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Astrocytes in mouse models of tauopathies acquire early deficits and lose neurosupportive functions

Sidoryk-Wegrzynowicz, Marta, Gerber, Yannick N., Ries, Miriam, Sastre, Magdalena, Tolkovsky, Aviva M., Spillantini, Maria Grazia·2017·Acta Neuropathologica Communications
DOI 10.1186/s40478-017-0478-9PMC PMC6389177
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Fig. 1 Astrocytes from P301S mice express more GFAP and S100β and less GS, GLT-1 and GLAST than astrocytes from control mice. a, d Representative blots of astrocyte-specific protein markers related to gliosis/proliferation (GFAP, S100β) and function (glutamine synthetase (GS) and the glutamate transporters (GLT-1 and GLAST)) in the superficial motor cortex of 3 month-old and 5 month-old C57 and P301S mice. h Expression of the same markers in primary pure cultured astrocytes from 7 day-old mice after days 8 in vitro (98% culture confluence). Mean ± SEM, *p < 0.05 vs control; unpaired t test, N = 3 independent experiments (mice: GFAP, S100β (b, c); GLT-1, GLAST, GS (e–g); primary cultures i). Vertical lines in (d) denote point were the picture of the Western blot was assembled from two parts cut from the same blot
Fig. 1 Astrocytes from P301S mice express more GFAP and S100β and less GS, GLT-1 and GLAST than astrocytes from control mice. a, d Representative blots of astrocyte-specific protein markers related to gliosis/proliferation (GFAP, S100β) and function (glutamine synthetase (GS) and the glutamate transporters (GLT-1 and GLAST)) in the superficial motor cortex of 3 month-old and 5 month-old C57 and P301S mice. h Expression of the same markers in primary pure cultured astrocytes from 7 day-old mice after days 8 in vitro (98% culture confluence). Mean ± SEM, *p < 0.05 vs control; unpaired t test, N = 3 independent experiments (mice: GFAP, S100β (b, c); GLT-1, GLAST, GS (e–g); primary cultures i). Vertical lines in (d) denote point were the picture of the Western blot was assembled from two parts cut from the same blotCC BY · PubMed Central
Fig. 2 Astrocytes from P301S mice are more proliferative. Proliferation assay using EdU was performed 1 day after passage of confluent astrocyte cultures from 7 day-old pups. A higher proliferation capacity was observed in P301SA compared to C57A astrocytes. a Representative images where red indicates nuclei undergoing proliferation. b Quantification of proliferating cells, mean ± SEM, *p < 0.05 vs control; statistical analysis was performed using unpaired t test. N = 3 independent experiments where counting from three technical replicates (wells) in which at least three fields per well were analyzed constitute one value for statistical purposes. EdU, 5-ethynyl-2'-deoxyuridine
Fig. 2 Astrocytes from P301S mice are more proliferative. Proliferation assay using EdU was performed 1 day after passage of confluent astrocyte cultures from 7 day-old pups. A higher proliferation capacity was observed in P301SA compared to C57A astrocytes. a Representative images where red indicates nuclei undergoing proliferation. b Quantification of proliferating cells, mean ± SEM, *p < 0.05 vs control; statistical analysis was performed using unpaired t test. N = 3 independent experiments where counting from three technical replicates (wells) in which at least three fields per well were analyzed constitute one value for statistical purposes. EdU, 5-ethynyl-2'-deoxyuridineCC BY · PubMed Central
