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Extracellular vesicles derived from astrocyte-treated with haFGF14-154 attenuate Alzheimer phenotype in AD mice

Peng, Dong, Wang, Youjin, Xiao, Yuanjie, Peng, Mengyuan, Mai, Wanwen, Hu, Bo, Jia, Yanbin, Chen, Hongxia, Yang, Yan, Xiang, Qi, Su, Zhijian, Zhang, Qihao, Huang, Yadong·2022·Theranostics
DOI 10.7150/thno.70951PMC PMC9131260
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Figures

Figure 1 AEVs-Aβ+H promote neurite outgrowth and diminish Aβ loading in neurons in vitro. (A) The representative images of MAP2+ cells (red) in rat primary cortical neurons treated with AEVs under the condition of Aβ-injury. (Scale bars, 50 µm). Quantification of the average neurite length of neurons (B), the proportion of the longest length of neural neurites over 100 µm (C) and the number of neural neurites per neuron (D), n = 6. (E) The representative immunoblots of PSD95, GAP43, SYN and Aβ. The quantified expression of PSD95 (F), GAP43 (G), SYN (H) and Aβ (I), n = 6. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test.
Figure 1 AEVs-Aβ+H promote neurite outgrowth and diminish Aβ loading in neurons in vitro. (A) The representative images of MAP2+ cells (red) in rat primary cortical neurons treated with AEVs under the condition of Aβ-injury. (Scale bars, 50 µm). Quantification of the average neurite length of neurons (B), the proportion of the longest length of neural neurites over 100 µm (C) and the number of neural neurites per neuron (D), n = 6. (E) The representative immunoblots of PSD95, GAP43, SYN and Aβ. The quantified expression of PSD95 (F), GAP43 (G), SYN (H) and Aβ (I), n = 6. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test.CC BY · PubMed Central
Figure 2 AEVs-Aβ+H ameliorate cognitive behavior deficits and promote synaptic plasticity in APP/PS1 mice. (A) Schedule of intranasal administration and behavior test of APP/PS1 mice. (B) Spontaneous alternation in Y-maze (n = 6-8). (C) The representative movement tracks of escape latency on day 5 in navigation test of MWM. (D-E) The escape latency (n = 8/9). Representative movement tracks in spatial probe test (F), numbers of crossing the removed platform area (G) and time spend in target quadrant (I) in spatial probe test of MWM, n = 8/9. (H) The representative images of synaptic structure in CA1 region of hippocampus observed by TEM. The length (J) and width (K) of PSD were quantified from 7 random fields per slide, 1 slide per animal, and 3 animals per group (n = 21). Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test and two-way ANOVA with Tukey's post-hoc test.
Figure 2 AEVs-Aβ+H ameliorate cognitive behavior deficits and promote synaptic plasticity in APP/PS1 mice. (A) Schedule of intranasal administration and behavior test of APP/PS1 mice. (B) Spontaneous alternation in Y-maze (n = 6-8). (C) The representative movement tracks of escape latency on day 5 in navigation test of MWM. (D-E) The escape latency (n = 8/9). Representative movement tracks in spatial probe test (F), numbers of crossing the removed platform area (G) and time spend in target quadrant (I) in spatial probe test of MWM, n = 8/9. (H) The representative images of synaptic structure in CA1 region of hippocampus observed by TEM. The length (J) and width (K) of PSD were quantified from 7 random fields per slide, 1 slide per animal, and 3 animals per group (n = 21). Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test and two-way ANOVA with Tukey's post-hoc test.CC BY · PubMed Central
Figure 3 AEVs-Aβ+H enhance the expression of synaptic proteins and alleviate brain Aβ burden in APP/PS1 mice. (A-H) The expression of PSD95, GAP43 and SYN in the prefrontal cortex (PFC) (A) and hippocampus (E) of APP/PS1 mice with intranasal administration of AEVs. The relative expression quantification of PSD95 (B), GAP43 (C), SYN (D) in the PFC and PSD95 (F), GAP43 (G), SYN (H) in hippocampus, n = 8-10. (I) The representative images of Aβ plaque in the dentate gyrus (DG), CA1 and CA3 regions of hippocampus (Scale: 100 µm). (J-L) The area of Aβ plaque is analyzed by image-pro plus software, n = 5-7. (M) Aβ in the PFC and hippocampus were detected by western blot. The quantified expression of Aβ in the PFC (N) and hippocampus (O), n = 8-10. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test.
