
“AC3 is a commonly accepted neuronal primary cilia marker protein, and ARL13B antibody is commonly used to label astrocytic primary cilia (Sipos, Komoly, and Ács 2018;Sterpka and Chen 2018).”
Quote in the paperSubstantial claim1 of 2 sources checkedProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationUpregulation of SSTR3 leads to an increase in the length of primary cilia.
“Previous studies have shown that the upregulation of SSTR3 will lead to an increase in the length of primary cilia (Wang et al. 2025).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Wang et al. 2025 source
May combine two claims.
InterpretationcitationPrimary cilia length plays a critical role in the proper formation and function of synapses, which is an important pathological feature of AD.
“Collectively, these findings underscore the critical role of primary cilia length in the proper formation and function of synapses, which is an important pathological feature of AD.”
Quote in the paperSubstantial claim3 of 3 sources checked- cites Kumamoto et al. 2012 source
The Discussion (“Essential roles of primary cilia in neuronal development”; page unavailable) reports that deleting primary cilia from newborn hippocampal neurons disrupted synaptic integration and reduced synaptic-event frequency. It does not establish that cilia length, specifically, controls synapse formation or function, and it does not connect these findings to Alzheimer’s disease. (LLM, conf=0.87)
Experimental — accuracy not yet measured - cites Guo et al. 2017 source
The Introduction and Results (page numbers unavailable) show that disrupting primary cilia signaling impairs interneuronal connectivity and inhibitory synaptic activity. They do not establish that cilia length is critical to synapse formation or function, or link this finding to Alzheimer’s disease (AD). (LLM, conf=0.88)
Experimental — accuracy not yet measured - cites Sheu et al. 2022 source
The Results ("FIB-SEM reveals axo-ciliary synapses"; page unavailable) document synapses contacting neuronal primary cilia. But the Results ("Axo-ciliary synapses are serotonergic"; page unavailable) find no significant correlation between cilia length and proximity to serotonergic axons, and the paper does not establish that cilia length is critical to synapse formation or function or link that claim to AD. (LLM, conf=0.84)
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationARL13B antibody is commonly used to label astrocytic primary cilia.
“AC3 is a commonly accepted neuronal primary cilia marker protein, and ARL13B antibody is commonly used to label astrocytic primary cilia (Sipos, Komoly, and Ács 2018;Sterpka and Chen 2018).”
Quote in the paperNot a substantial claim1 of 2 sources checkedMay combine two claims.
PremisecitationIn APP/PS1 mice, Aβ plaques begin to appear in the cerebral cortex around 4 months of age and in the hippocampus around 6 months.
“In APP/PS1 mice, Aβ plaques begin to appear in the cerebral cortex around 4 months of age and in the hippocampus around 6 months.”
Quote in the paperSubstantial claim1 of 2 sources checked- cites Lalonde et al. 2005 source
- cites Zhong et al. 2024 source
The Introduction’s transgenic-mouse-models section (page unavailable) reports Aβ deposits in APP/PS1 mice as early as 4 months, but does not locate those early deposits in the cortex. It reports plaques in both the hippocampus and cortex by 9 months; its 6-month finding concerns memory deficits, not hippocampal plaque onset. (LLM, conf=0.87)
Experimental — accuracy not yet measured
May combine two claims.
InterpretationcitationAbnormalities in ciliary function could lead to excitatory imbalances in neurons, disrupting brain electrical activity, and may be closely related to abnormal electrical activity in AD pathology.
“Abnormalities in ciliary function could lead to excitatory imbalances in neurons, disrupting brain electrical activity (Vien et al. 2023), and it may be closely related to abnormal electrical activity in AD pathology.”
Quote in the paperSubstantial claim1 of 1 sources checked- cites Vien et al. 2023 source
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationThe dynamic composition of ciliary proteins endows primary cilia with the capacity to transduce a multitude of signal inputs through an intricate signalling network.