Fig. 3 Astrocytes from P301S mice have a reduced capacity to support neuronal survival. Primary astrocytes (C57A and P301SA) cultured from cerebral cortex of 7 day-old mice (98% purity) were plated on top of primary neurons cultured from mice of similar age and brain region for 4–5 days. Co-cultures were maintained for 4 and 8 days. a Representative images of co-cultures immunostained for β-III-tubulin (red), GFAP (green) and Dapi (blue). Quantification of neuron (b, c) and astrocyte (d, e) numbers after 4 and 8 days of co-culture. Each experiment consisted of six technical replicates (wells) in which at least five fields were analyzed. Data show mean per field ± SEM from at least four independent experiments. Data were analysed using ANOVA followed by Tukey’s multiple comparison test; *p < 0.05 for these comparisons: C57N vs C57N + P301SA; C57N vs P301SN + P301SA; C57N vs C57N + C57A; C57N + C57A vs P301SN + C57A; C57N + C57A vs C57N + P301SA; C57N + C57A vs P301SN + P301SA; P301SN + C57A vs P301SN + P301SA; ANOVA of results from 4 day co-cultures revealed a significant interaction between genotype and co-culture condition [F (2, 21) = 4.477; p = 0.0240], significant effects of co-culture type [F (2, 21) = 14.27; p = 0.0001] and genotype [F (1, 21) = 14.8; p = 0.0009]. In 8 day of co-cultures, ANOVA revealed no interaction between genotype and culture conditions [F (2, 22) = 3.048; p = 0.0678], the significant effect being co-culture type [F (2, 22) = 17.51; p < 0.0001] and co-culture condition [F (1, 22) = 6.54; p = 0.0180]. No significant differences in the numbers of astrocytes were present between the various cultures
Fig. 3 Astrocytes from P301S mice have a reduced capacity to support neuronal survival. Primary astrocytes (C57A and P301SA) cultured from cerebral cortex of 7 day-old mice (98% purity) were plated on top of primary neurons cultured from mice of similar age and brain region for 4–5 days. Co-cultures were maintained for 4 and 8 days. a Representative images of co-cultures immunostained for β-III-tubulin (red), GFAP (green) and Dapi (blue). Quantification of neuron (b, c) and astrocyte (d, e) numbers after 4 and 8 days of co-culture. Each experiment consisted of six technical replicates (wells) in which at least five fields were analyzed. Data show mean per field ± SEM from at least four independent experiments. Data were analysed using ANOVA followed by Tukey’s multiple comparison test; *p < 0.05 for these comparisons: C57N vs C57N + P301SA; C57N vs P301SN + P301SA; C57N vs C57N + C57A; C57N + C57A vs P301SN + C57A; C57N + C57A vs C57N + P301SA; C57N + C57A vs P301SN + P301SA; P301SN + C57A vs P301SN + P301SA; ANOVA of results from 4 day co-cultures revealed a significant interaction between genotype and co-culture condition [F (2, 21) = 4.477; p = 0.0240], significant effects of co-culture type [F (2, 21) = 14.27; p = 0.0001] and genotype [F (1, 21) = 14.8; p = 0.0009]. In 8 day of co-cultures, ANOVA revealed no interaction between genotype and culture conditions [F (2, 22) = 3.048; p = 0.0678], the significant effect being co-culture type [F (2, 22) = 17.51; p < 0.0001] and co-culture condition [F (1, 22) = 6.54; p = 0.0180]. No significant differences in the numbers of astrocytes were present between the various culturesCC BY · PubMed Central
Fig. 4 Astrocytes from P301S and P301L tau mice develop a reduced capacity to support neuronal survival during the first postnatal week. Serum-free medium conditioned by pure astrocytes derived from ≥7 day-old C57, P301S and P301L tau mice over 24 h was centrifuged to remove cellular debris and immediately added to 7 day cultured neurons extracted from 7 day-old mice. After 8 days, cells were fixed, stained with β-III-tubulin and counted. Mean ± SEM of four independent experiments where a single value is from four technical replicates (wells) in which at least five fields per well were analyzed. a Images of neurons treated with the various ACMs as indicated. b ACM from 7 day-old C57 and P301S mice; *p < 0.05 for these comparisons: no ACM C57N vs C57N + C57ACM; no ACM P301SN vs C57N + C57ACM; C57N + C57ACM vs P301SN + C57ACM, C57N + C57ACM vs C57N + P301SACM, C57N + C57ACM vs P301SN + P301SACM, P301SN + C57ACM vs P301SN + P301SACM. c ACM from 7 day-old C57A and P301LA; *p < 0.05 for these comparisons: no ACM C57N vs C57N + C57ACM; C57N + C57ACM vs C57N + P301LACM; Tukey’s multiple comparisons test. For 8 day of cultures, ANOVA revealed no interaction between genotype and culture conditions [F (2, 18) = 1.174; p = 0.3317], significant effect of culture condition [F (2, 18) = 19.73; p = 0.0001] and significant effect of genotype [F (1, 18) = 