Figure 3 AEVs-Aβ+H enhance the expression of synaptic proteins and alleviate brain Aβ burden in APP/PS1 mice. (A-H) The expression of PSD95, GAP43 and SYN in the prefrontal cortex (PFC) (A) and hippocampus (E) of APP/PS1 mice with intranasal administration of AEVs. The relative expression quantification of PSD95 (B), GAP43 (C), SYN (D) in the PFC and PSD95 (F), GAP43 (G), SYN (H) in hippocampus, n = 8-10. (I) The representative images of Aβ plaque in the dentate gyrus (DG), CA1 and CA3 regions of hippocampus (Scale: 100 µm). (J-L) The area of Aβ plaque is analyzed by image-pro plus software, n = 5-7. (M) Aβ in the PFC and hippocampus were detected by western blot. The quantified expression of Aβ in the PFC (N) and hippocampus (O), n = 8-10. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test.CC BY · PubMed Central
Figure 4 aFGF down-regulates the level of miR-206-3p targeting BDNF in AEVs secreted in AD microenvironment. (A) Heatmap of miRNA expression profile showing the expression difference in AEVs-Ctrl, AEVs-Aβ and AEVs-Aβ+H by color bar. Red represents increased expression and blue represents decreased expression. Scale is 1.0 to -1.0. (B) Heatmap image displays the significant difference of miRNAs in AEVs-Ctrl, AEVs-Aβ and AEVs-Aβ+H, and the miRNA level is showed as number in each square. (C) Representative signaling pathways of genes targeted by significantly differential miRNAs according to KEGG analysis. (D) The differential miRNAs verified by qPCR in AEVs, n = 3-5. (E) The expression of miR-206-3p detected by qPCR in astrocytes damaged by Aβ accompanied with haFGF14-154 treatment, n = 3. (F) Comparison of miR-206-3p level between neurons and astrocytes subjected to Aβ1-42 oligomer, n = 3/4. (G) The distribution of miR-206-3p (green) in the PFC and hippocampal DG region of APP/PS1 mice measured by FISH and the quantified levels in the PFC (H) and DG region (I), n = 4/5. (J) The plasma miR-206-3p level detected by qPCR in wild-type mice and APP/PS1 mice with intranasal administration of AEVs or PBS, n = 6-8. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test and two-way ANOVA with Tukey's post-hoc test.
Figure 4 aFGF down-regulates the level of miR-206-3p targeting BDNF in AEVs secreted in AD microenvironment. (A) Heatmap of miRNA expression profile showing the expression difference in AEVs-Ctrl, AEVs-Aβ and AEVs-Aβ+H by color bar. Red represents increased expression and blue represents decreased expression. Scale is 1.0 to -1.0. (B) Heatmap image displays the significant difference of miRNAs in AEVs-Ctrl, AEVs-Aβ and AEVs-Aβ+H, and the miRNA level is showed as number in each square. (C) Representative signaling pathways of genes targeted by significantly differential miRNAs according to KEGG analysis. (D) The differential miRNAs verified by qPCR in AEVs, n = 3-5. (E) The expression of miR-206-3p detected by qPCR in astrocytes damaged by Aβ accompanied with haFGF14-154 treatment, n = 3. (F) Comparison of miR-206-3p level between neurons and astrocytes subjected to Aβ1-42 oligomer, n = 3/4. (G) The distribution of miR-206-3p (green) in the PFC and hippocampal DG region of APP/PS1 mice measured by FISH and the quantified levels in the PFC (H) and DG region (I), n = 4/5. (J) The plasma miR-206-3p level detected by qPCR in wild-type mice and APP/PS1 mice with intranasal administration of AEVs or PBS, n = 6-8. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test and two-way ANOVA with Tukey's post-hoc test.CC BY · PubMed Central
Figure 5 miR-206-3p inhibitors promote neurite growth. (A) Representative morphology of MAP2+ cells in primary cortical neurons (red) transfected with miR-206-3p mimics and inhibitors (Scale bars: 50 µm). Quantification of the average neurite length of neurons (B), the proportion of the longest length of neural neurites over 100 µm (C) and the number of neural neurites per neuron (D), n = 6. (E-H) The expression of PSD95, GAP43 and SYN in rat primary cortical neurons transfected with miR-206-3p mimics and inhibitors, n = 6. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by student's t-test.