“The dynamic composition of ciliary proteins endows primary cilia with the capacity to transduce a multitude of signal inputs through an intricate signalling network.This mechanism enables primary cilia to process information in both temporal and spatial dimensions, integrating complex cellular cues with high precision (Anvarian et al. 2019).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Anvarian et al. 2019 source
May combine two claims.
PremisecitationMicroglia form a barrier to prevent Aβ plaques from expanding outward, and areas deficient in microglia exhibit increased Aβ plaque burden and severe axonal degeneration.
“High-resolution confocal and in vivo two-photon imaging have demonstrated that microglia form a barrier to prevent Aβ plaques from expanding outward, with areas deficient in microglia exhibiting increased Aβ plaque burden and severe axonal degeneration (Condello et al. 2015).”
Quote in the paperSubstantial claim1 of 1 sources checked- cites Condello et al. 2015 source
The Introduction says the imaging showed that microglia restrict the radial expansion of plaques. The Results section on neuritic dystrophy reports greater axonal dystrophy in plaque regions lacking microglial processes, alongside local accumulation of protofibrillar Aβ42. It does not establish increased overall Aβ plaque burden in those areas; local hotspots are narrower than that claim. The indexed passages provide section labels but no page numbers. (LLM, conf=0.86)
Experimental — accuracy not yet measured
May combine two claims.
PremisecitationPrimary cilia serve as key sensory organelles that detect extracellular signals and mediate intracellular signalling pathways, playing a crucial role in the function and health of neurons.
“Primary cilia serve as key sensory organelles that detect extracellular signals and mediate intracellular signalling pathways, playing a crucial role in the function and health of neurons”
Quote in the paperSubstantial claim1 of 1 sources checked- cites Goetz and Anderson 2010 source
The Abstract describes primary cilia as necessary for responses to developmental signals, and the section on Hedgehog signaling in adult tissues reports roles in cerebellar growth and the maintenance of neural progenitors. These passages support a role in neural signaling and development, but do not establish the broader claim that cilia are crucial to the function and health of neurons generally. Page numbers are not available in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measured
May combine two claims.
PremisecitationDefects in primary cilia can lead to reduced neuronal dendrite length and prevent neurons from being properly integrated into neural circuits.
“Primary cilia are also of vital importance for neuronal synaptogenesis.Defects in primary cilia can lead to reduced neuronal dendrite length and prevent neurons from being properly integrated into neural circuits (Kumamoto et al. 2012).”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Kumamoto et al. 2012 source
May combine two claims.
PremisecitationSuch defects can be rescued by activating ciliary G-protein-coupled receptors (GPCRs), highlighting the significance of these receptors on primary cilia for neural circuit formation.
“Such defects can be rescued by activating ciliary G-protein-coupled receptors (GPCRs), highlighting the significance of these receptors on primary cilia for neural circuit formation.”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites Guo et al. 2017 source
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationThe regulation of ciliary length, such as ciliary elongation, is recognized as a key mechanism to modulate the signalling activities of organelles in response to changes in the extracellular environment.
“The regulation of ciliary length, such as ciliary elongation, is recognized as a key mechanism to modulate the signalling activities of organelles in response to changes in the extracellular environment (Dummer et al. 2016;Hilgendorf, Johnson, and Jackson 2016).”
Quote in the paperNot a substantial claim2 of 2 sources checked- cites Dummer et al. 2016 source
The Background says that cilium elongation may change receptor availability and that length differences might fine-tune signaling; it also describes greater sensitivity to flow changes in longer cilia. It does not establish length regulation as a key mechanism: its conclusion about signaling is tentative. Page numbers are not available in our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measured - cites Hilgendorf, Johnson, and Jackson 2016 source
The Introduction (page unavailable) says cilia vary in length between tissues and that tissue-specific structures may tune ciliary signaling. It does not establish that ciliary elongation in response to extracellular changes is a key mechanism for modulating signaling. (LLM, conf=0.85)
Experimental — accuracy not yet measured
May combine two claims.
PremisecitationIn AD pathology, microglia play a crucial role in clearing Aβ depositions and inhibiting Tau hyperphosphorylation.