8.725; p = 0.0085]. d Neurons from 1 to 2 day-old mice were cultured for 4 days after which ACM derived from astrocytes cultured from 1 to 2 day-old mice was added for 4 days. e Neurons from 7 day-old mice were cultured for 4 days after which ACM derived from astrocytes cultured from 1 to 2 day-old mice was added for 4 days. Note that in both cases, there is no difference between the effects of ACMs from C57 or P301S mice. Mean ± SEM from three independent experiments; each value was obtained from four technical replicates (wells) in which at least five fields were examined. Values were analysed by the Mann–Whitney test
Fig. 4 Astrocytes from P301S and P301L tau mice develop a reduced capacity to support neuronal survival during the first postnatal week. Serum-free medium conditioned by pure astrocytes derived from ≥7 day-old C57, P301S and P301L tau mice over 24 h was centrifuged to remove cellular debris and immediately added to 7 day cultured neurons extracted from 7 day-old mice. After 8 days, cells were fixed, stained with β-III-tubulin and counted. Mean ± SEM of four independent experiments where a single value is from four technical replicates (wells) in which at least five fields per well were analyzed. a Images of neurons treated with the various ACMs as indicated. b ACM from 7 day-old C57 and P301S mice; *p < 0.05 for these comparisons: no ACM C57N vs C57N + C57ACM; no ACM P301SN vs C57N + C57ACM; C57N + C57ACM vs P301SN + C57ACM, C57N + C57ACM vs C57N + P301SACM, C57N + C57ACM vs P301SN + P301SACM, P301SN + C57ACM vs P301SN + P301SACM. c ACM from 7 day-old C57A and P301LA; *p < 0.05 for these comparisons: no ACM C57N vs C57N + C57ACM; C57N + C57ACM vs C57N + P301LACM; Tukey’s multiple comparisons test. For 8 day of cultures, ANOVA revealed no interaction between genotype and culture conditions [F (2, 18) = 1.174; p = 0.3317], significant effect of culture condition [F (2, 18) = 19.73; p = 0.0001] and significant effect of genotype [F (1, 18) = 8.725; p = 0.0085]. d Neurons from 1 to 2 day-old mice were cultured for 4 days after which ACM derived from astrocytes cultured from 1 to 2 day-old mice was added for 4 days. e Neurons from 7 day-old mice were cultured for 4 days after which ACM derived from astrocytes cultured from 1 to 2 day-old mice was added for 4 days. Note that in both cases, there is no difference between the effects of ACMs from C57 or P301S mice. Mean ± SEM from three independent experiments; each value was obtained from four technical replicates (wells) in which at least five fields were examined. Values were analysed by the Mann–Whitney testCC BY · PubMed Central
Fig. 5 ACM from P301SA reduces synaptic protein expression in cultured neurons. C57N or P301SN cultures were exposed to C57ACM or P301SACM for 8 days after which cell lysates were analysed by immunoblotting. a Representative immunoblot of synaptophysin (SNP) and PSD95 in neuronal cultures with and without ACM exposure. Note the significant decline of both (b) SNP and (c) PSD95 when C57N or P301SN were cultured with P301SACM compared to neurons maintained in C57ACM. Data were normalised to β actin and represent mean ± SEM of three independent experiments performed in triplicate. *p < 0.05 for these comparisons: C57N vs C57N + P301SACM; C57N + P301SACM vs C57N + C57ACM; P301SN vs P301SN + P301SACM; P301SN vs P301SN + C57ACM; Tukey’s multiple comparisons test both for SNP and PSD95. ANOVA for SNP values revealed a significant interaction between genotype and culture condition [F (2, 12) = 29.88; p = 0.0001], significant effect of genotype [F (1, 12) = 307.2; p = 0.0001] and significant effect of culture treatment [F (2, 12) = 34.68; p = 0.0001]. ANOVA for PSD95 values revealed a significant interaction between genotype and culture condition (ACM) [F (2, 12) = 18.08; p = 0.0002], significant effect of genotype [F (1, 12) = 112.2; p = 0.0001] and culture treatments [F (2, 12) = 37.01; p = 0.0001]