Figure 5 miR-206-3p inhibitors promote neurite growth. (A) Representative morphology of MAP2+ cells in primary cortical neurons (red) transfected with miR-206-3p mimics and inhibitors (Scale bars: 50 µm). Quantification of the average neurite length of neurons (B), the proportion of the longest length of neural neurites over 100 µm (C) and the number of neural neurites per neuron (D), n = 6. (E-H) The expression of PSD95, GAP43 and SYN in rat primary cortical neurons transfected with miR-206-3p mimics and inhibitors, n = 6. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by student's t-test.CC BY · PubMed Central
Figure 6 miR-206-3p antagomirs alleviate learning and memory deficits in AD mice. (A) Schematic protocol for the hippocampal injection of miR-206-3p antagomirs and behavior test. (B-C) miR-206-3p level in the PFC (B, n = 4) and hippocampus (C, n = 6) of AD mice with brain injection of miR-206-3p antagomirs. (D) The representative movement tracks of escape latency on day 5 in navigation test of MWM. (F) The escape latencies of mice. Representative movement tracks in spatial probe test (E), numbers of crossing the removed platform area (G) and time spend in target quadrant (H) in spatial probe test of MWM, n = 9/10. (I) Spontaneous alternation in Y-maze, n = 9-12. The expression of PSD95, GAP43 and SYN in the PFC (J-M) and hippocampus (N-Q) of AD mice with brain injection of miR-206-3p antagomirs and antagomir NC, n = 8/9. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test and two-way ANOVA with Tukey's post-hoc test.
Figure 6 miR-206-3p antagomirs alleviate learning and memory deficits in AD mice. (A) Schematic protocol for the hippocampal injection of miR-206-3p antagomirs and behavior test. (B-C) miR-206-3p level in the PFC (B, n = 4) and hippocampus (C, n = 6) of AD mice with brain injection of miR-206-3p antagomirs. (D) The representative movement tracks of escape latency on day 5 in navigation test of MWM. (F) The escape latencies of mice. Representative movement tracks in spatial probe test (E), numbers of crossing the removed platform area (G) and time spend in target quadrant (H) in spatial probe test of MWM, n = 9/10. (I) Spontaneous alternation in Y-maze, n = 9-12. The expression of PSD95, GAP43 and SYN in the PFC (J-M) and hippocampus (N-Q) of AD mice with brain injection of miR-206-3p antagomirs and antagomir NC, n = 8/9. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test and two-way ANOVA with Tukey's post-hoc test.CC BY · PubMed Central
Figure 7 miR-206-3p antagomirs reduce the deposition of Aβ in AD mice. (A) Representative images of Aβ plaque in the DG, CA1 and CA3 regions of AD mice with hippocampal injection of miR-206-3p antagomirs (Scale: 100 µm). (B-D) Quantitative analysis for Aβ plaque area by image-pro plus software, n = 3-5. (E-G) The level of Aβ in the PFC and hippocampal tissue of AD mice, n = 5-6. Data are as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test.
Figure 7 miR-206-3p antagomirs reduce the deposition of Aβ in AD mice. (A) Representative images of Aβ plaque in the DG, CA1 and CA3 regions of AD mice with hippocampal injection of miR-206-3p antagomirs (Scale: 100 µm). (B-D) Quantitative analysis for Aβ plaque area by image-pro plus software, n = 3-5. (E-G) The level of Aβ in the PFC and hippocampal tissue of AD mice, n = 5-6. Data are as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test.CC BY · PubMed Central
Figure 8 AEVs-Aβ+H and miR-206-3p antagomirs increase BDNF levels. (A) Potential binding sites in 3'UTR of BDNF. (B) Identification of miR-206-3p potential binding sites to BDNF 3'UTR performed by luciferase reporter assay, n = 4. (C-D) The expression of BDNF in rat primary cortical neurons transfected with miR-206-3p mimics and inhibitors, n = 4. (E-G) BDNF expression in the PFC and hippocampus of APP/PS1 with intranasal administration of AEVs, n = 8-10. (H-J) The expression of BDNF in the PFC and hippocampus of AD mice with hippocampal injection of miR-206-3p antagomirs and antagomir NC, n = 8/9. (K-M) The level of AEP (full-length and cleaved AEP) in the PFC and hippocampus of APP/PS1 mice with intranasal administration of AEVs, n = 8-10. (N-P) The level of AEP (full-length and cleaved AEP) in the PFC and hippocampus of AD mice with hippocampal injection of miR-206-3p antagomirs, n = 11/12. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test.