“In AD pathology, microglia play a crucial role in clearing Aβ depositions and inhibiting Tau hyperphosphorylation (Wang et al. 2016).”
Quote in the paperSubstantial claim1 of 1 sources checked- cites Wang et al. 2016 source
In Results and Discussion, the paper reports that TREM2-sufficient microglia engulf portions of Aβ plaques and that TREM2-deficient mice have more hyperphosphorylated tau puncta near plaques. This supports a protective role in the studied mouse model, but the paper emphasizes plaque containment rather than demonstrating clearance of Aβ deposits, and it does not establish that microglia directly inhibit tau hyperphosphorylation across AD pathology. Page numbers are unavailable in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measured
May combine two claims.
Findingown dataAfter the onset of Aβ deposition, primary cilia growth ceased at 6 months in APP/PS1 mice and at 2 months in 5xFAD mice.
“However, after the onset of Aβ deposition, primary cilia growth ceased at 6 months in APP/PS1 mice (Figure 2E,G) and at 2 months in 5 × FAD mice (Figure 2F,H).”
Quote in the paperSubstantial claimThe quote only partly states this claim.
Findingown dataIn APP/PS1 and 5xFAD mice, primary cilia length in neurons increased with increasing distance from Aβ deposition.
“Immunohistochemical staining revealed that the length of primary cilia in neurons increased with increasing distance from the Aβ deposition (Figure 2C).”
- Also stated in: § 3.2 | Aβ Deposition Affected Primary Ciliary Length in AD Model Mice · plain
“Consistent results were observed using immunohistochemical staining (Figure 2D).”
Quote in the paperSubstantial claim- Also stated in: § 3.2 | Aβ Deposition Affected Primary Ciliary Length in AD Model Mice · plain
May combine two claims.
Findingown dataPrimary cilia of neurons in AD model mice exhibited abnormalities, along with altered expression of the ciliary protein SSTR3.
“The primary cilia of neurons in AD models mice exhibited abnormalities, along with altered expression of the ciliary protein SSTR3.”
Quote in the paperSubstantial claimThe quote only partly states this claim.
Findingown dataSSTR3 expression in the hippocampus of APP/PS1, 5xFAD, and 3xTg mice at 12 months was significantly increased compared to control.
“Quantitative analysis of western blot results.Control vs. APP/PS1, p = 0.0022; control vs. 5 × FAD, p = 0.0038; control vs. 3*Tg, p = 0.0030.control, n = 9; APP/PS1, n = 9; 5 × FAD, n = 9; 3*Tg, n = 9.”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataIn APP/PS1 mice, ciliary length in brain slices decreased significantly from 2 months to 6 and 12 months, but not between 6 and 12 months.
“Statistical analysis of ciliary length in brain slices from APP/PS1 mice at different ages.One-way ANOVA followed by Šídák post hoc test.F (2, 339) = 50.70; 2 months vs. 6 months, p < 0.001; 2 months vs. 12 months, p < 0.001; 6 months vs. 12 months, p = 0.9668.”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataIn 5xFAD mice, ciliary length in brain slices decreased significantly from 1 month to 2 and 6 months, but not between 2 and 6 months.
“Statistical analysis of ciliary length in brain slices from 5 × FAD mice at different ages.One-way ANOVA followed by Šídák post hoc test.F (2, 365) = 19.79; 1 month vs. 2 months, p < 0.001; 1 month vs. 6 months, p = 0.0154; 2 months vs. 6 months, p = 0.4458.”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataAD pathology directly impacts primary cilia, affecting both their morphology and associated proteins.
“In summary, our investigation provides further evidence that AD pathology directly impacts primary cilia, affecting both their morphology and associated proteins.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone givenMice were randomly selected as biological replicates in all experiments to make the study reliable.
“In all the experiments, mice were randomly selected as biological replicates to make the study reliable.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationThe accumulation of Aβ in the brain is widely regarded as a toxic event in the pathogenesis of AD, initiating a cascade of pathological processes detrimental to neuronal health.