Fig. 5 ACM from P301SA reduces synaptic protein expression in cultured neurons. C57N or P301SN cultures were exposed to C57ACM or P301SACM for 8 days after which cell lysates were analysed by immunoblotting. a Representative immunoblot of synaptophysin (SNP) and PSD95 in neuronal cultures with and without ACM exposure. Note the significant decline of both (b) SNP and (c) PSD95 when C57N or P301SN were cultured with P301SACM compared to neurons maintained in C57ACM. Data were normalised to β actin and represent mean ± SEM of three independent experiments performed in triplicate. *p < 0.05 for these comparisons: C57N vs C57N + P301SACM; C57N + P301SACM vs C57N + C57ACM; P301SN vs P301SN + P301SACM; P301SN vs P301SN + C57ACM; Tukey’s multiple comparisons test both for SNP and PSD95. ANOVA for SNP values revealed a significant interaction between genotype and culture condition [F (2, 12) = 29.88; p = 0.0001], significant effect of genotype [F (1, 12) = 307.2; p = 0.0001] and significant effect of culture treatment [F (2, 12) = 34.68; p = 0.0001]. ANOVA for PSD95 values revealed a significant interaction between genotype and culture condition (ACM) [F (2, 12) = 18.08; p = 0.0002], significant effect of genotype [F (1, 12) = 112.2; p = 0.0001] and culture treatments [F (2, 12) = 37.01; p = 0.0001]CC BY · PubMed Central
Fig. 6 The active components in C57ACM are macromolecules with a MW above 10 kDa. C57N and P301SN cultures were exposed to complete C57ACM and the same ACM fractionated through a filter with a cut off of ≥10 kDa. The fraction ≥10 kDa (which was diluted to the original volume to offset changes due to concentrating the ACM) or ≤10 kDa was added to the neurons for 8 days. Neurons were counted after immunostaining with the neuronal marker β-III-tubulin. *p < 0.05 for comparisons between number of neurons in: NB vs C57ACM; C57ACM vs C57ACM-10 kDa; C57ACM-10 kDa vs C57ACM + 10 kDa; similar significance was found when C57N or P301SN were treated, statistical analyses was done using Tukey’s multiple comparisons test. ANOVA revealed no interaction on genotype and culture condition (ACM) [F (3, 22 = 0.1457; p = 0.9314], no effect for genotype [F (1, 22) = 0.03553; p = 0.8522] but a significant effect of culture type (ACM) [F (3, 22) = 30.6; p = 0.0001]. The data represent a mean of at least three independent experiments. Each experiment consisted of four technical replicates (wells) in which at least three fields were analyzed
Fig. 6 The active components in C57ACM are macromolecules with a MW above 10 kDa. C57N and P301SN cultures were exposed to complete C57ACM and the same ACM fractionated through a filter with a cut off of ≥10 kDa. The fraction ≥10 kDa (which was diluted to the original volume to offset changes due to concentrating the ACM) or ≤10 kDa was added to the neurons for 8 days. Neurons were counted after immunostaining with the neuronal marker β-III-tubulin. *p < 0.05 for comparisons between number of neurons in: NB vs C57ACM; C57ACM vs C57ACM-10 kDa; C57ACM-10 kDa vs C57ACM + 10 kDa; similar significance was found when C57N or P301SN were treated, statistical analyses was done using Tukey’s multiple comparisons test. ANOVA revealed no interaction on genotype and culture condition (ACM) [F (3, 22 = 0.1457; p = 0.9314], no effect for genotype [F (1, 22) = 0.03553; p = 0.8522] but a significant effect of culture type (ACM) [F (3, 22) = 30.6; p = 0.0001]. The data represent a mean of at least three independent experiments. Each experiment consisted of four technical replicates (wells) in which at least three fields were analyzedCC BY · PubMed Central
Fig. 7 TSP-1 expression is reduced in the superficial cortex and in cultured astrocytes or ACM from P301S mice. a Lysates from the superficial cortex of 3 and 5 month-old mice or b from astrocytes from 98% pure cultures from 7 day-old mice were analysed for TSP-1 expression by immunoblotting. c Quantitative analysis of TSP-1 expression normalised to actin. Values for C57-derived controls are set to 1. *p < 0.05 for these comparisons: C57 3 m vs P301S 3 m; C57 5 m vs P301S 5 mo; C57A vs P301SA. d Analysis of ACM from C57A or P301SA after fractionation on an Amicon filter with a 10 kDa cutoff. A significant decrease in TSP-1 was observed in P301SACM compared to C57ACM, *p < 0.05; e Representative blot, and f quantification of TSP-1.expression in C57ACM, pure C57 neuronal cultures (C57NCM), and C57 neurons co-cultured with C57ACM or P301SACM. Ponceau S staining of ACM blot to show equal loading. *p < 0.05 for these comparisons: C57N + C57ACM vs C57N + P301SACM. C57A released more TSP-1 than C57N, C57A vs C57N. The data represent a mean of three independent experiments performed in triplicates; mean ± S.E.M, statistical analyses performed with Mann–Whitney test