Figure 8 AEVs-Aβ+H and miR-206-3p antagomirs increase BDNF levels. (A) Potential binding sites in 3'UTR of BDNF. (B) Identification of miR-206-3p potential binding sites to BDNF 3'UTR performed by luciferase reporter assay, n = 4. (C-D) The expression of BDNF in rat primary cortical neurons transfected with miR-206-3p mimics and inhibitors, n = 4. (E-G) BDNF expression in the PFC and hippocampus of APP/PS1 with intranasal administration of AEVs, n = 8-10. (H-J) The expression of BDNF in the PFC and hippocampus of AD mice with hippocampal injection of miR-206-3p antagomirs and antagomir NC, n = 8/9. (K-M) The level of AEP (full-length and cleaved AEP) in the PFC and hippocampus of APP/PS1 mice with intranasal administration of AEVs, n = 8-10. (N-P) The level of AEP (full-length and cleaved AEP) in the PFC and hippocampus of AD mice with hippocampal injection of miR-206-3p antagomirs, n = 11/12. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test.CC BY · PubMed Central
Figure 9 haFGF14-154 inhibits AEP activity via miR-206-3p/BDNF pathway in the brain of APP/PS1 mice. (A-C) miR-206-3p level in the PFC and hippocampal DG region of APP/PS1 mice with intranasal administration of 600 µg/kg haFGF14-154-loaded cationic liposomes (L+H600) or 0.9% saline (vehicle), measured by fluorescence in situ hybridization (FISH), n = 4/5. (D-F) The expression of BDNF and AEP (full-length and cleaved AEP) in the PFC of APP/PS1 mice with intranasal administration of L+H600 or vehicle, n = 6. The plasma levels of miR-206-3p (G) and BDNF (H) in patients with Alzheimer's disease (AD), PD and Schizophrienia detected by qPCR. P values are calculated by age-adjusted ANCOVA model with Tukey's post-hoc test. n = 25/16, 18/18, 15/13 and 12/8 for normal control and patients with AD, PD and Schizophrienia in the experiments of qPCR and ELISA, respectively. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test and student's t-test.
Figure 9 haFGF14-154 inhibits AEP activity via miR-206-3p/BDNF pathway in the brain of APP/PS1 mice. (A-C) miR-206-3p level in the PFC and hippocampal DG region of APP/PS1 mice with intranasal administration of 600 µg/kg haFGF14-154-loaded cationic liposomes (L+H600) or 0.9% saline (vehicle), measured by fluorescence in situ hybridization (FISH), n = 4/5. (D-F) The expression of BDNF and AEP (full-length and cleaved AEP) in the PFC of APP/PS1 mice with intranasal administration of L+H600 or vehicle, n = 6. The plasma levels of miR-206-3p (G) and BDNF (H) in patients with Alzheimer's disease (AD), PD and Schizophrienia detected by qPCR. P values are calculated by age-adjusted ANCOVA model with Tukey's post-hoc test. n = 25/16, 18/18, 15/13 and 12/8 for normal control and patients with AD, PD and Schizophrienia in the experiments of qPCR and ELISA, respectively. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test and student's t-test.CC BY · PubMed Central

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Cites

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Research works printed but not linked: 46

  1. [1]Goedert M Spillantini MG A century of Alzheimer's disease Science 2006 314 777 81 17082447
  2. [2]Hardy J Selkoe DJ The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics Science 2002 297 353 6 12130773