“The accumulation of Aβ in the brain is widely regarded as a toxic event in the pathogenesis of AD, initiating a cascade of pathological processes that are detrimental to neuronal health (Thal et al. 2015).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Thal et al. 2015 source
May combine two claims.
PremisecitationOnly SSTR3 among the five somatostatin receptor subtypes contains ciliated localization sequences and has been shown to enhance cortical staining in patients with AD.
“Of the five subtypes of somatostatin receptors (SSTRs), only SSTR3 contains ciliated localization sequences and has been shown to enhance cortical staining in patients with AD (Kumar 2005;Barbeito and Garcia-Gonzalo 2021).”
Quote in the paperSubstantial claim0 of 2 sources checkedProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductown dataStatistical analysis of ciliary lengths was performed combining three experimental replicates.
“Statistical analysis of the ciliary lengths was performed, combining three experimental replicates, and all the data were represented as scatter plots.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationSSTR3 is present on primary ciliary membranes of insulin-secreting β cells in the pancreas and growth hormone-secreting pituitary cells in the anterior pituitary gland, making SSTR3 another common ciliary marker.
“It is also present on the primary ciliary membranes of insulin-secreting β cells in the pancreas and growth hormone-secreting pituitary cells in the anterior pituitary gland, making SSTR3 another common ciliary marker (Barbeito et al. 2021).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Barbeito et al. 2021 source
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationAβ deposition is known to cause structural and functional neuronal damage.
“Aβ deposition is known to cause structural and functional neuronal damage (Jawhar et al. 2012).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Jawhar et al. 2012 source
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationSST deficiency is correlated with Aβ deposition.
“Furthermore, SST deficiency has been correlated with Aβ deposition (Morrison et al. 1985).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Morrison et al. 1985 source
Classified as probably not a substantial claim.
Study design and conductreasoningTo minimize confounding effects of multiple Aβ deposits, analysis focused on neurons within 160 μm of a single Aβ deposition.
“To minimize the confounding effects of multiple Aβ deposits, we focused on neurons within 160 μm of a single Aβ deposition.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationSST deficiency is strongly linked to cognitive and memory impairments.
“with this deficit strongly linked to cognitive and memory impairments (Grouselle et al. 1998).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Grouselle et al. 1998 source
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationBrain regions affected in the early stages of AD, such as the hippocampus and cortex, are also areas where neuropeptides like bradykinin and SST, along with their receptors, are changed.
“Notably, brain regions affected in the early stages of AD, such as the hippocampus and cortex, are also areas where neuropeptides like bradykinin and SST, along with their receptors, are changed (Corrêa et al. 1979;Johansson, Hökfelt, and Elde 1984).”
Quote in the paperNot a substantial claim0 of 2 sources checkedProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationPrimary cilia in neurons and astrocytes exhibit specific distribution patterns in the brain, with marker proteins displaying an orderly arrangement, suggesting potential functional differences among cilia of distinct cell types.
“Studies have highlighted that primary cilia in neurons and astrocytes exhibit specific distribution patterns in the brain, with marker proteins displaying an orderly arrangement, suggesting potential functional differences among cilia of distinct cell types (Sipos, Komoly, and Ács 2018).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Sipos, Komoly, and Ács 2018 source
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationSipos et al. reported that microglia in mouse hippocampus do not display primary cilia marked by AC3 and ARL13B.
“Sipos et al. reported that microglia in mouse hippocampus do not display primary cilia marked by AC3 and ARL13B (Sipos, Komoly, and Ács 2018).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Sipos, Komoly, and Ács 2018 source
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationSSTR3 is the only subtype in the cortical region of AD that exhibits enhanced staining.
“A previous study demonstrated that SSTR3 is the only subtype in the cortical region of AD that exhibits enhanced staining (Kumar 2005).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Kumar 2005 source
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationMicroglia are the main phagocytes in the central nervous system.
“Microglia are the main phagocytes in the central nervous system (Prinz, Jung, and Priller 2019).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Prinz, Jung, and Priller 2019 source
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationCertain neuropeptides exhibit significant declines with aging, even before the onset of AD.