Fig. 7 TSP-1 expression is reduced in the superficial cortex and in cultured astrocytes or ACM from P301S mice. a Lysates from the superficial cortex of 3 and 5 month-old mice or b from astrocytes from 98% pure cultures from 7 day-old mice were analysed for TSP-1 expression by immunoblotting. c Quantitative analysis of TSP-1 expression normalised to actin. Values for C57-derived controls are set to 1. *p < 0.05 for these comparisons: C57 3 m vs P301S 3 m; C57 5 m vs P301S 5 mo; C57A vs P301SA. d Analysis of ACM from C57A or P301SA after fractionation on an Amicon filter with a 10 kDa cutoff. A significant decrease in TSP-1 was observed in P301SACM compared to C57ACM, *p < 0.05; e Representative blot, and f quantification of TSP-1.expression in C57ACM, pure C57 neuronal cultures (C57NCM), and C57 neurons co-cultured with C57ACM or P301SACM. Ponceau S staining of ACM blot to show equal loading. *p < 0.05 for these comparisons: C57N + C57ACM vs C57N + P301SACM. C57A released more TSP-1 than C57N, C57A vs C57N. The data represent a mean of three independent experiments performed in triplicates; mean ± S.E.M, statistical analyses performed with Mann–Whitney testCC BY · PubMed Central
Fig. 8 TSP-1 depletion reduces the synaptogenic effects of C57ACM. a TSP-1 was immunodepleted from crude C57ACM or from the ≥10 kDa fraction and depletion validated by immunoblotting. Blot showsTSP-1 amounts in input, fraction bound to beads, and eluted supernatant after magnetic separation. b Representative pictures of SNP and NeuN immunocytochemistry. Complete ACM and TSP-1-depleted ACM were added to the neuronal cultures for 8 days after which cultures were fixed and immunolabelled with antibodies against SNP and NeuN. c Quantification of SNP intensity. For quantification of staining intensity of SNP in the green channel from three slides for each experimental condition were analysed. Results indicate a mean which corresponds in each case to the mean of four fields. *p < 0.05 for these comparisons: C57N + C57ACM vs C57N + C57ACM-TSP-1; P301SN + C57ACM vs P301SN + C57ACM-TSP-1. Values were analysed using Tukey’s multiple comparisons test. ANOVA revealed no interaction between genotype and culture condition (ACM or ACM-TSP-1) [F (1, 12) = 0.9814; p = 0.3414] but a significant effect was found for genotype [F (1, 12) = 62.94; P < 0.0001] while no effect for culture type [F (1, 12) = 1.476; p = 0.2478]
Fig. 8 TSP-1 depletion reduces the synaptogenic effects of C57ACM. a TSP-1 was immunodepleted from crude C57ACM or from the ≥10 kDa fraction and depletion validated by immunoblotting. Blot showsTSP-1 amounts in input, fraction bound to beads, and eluted supernatant after magnetic separation. b Representative pictures of SNP and NeuN immunocytochemistry. Complete ACM and TSP-1-depleted ACM were added to the neuronal cultures for 8 days after which cultures were fixed and immunolabelled with antibodies against SNP and NeuN. c Quantification of SNP intensity. For quantification of staining intensity of SNP in the green channel from three slides for each experimental condition were analysed. Results indicate a mean which corresponds in each case to the mean of four fields. *p < 0.05 for these comparisons: C57N + C57ACM vs C57N + C57ACM-TSP-1; P301SN + C57ACM vs P301SN + C57ACM-TSP-1. Values were analysed using Tukey’s multiple comparisons test. ANOVA revealed no interaction between genotype and culture condition (ACM or ACM-TSP-1) [F (1, 12) = 0.9814; p = 0.3414] but a significant effect was found for genotype [F (1, 12) = 62.94; P < 0.0001] while no effect for culture type [F (1, 12) = 1.476; p = 0.2478]CC BY · PubMed Central