  3. [3]Guo T Zhang D Zeng Y Huang TY Xu H Zhao Y Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer's disease Mol Neurodegener 2020 15 40 32677986 PMC7364557
  4. [4]Gorshkov K Aguisanda F Thorne N Zheng W Astrocytes as targets for drug discovery Drug Discov Today 2018 23 673 80 29317338 PMC5937927
  5. [5]Phatnani H Maniatis T Astrocytes in neurodegenerative disease Cold Spring Harb Perspect Biol 2015 7 PMC4448607 25877220
  6. [9]Wang G Dinkins M He Q Zhu G Poirier C Campbell A Astrocytes secrete exosomes enriched with proapoptotic ceramide and prostate apoptosis response 4 (PAR-4): potential mechanism of apoptosis induction in Alzheimer disease (AD) J Biol Chem 2012 287 21384 95 22532571 PMC3375560
  7. [10]Elsherbini A Kirov AS Dinkins MB Wang G Qin H Zhu Z Association of Abeta with ceramide-enriched astrosomes mediates Abeta neurotoxicity Acta Neuropathol Commun 2020 8 60 32345374 PMC7189561
  8. [11]Mao S Sun Q Xiao H Zhang C Li L Secreted miR-34a in astrocytic shedding vesicles enhanced the vulnerability of dopaminergic neurons to neurotoxins by targeting Bcl-2 Protein Cell 2015 6 529 40 26091620 PMC4491052
  9. [13]Long Q Upadhya D Hattiangady B Kim DK An SY Shuai B Intranasal MSC-derived A1-exosomes ease inflammation, and prevent abnormal neurogenesis and memory dysfunction after status epilepticus Proc Natl Acad Sci U S A 2017 114 E3536 E45 28396435 PMC5410779
  10. [14]Long X Yao X Jiang Q Yang Y He X Tian W Astrocyte-derived exosomes enriched with miR-873a-5p inhibit neuroinflammation via microglia phenotype modulation after traumatic brain injury Journal of neuroinflammation 2020 17 89 32192523 PMC7082961
  11. [15]Chen W Wang H Zhu Z Feng J Chen L Exosome-Shuttled circSHOC2 from IPASs Regulates Neuronal Autophagy and Ameliorates Ischemic Brain Injury via the miR-7670-3p/SIRT1 Axis Molecular therapy Nucleic acids 2020 22 657 72 33230464 PMC7581834
  12. [16]Deng Z Wang J Xiao Y Li F Niu L Liu X Ultrasound-mediated augmented exosome release from astrocytes alleviates amyloid-beta-induced neurotoxicity Theranostics 2021 11 4351 62 33754065 PMC7977450
  13. [17]Kang W Hebert JM FGF Signaling Is Necessary for Neurogenesis in Young Mice and Sufficient to Reverse Its Decline in Old Mice J Neurosci 2015 35 10217 23 26180198 PMC4502262
  14. [18]Bouleau S Parvu-Ferecatu I Rodriguez-Enfedaque A Rincheval V Grimal H Mignotte B Fibroblast Growth Factor 1 inhibits p53-dependent apoptosis in PC12 cells Apoptosis 2007 12 1377 87 17473910
  15. [19]Wu Y Wu C Ye L Wang B Yuan Y Liu Y Exogenous fibroblast growth factor 1 ameliorates diabetes-induced cognitive decline via coordinately regulating PI3K/AKT signaling and PERK signaling Cell Commun Signal 2020 18 81 32460803 PMC7251863
  16. [20]Damon DH D'Amore PA Wagner JA Nerve growth factor and fibroblast growth factor regulate neurite outgrowth and gene expression in PC12 cells via both protein kinase C- and cAMP-independent mechanisms J Cell Biol 1990 110 1333 9 2157719 PMC2116059
  17. [21]Mashayekhi F Hadavi M Vaziri HR Naji M Increased acidic fibroblast growth factor concentrations in the serum and cerebrospinal fluid of patients with Alzheimer's disease J Clin Neurosci 2010 17 357 9 20079650
  18. [22]Lou G Zhang Q Xiao F Xiang Q Su Z Huang Y Intranasal TAT-haFGF Improves Cognition and Amyloid-beta Pathology in an AbetaPP/PS1 Mouse Model of Alzheimer's Disease Journal of Alzheimer's disease: JAD 2016 51 985 90 26890786