“Previous studies have shown that certain neuropeptides exhibit significant declines with aging, even before the onset of AD (Fliers and Swaab 1986).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Fliers and Swaab 1986 source
The paper relies on this without support.
Primary cilia have not been extensively studied in the context of AD progression.
“Primary cilia, organelles associated with age-related diseases, have not been extensively studied in the context of AD progression.”
The paper relies on this without support.
The changes in neuronal primary cilia during the pathological progression of AD and their specific role in the disease process remain unclear.
“However, the changes in neuronal primary cilia during the pathological progression of AD and their specific role in the disease process remain unclear.”
The paper relies on this without support.
Primary cilia exist transiently in microglia, and their number is significantly reduced in microglia from AD mice.
“Recent studies have also shown that primary cilia exist transiently in microglia, and their number is significantly reduced in microglia from AD mice.”
The paper relies on this without support.
Inhibiting the primary cilia of microglia in AD mice leads to the expansion of extracellular amyloid plaques and damage to adjacent neurites.
“Inhibiting the primary cilia of microglia in AD mice leads to the expansion of extracellular amyloid plaques and damage to adjacent neurites, indicating that the primary cilia signalling system is crucial for maintaining the normal function of microglia and inhibiting the progression of AD.”
The paper relies on this without support.
The primary cilia signalling system is crucial for maintaining the normal function of microglia and inhibiting the progression of AD.
“Inhibiting the primary cilia of microglia in AD mice leads to the expansion of extracellular amyloid plaques and damage to adjacent neurites, indicating that the primary cilia signalling system is crucial for maintaining the normal function of microglia and inhibiting the progression of AD.”
The paper relies on this without support.
SSTR3 is a unique GPCR localized to the primary cilia.
“SSTR3 is a unique GPCR localized to the primary cilia.”
The paper relies on this without support.
SST-expressing neurons form extensive neural connections and play a critical role in regulating hippocampal activity, learning, and memory.
“SST-expressing neurons have been found to form extensive neural connections, playing a critical role in regulating hippocampal activity, learning, and memory.”
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?
Aβ deposition can cause cilia length to shorten in vitro and in vivo.
“In relation to AD, it has been shown that Aβ deposition can cause cilia length to shorten in vitro and in vivo [47,48].”
From Primary Cilia and Cardiovascular Risk Factors in Alzheimer's Disease (2025) · cites this paper as [47]
Section 3.1 reports that Aβ 1-42 treatment shortened primary cilia in cultured cells and neurons. Section 3.2 finds shorter neuronal cilia closer to Aβ deposits in AD-model mice, but this in vivo association does not establish that deposition caused the shortening. Page numbers were not available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIn Alzheimer's disease mouse models, both the number and morphology of microglial primary cilia are significantly reduced.
“In AD mouse models, both the number and morphology of microglial PC are significantly reduced [84,85,86].”
From The Impact of Neurotoxin Proteins Trafficked by Primary Cilia and Extracellular Vesicles in Neurodegenerative Diseases (2025) · cites this paper as [85]
The Discussion (section 4; page unavailable) says the number of primary cilia is significantly reduced in microglia from AD mice. It does not report a reduction in microglial cilia morphology; the morphological changes described in the Results (sections 3.2–3.3; pages unavailable) concern neuronal cilia. (LLM, conf=0.88)
Experimental — accuracy not yet measuredHippocampal neurons derived from multiple transgenic AD mouse models (APP/PS1, 5 × FAD, and 3 × Tg) exhibit elongated cilia during early in vitro development (Day 7), even before detectable Aβ deposition or altered secretion.
“Intriguingly, hippocampal neurons derived from multiple transgenic AD mouse models (APP/PS1, 5 × FAD, and 3 × Tg) exhibit elongated cilia during early in vitro development (Day 7), even before detectable Aβ deposition or altered secretion (Guo et al., 2025).”