Fig. 9 Effect of TSP-1 depletion of C57ACM or supplementation to P301SACM on neuronal survival. To study the effect of TSP-1 on neuronal survival C57N and P301SN were cultured in (a, b) C57ACM or C57ACM depleted of TSP-1 or (c, d) P301SACM or P301SACM supplemented with TSP-1 for 8 days. a, c Neuronal cultures were fixed and immunolabelled with anti-β-III-tubulin antibody to determine neuronal number. The data represent a mean of three independent experiments. Each experiment consisted of three technical replicates (wells) in which at least three fields were analyzed. b *p < 0.05 for these comparisons: number of neurons in C57N + NB vs C57N + C57ACM; C57N + C57ACM vs C57N + C57ACM-TSP-1; C57N + NB vs C57N + C57ACM-TSP-1; P301SN + C57ACM vs P301SN + C57ACM-TSP-1. d *p < 0.05 for these comparisons: number of neurons in C57N + NB vs C57N + P301SACM; C57N + P301SACM vs C57N + P301SACM + TSP-1; P301SN + NB vs P301SN + P301SACM + TSP-1; P301SN + P301SACM vs P301SN + P301SACM + TSP-1. Results were evaluated with Tukey’s multiple comparisons. For experiments where TSP-1 was depleted ANOVA revealed significant interaction on genotype and culture condition (ACM) [F (2, 12) = 18.01; p = 0.0002], a significant effect for genotype [F (1, 12) = 22.87; p = 0.0004] and significant effect of culture type (ACM) [F (2, 12) = 32.75; p = 0.0001]. For experiments where TSP-1 were added, ANOVA revealed no difference between genotype and culture condition (ACM) [F (2, 12) = 2.524; p = 0.1217], a significant effect of the genotype [F (1, 12) = 9.39; p = 0.0098] and significant effect of culture type (ACM) [F (2, 12) = 32.75; p = 0.0001]
Fig. 9 Effect of TSP-1 depletion of C57ACM or supplementation to P301SACM on neuronal survival. To study the effect of TSP-1 on neuronal survival C57N and P301SN were cultured in (a, b) C57ACM or C57ACM depleted of TSP-1 or (c, d) P301SACM or P301SACM supplemented with TSP-1 for 8 days. a, c Neuronal cultures were fixed and immunolabelled with anti-β-III-tubulin antibody to determine neuronal number. The data represent a mean of three independent experiments. Each experiment consisted of three technical replicates (wells) in which at least three fields were analyzed. b *p < 0.05 for these comparisons: number of neurons in C57N + NB vs C57N + C57ACM; C57N + C57ACM vs C57N + C57ACM-TSP-1; C57N + NB vs C57N + C57ACM-TSP-1; P301SN + C57ACM vs P301SN + C57ACM-TSP-1. d *p < 0.05 for these comparisons: number of neurons in C57N + NB vs C57N + P301SACM; C57N + P301SACM vs C57N + P301SACM + TSP-1; P301SN + NB vs P301SN + P301SACM + TSP-1; P301SN + P301SACM vs P301SN + P301SACM + TSP-1. Results were evaluated with Tukey’s multiple comparisons. For experiments where TSP-1 was depleted ANOVA revealed significant interaction on genotype and culture condition (ACM) [F (2, 12) = 18.01; p = 0.0002], a significant effect for genotype [F (1, 12) = 22.87; p = 0.0004] and significant effect of culture type (ACM) [F (2, 12) = 32.75; p = 0.0001]. For experiments where TSP-1 were added, ANOVA revealed no difference between genotype and culture condition (ACM) [F (2, 12) = 2.524; p = 0.1217], a significant effect of the genotype [F (1, 12) = 9.39; p = 0.0098] and significant effect of culture type (ACM) [F (2, 12) = 32.75; p = 0.0001]CC BY · PubMed Central

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Cited by

Metadata

Authors
Sidoryk-Wegrzynowicz, M., Gerber, Y. N., Ries, M., Sastre, M., Tolkovsky, A. M., & Spillantini, M. G.
Venue
Acta Neuropathologica Communications
Publisher
Springer Science and Business Media LLC
Published
2017-12
Volume
5
Issue
1
ISSN
2051-5960
DOI
10.1186/s40478-017-0478-9
PMC
PMC6389177
Cited by
92
References
11
Language
en
Funders
  • Alzheimer’s Research UK (RG62844, RG80005)
  • National Centre for the Replacement, Refinement and Reduction of Animals in Research (NC/L000741/1)

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