  19. [23]Meng T Cao Q Lei P Bush AI Xiang Q Su Z Tat-haFGF14-154 Upregulates ADAM10 to Attenuate the Alzheimer Phenotype of APP/PS1 Mice through the PI3K-CREB-IRE1alpha/XBP1 Pathway Molecular therapy Nucleic acids 2017 7 439 52 28624220 PMC5443968
  20. [24]Kang W Balordi F Su N Chen L Fishell G Hebert JM Astrocyte activation is suppressed in both normal and injured brain by FGF signaling Proc Natl Acad Sci U S A 2014 111 E2987 95 25002516 PMC4115557
  21. [25]Chompre G Cruz E Maldonado L Rivera-Amill V Porter JT Noel RJ Jr Astrocytic expression of HIV-1 Nef impairs spatial and recognition memory Neurobiol Dis 2013 49 128 36 22926191 PMC3530662
  22. [27]Seo J Giusti-Rodriguez P Zhou Y Rudenko A Cho S Ota KT Activity-dependent p25 generation regulates synaptic plasticity and Abeta-induced cognitive impairment Cell 2014 157 486 98 24725413 PMC4327772
  23. [28]Abdullah M Takase H Nunome M Enomoto H Ito J Gong JS Amyloid-beta Reduces Exosome Release from Astrocytes by Enhancing JNK Phosphorylation Journal of Alzheimer's disease: JAD 2016 53 1433 41 27392863
  24. [29]Ma X Huang M Zheng M Dai C Song Q Zhang Q ADSCs-derived extracellular vesicles alleviate neuronal damage, promote neurogenesis and rescue memory loss in mice with Alzheimer's disease J Control Release 2020 327 688 702 32931898
  25. [30]Nogueras-Ortiz CJ Mahairaki V Delgado-Peraza F Das D Avgerinos K Eren E Astrocyte- and Neuron-Derived Extracellular Vesicles from Alzheimer's Disease Patients Effect Complement-Mediated Neurotoxicity Cells 2020 9 PMC7407141 32635578
  26. [31]Chen C Wang Z Zhang Z Liu X Kang SS Zhang Y The prodrug of 7,8-dihydroxyflavone development and therapeutic efficacy for treating Alzheimer's disease Proc Natl Acad Sci U S A 2018 115 578 83 29295929 PMC5777001
  27. [32]Wang ZH Xiang J Liu X Yu SP Manfredsson FP Sandoval IM Deficiency in BDNF/TrkB Neurotrophic Activity Stimulates delta-Secretase by Upregulating C/EBPbeta in Alzheimer's Disease Cell Rep 2019 28 655 69 e5 31315045 PMC6684282
  28. [33]Baldwin KT Eroglu C Molecular mechanisms of astrocyte-induced synaptogenesis Curr Opin Neurobiol 2017 45 113 20 28570864 PMC5573249
  29. [34]Blanco-Suarez E Caldwell AL Allen NJ Role of astrocyte-synapse interactions in CNS disorders J Physiol 2017 595 1903 16 27381164 PMC5350444
  30. [35]Kim SK Nabekura J Koizumi S Astrocyte-mediated synapse remodeling in the pathological brain Glia 2017 65 1719 27 28569048
  31. [36]Allaman I Belanger M Magistretti PJ Astrocyte-neuron metabolic relationships: for better and for worse Trends Neurosci 2011 34 76 87 21236501
  32. [37]Verkhratsky A Parpura V Pekna M Pekny M Sofroniew M Glia in the pathogenesis of neurodegenerative diseases Biochem Soc Trans 2014 42 1291 301 25233406
  33. [38]Williams CJ Dexter DT Neuroprotective and symptomatic effects of targeting group III mGlu receptors in neurodegenerative disease J Neurochem 2014 129 4 20 24224472
  34. [39]Harada K Kamiya T Tsuboi T Gliotransmitter Release from Astrocytes: Functional, Developmental, and Pathological Implications in the Brain Front Neurosci 2015 9 499 26793048 PMC4709856
  35. [40]Kim YS Jung HM Yoon BE Exploring glia to better understand Alzheimer's disease Anim Cells Syst (Seoul) 2018 22 213 8 30460100 PMC6138241