From Primary cilia in the mature brain: emerging roles in Alzheimer's disease pathogenesis (2025) · cites this paper as Guo et al., 2025
Section 3.3 reports significantly longer cilia on day 7 in cultured hippocampal neurons from all three AD mouse models. It reports no significant Aβ deposits in neurons from 5 × FAD mice and no significant change in Aβ42 secretion, but does not establish those findings for all three models as the claim implies. (LLM, conf=0.84)
Experimental — accuracy not yet measuredExogenous Aβ1-42 exposure shortens the primary cilia of cultured mouse neurons without affecting the ciliation rates, whereas tau overexpression does not alter ciliary length or ciliation rate.
“Exogenous Aβ1–42 exposure shortened the primary cilia of cultured mouse neurons without affecting the ciliation rates, whereas tau overexpression does not alters ciliary length or ciliation rate (Guo et al., 2025), suggesting a selective vulnerability to Aβ.”
From Primary cilia in the mature brain: emerging roles in Alzheimer's disease pathogenesis (2025) · cites this paper as Guo et al., 2025
Section 3.1 (page not provided) reports that exogenous Aβ1–42 shortened cilia in cultured mouse hippocampal neurons without changing the proportion of ciliated cells. It also reports no significant change in ciliary length after tau overexpression, but the unchanged ciliation rate was measured after exogenous tau treatment, not tau overexpression. (LLM, conf=0.88)
Experimental — accuracy not yet measuredShortening of cilia can impair their ability to sense and regulate external signals, leading to the promotion of AD.
“The shortening of cilia can impair their ability to sense and regulate external signals, leading to the promotion of AD [47].”
From Primary Cilia and Cardiovascular Risk Factors in Alzheimer's Disease (2025) · cites this paper as [47]
Sstr3 expression is significantly elevated in the hippocampus of 12-month-old APP/PS1, 5 × FAD, and 3 × Tg mice relative to wild-type controls.
“Similarly, Sstr3 expression was significantly elevated in the hippocampus of 12-month-old APP/PS1, 5 × FAD, and 3 × Tg mice relative to wild-type controls (Guo et al., 2025).”
From Primary cilia in the mature brain: emerging roles in Alzheimer's disease pathogenesis (2025) · cites this paper as Guo et al., 2025
In the hippocampal CA1 region of APP/PS1 and 5×FAD mice, neuronal primary cilia length gradually increases with age but ceases to elongate following the onset of Aβ accumulation.
“In the hippocampal CA1 region of both models, neuronal primary cilia length gradually increases with age but ceases to elongate following the onset of Aβ accumulation (Guo et al., 2025).”
From Primary cilia in the mature brain: emerging roles in Alzheimer's disease pathogenesis (2025) · cites this paper as Guo et al., 2025
In offspring of Sstr3 knockout mice crossed with 5 × FAD mice (Sstr3−/− × 5 × FAD, 4 months old), the loss of Sstr3 worsens Aβ accumulation, increases hippocampal neuronal apoptosis, and heightens microglial reactivity in the CA1 region, but reduces microglial clustering around Aβ plaques compared to 5 × FAD controls.
“In offspring of Sstr3 knockout mice crossed with 5 × FAD mice (Sstr3−/− × 5 × FAD, 4 months old), the loss of the primary ciliary-localized receptor Sstr3 worsened Aβ accumulation, increased hippocampal neuronal apoptosis, and heightened microglial reactivity in the CA1 region. However, paradoxically, it reduced microglial clustering around Aβ plaques compared to 5 × FAD controls (Guo et al., 2025”
From Primary cilia in the mature brain: emerging roles in Alzheimer's disease pathogenesis (2025) · cites this paper as Guo et al., 2025
In the brains of 12-month-old APP/PS1 and 4-month-old 5 × FAD mice, AC3-labeled neuronal primary cilia are significantly shorter in regions adjacent to Aβ plaques compared to more distant areas.
“In the brains of 12-month-old amyloid precursor protein/presenilin-1 (APP/PS1) and 4-month-old 5 × FAD mice, AC3-labeled neuronal primary cilia are significantly shorter in regions adjacent to Aβ plaques compared to more distant areas.”
