rotarod 1 2 0 software  (Med Associates Inc)

Journal: iScience

Article Title: Targeting Cdc42 improves motor phenotype in Parkinson’s disease mice and reveals age-dependent susceptibility to α-synuclein

doi: 10.1016/j.isci.2025.114217

Figure Lengend Snippet: S1/S2 PD mouse model shows age and α-syn-related motoric deficits (A) Schematic principle of the S1/S2 PD mouse model, which includes a protein complementation assay expressing α-syn coupled to either the N- or C-terminal part of a Gaussia luciferase. The expression takes place under the neuron-specific CamKIIα promoter and is modeled as a Tet-off system driven by doxycycline. Figure modified from Kiechle et al., 2019. (B) Overview of all different S1/S2 mouse cohorts that differ in their age (6, 16, and 24 M) and length of S1/S2 expression (short, long, and non-expressing). (C–E) Accelerating Rotarod was used to determine motor balance and coordination of all S1/S2 mouse cohorts, comparing short-, long-, and non-expressing animals (C) 1–6 M, (D) 11–16 M, and (E) 19–24 M of age by measuring the latency to fall in seconds (s) ( n = 12 male and female mice, repeated measures two-way ANOVA, ∗∗∗ p < 0.001, ∗∗ p < 0.01; data: mean ± SEM).

Article Snippet: Rotarod 1.2.0 software , Med Associates, Fairfax, VT, USA , N/A.

Techniques: Expressing, Luciferase, Modification

Journal: iScience

Article Title: Targeting Cdc42 improves motor phenotype in Parkinson’s disease mice and reveals age-dependent susceptibility to α-synuclein

doi: 10.1016/j.isci.2025.114217

Figure Lengend Snippet: CASIN treatment alleviates motoric phenotype (A) Overview of the different S1/S2 mouse cohorts for CASIN treatment. They are categorized by age (16 and 24 M), levels of S1/S2 expression (ON vs. OFF), and treatment with CASIN. (B and C) Accelerating Rotarod was used to evaluate motor balance and coordination across S1/S2 mouse cohorts. The performance of expressing and non-expressing animals with and without CASIN treatment was compared, and the latency to fall (in seconds) was measured. Performance was assessed at (B) 11–16 M: significant differences were found between synON16M + CASIN vs. synOFF16M + CASIN (∗), synOFF16M + CASIN vs. synON16M (∗∗∗), synON16M + CASIN vs. synON16M (∗∗∗), and synOFF16M vs. synON16M (∗∗∗), and (C) 19–24 M: significant differences occurred between synON24M vs. synOFF24M (∗∗∗), synON24M vs. synON24M + CASIN (∗∗), synON24M vs. synOFF24M + CASIN (∗∗∗), synOFF24M vs. synON24M + CASIN (∗∗∗), and synON24M + CASIN vs. synOFF24M + CASIN (∗∗∗) ( n = 12 male and female mice, repeated-measures two-way ANOVA, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; data: mean ± SEM). (D and E) Gaussia luciferase activity analysis was performed on SEC fractions from S1/S2 mice aged (D) 16 M and (E) 24 M. Comparisons included groups with and without S1/S2 expression, as well as with or without CASIN treatment ( n = 6 male and female mice per group, data: mean ± SEM). (F) Quantification of the AUC for total luciferase activity in SEC fractions (one-way ANOVA with Tukey’s post hoc test; data: mean ± SEM). (G) Quantification of S1/S2 transgene expression in lysates from S1/S2 mice performed by capillary-based western blot analysis (simple western), normalized to Actin (Student’s t test; data: mean ± SEM).

Article Snippet: Rotarod 1.2.0 software , Med Associates, Fairfax, VT, USA , N/A.

Techniques: Expressing, Luciferase, Activity Assay, Western Blot, Simple Western

Journal: iScience

Article Title: Targeting Cdc42 improves motor phenotype in Parkinson’s disease mice and reveals age-dependent susceptibility to α-synuclein

doi: 10.1016/j.isci.2025.114217

Figure Lengend Snippet: PD Signature points to early cAMP disruption and downstream actin/proteasome dysregulation (A) Defining the “PD Signature” and “PD Beginning” gene set. Based on the Rotarod data we decided to only consider intersection genes between the comparisons “synON vs. synOFF” and “synlateON vs. synOFF” at 16 M and 24 M for PD Signatures. From those intersections the genes that were not differentially expressed in “synON6M vs. synOFF6M” were assigned to “PD Signature,” while genes present in “synON6M vs. synOFF6M” and the intersections were defined as “PD Beginning.” (B) Functional network using the central regulators from snRNA-seq PD Signature, PD Beginning genes, and bulk Protein (bProtein) PD Signature from MassSpec data. The interaction between genes/proteins and the p values (pval) for topic-topic interactions were obtained based on omniPath and STRING databases. Network only showed topics with at least two genes/proteins and the top 2 topic-topic connections for each topic. The network suggests an upstream role of cAMP even before onset of motor deficits. This is followed by calcium pathway and Grm5. Grm5 acts as an intersection between the more upstream pathways and the downstream effectors like Proteasome or Axon/Actin. Especially Axon/Actin showed high number of strongly interconnected genes/proteins. Additionally, it should be noted that the “Synapse” topic serves as a fallback category for genes/proteins with broad synaptic functions. Most genes/proteins assigned to other topics are also located in the synapse but have more specific subcellular roles.

Article Snippet: Rotarod 1.2.0 software , Med Associates, Fairfax, VT, USA , N/A.

Techniques: Disruption, Functional Assay