  36. [41]Niranjan R The role of inflammatory and oxidative stress mechanisms in the pathogenesis of Parkinson's disease: focus on astrocytes Molecular neurobiology 2014 49 28 38 23783559
  37. [42]Goetzl EJ Schwartz JB Abner EL Jicha GA Kapogiannis D High complement levels in astrocyte-derived exosomes of Alzheimer disease Annals of neurology 2018 83 544 52 29406582 PMC5867263
  38. [43]Trotta T Panaro MA Cianciulli A Mori G Di Benedetto A Porro C Microglia-derived extracellular vesicles in Alzheimer's Disease: A double-edged sword Biochem Pharmacol 2018 148 184 92 29305855
  39. [45]Pascua-Maestro R Gonzalez E Lillo C Ganfornina MD Falcon-Perez JM Sanchez D Extracellular Vesicles Secreted by Astroglial Cells Transport Apolipoprotein D to Neurons and Mediate Neuronal Survival Upon Oxidative Stress Frontiers in cellular neuroscience 2018 12 526 30687015 PMC6335244
  40. [46]Mignani S Shi X Karpus A Majoral JP Non-invasive intranasal administration route directly to the brain using dendrimer nanoplatforms: An opportunity to develop new CNS drugs Eur J Med Chem 2021 209 112905 33069435 PMC7548078
  41. [47]Lee ST Chu K Jung KH Kim JH Huh JY Yoon H miR-206 regulates brain-derived neurotrophic factor in Alzheimer disease model Annals of neurology 2012 72 269 77 22926857
  42. [49]Ji Y Lu Y Yang F Shen W Tang TT Feng L Acute and gradual increases in BDNF concentration elicit distinct signaling and functions in neurons Nat Neurosci 2010 13 302 9 20173744 PMC4780419
  43. [50]Tyler WJ Pozzo-Miller L Miniature synaptic transmission and BDNF modulate dendritic spine growth and form in rat CA1 neurones J Physiol 2003 553 497 509 14500767 PMC2343578
  44. [51]Bates KA Verdile G Li QX Ames D Hudson P Masters CL Clearance mechanisms of Alzheimer's amyloid-beta peptide: implications for therapeutic design and diagnostic tests Mol Psychiatry 2009 14 469 86 18794889
  45. [52]Cone AS Yuan X Sun L Duke LC Vreones MP Carrier AN Mesenchymal stem cell-derived extracellular vesicles ameliorate Alzheimer's disease-like phenotypes in a preclinical mouse model Theranostics 2021 11 8129 42 34373732 PMC8344012
  46. [53]Wang ZH Gong K Liu X Zhang Z Sun X Wei ZZ C/EBPbeta regulates delta-secretase expression and mediates pathogenesis in mouse models of Alzheimer's disease Nat Commun 2018 9 1784 29725016 PMC5934399

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Metadata

Authors
Peng, D., Wang, Y., Xiao, Y., Peng, M., Mai, W., Hu, B., Jia, Y., Chen, H., Yang, Y., Xiang, Q., Su, Z., Zhang, Q., & Huang, Y.
Venue
Theranostics
Publisher
Ivyspring International Publisher
Published
2022
Volume
12
Issue
8
Pages
3862-3881
ISSN
1838-7640
DOI
10.7150/thno.70951
PMC
PMC9131260
Cited by
52
References
8
Language
en

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.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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How to cite

Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: Extracellular vesicles derived from astrocyte-treated with haFGF14-154 attenuate Alzheimer phenotype in AD mice. https://app.cochat.ai/papers/10.7150/thno.70951
The paper
Peng, D., Wang, Y., Xiao, Y., Peng, M., Mai, W., Hu, B., Jia, Y., Chen, H., Yang, Y., Xiang, Q., Su, Z., Zhang, Q., & Huang, Y. (2022). Extracellular vesicles derived from astrocyte-treated with haFGF14-154 attenuate Alzheimer phenotype in AD mice. Theranostics. https://doi.org/10.7150/thno.70951