From Primary cilia in the mature brain: emerging roles in Alzheimer's disease pathogenesis (2025) · cites this paper as Guo et al., 2025
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Tau-treated neuron counts do not match the ANOVA degrees of freedom
MinorThe five reported groups total 250 observations, implying 245 residual degrees of freedom for the stated one-way ANOVA, rather than 226.
Reported 226 · recomputed 250
“F (4, 226) = 0.4447.0 μM, n = 51; 0.05 μM, n = 45; 0.1 μM, n = 56; 0.2 μM, n = 49; 1 μM, n = 49.”
Aβ-treated HEK293T cilia counts do not match the ANOVA degrees of freedom
MinorThe four reported groups contain 293 observations. A one-way ANOVA with four groups would therefore have 289 residual degrees of freedom, not 283.
Reported 283 · recomputed 293
“F (3, 283) = 20.14;0 μM vs. 1 μM, p < 0.001; 0 μM vs. 2 μM, p < 0.001.0 μM, n = 75; 0.5 μM, n = 85; 1 μM, n = 77; 2 μM, n = 56.”
Figure 2C cilia counts do not match the ANOVA degrees of freedom
MinorThe four distance groups total 259 observations. Their one-way ANOVA would have 255 residual degrees of freedom, rather than the reported 225.
Reported 225 · recomputed 259
“F (3, 225) = 23.06;40 μm vs. 80 μm, p = 0.0861; 40 μm vs. 120 μm, p < 0.001; 40 μm vs. 160 μm, p < 0.001; 80 μm vs. 120 μm, p < 0.001; 80 μm vs. 160 μm, p < 0.001.40 μm, n = 59; 80 μm, n = 88; 120 μm, n = 53; 160 μm, n = 59.”
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Primary cilia in the mature brain: emerging roles in Alzheimer's disease pathogenesis
Huang, A. S., Li, A. S. M., & Hor, C. H. H. (2025) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2025.1650884 · Cited by 4 · see citing works
“Exogenous Aβ 1 – 42 exposure shortened the primary cilia of cultured mouse neurons without affecting the ciliation rates, whereas tau overexpression does not alters ciliary length or ciliation rate (Guo et al., 2025), suggesting a selective vulnerability to Aβ.”
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Primary Cilia and Cardiovascular Risk Factors in Alzheimer's Disease
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“The shortening of cilia can impair their ability to sense and regulate external signals, leading to the promotion of AD [47].”
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“Guo et al. (2025) demonstrated that primary cilia undergo shortening — not merely dysfunction — upon Aβ deposition (NJ et al., 2025), a finding confirmed and extended in a comprehensive review of ciliary roles in the mature AD brain (R et al., 1998).”
- Authors
- Guo, A., Wang, H., Zhang, Y., & Huang, H.
- Affiliations
- Capital Medical University (CN)
- Peking University (CN)
- Yantai Laiyang Central Hospital (CN)
- Corresponding author
- Huang, Hongbin
- Venue
- European Journal of Neuroscience
- Publisher
- Wiley
- Published
- 2025-05
- Volume
- 61
- Issue
- 9
- Pages
- e70125-e70125
- ISSN
- 0953-816X (ISSN-L)
- 1460-9568
- OpenAlex
- W4410136799
- Cited by
- 7
- References
- 73
- Citations by year
- 2026: 4 · 2025: 3
- FWCI
- 4.46
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- European Journal of Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Natural Science Foundation of Zhejiang Province (TGY24H090008)
- Ministry of Science and Technology (2018YFA0507600, 2017YFA0503600)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic and Kidney Cyst Diseases
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, primary cilia, amyloid plaques, SSTR3, hippocampus, neurodegeneration, aging
- MeSH terms
- Alzheimer Disease, Animals, Cilia, Hippocampus, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Amyloid beta-Peptides, Receptors, Somatostatin, Mice, Knockout, Mice, Plaque, Amyloid
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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.
Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-11.
Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-11.
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