Semax · research summary

A Mouse Model of Nigrostriatal Dopaminergic Axonal Degeneration As a Tool for Testing Neuroprotectors.

Acta naturae · 2021. Summary drawn from the study's full text. Each statement is followed by the exact sentence it comes from. This is a research summary, not medical advice.

Study type

Animal study using a mouse model of Parkinson's disease to test neuroprotective agents
“We used male C57BL/6 mice (2–2.5 months of age).”

Subjects

Male C57BL/6 mice
“We used male C57BL/6 mice (2–2.5 months of age).”

Sample size

Groups ranged from n=3 to n=9 depending on the specific experiment and measurement
“Tyrosine hydroxylase (TH) (n = 3–4) in striatal slices was detected by immunohistochemistry (IHC), followed by the counting of axonal terminals in four areas of the dorsal striatum as described previously [7].”

Duration

Observations were conducted at specific time points up to 12 hours after the final MPTP injection
“Material (striatum) for all neuroprotectors was collected 12 h after the last MPTP injection, and the DA concentration in the tissue was determined by HPLC-ED.”

Reported findings

The rate of dopaminergic axonal terminal degeneration is nonlinear, decreasing from approximately 7%/h in the first 4 hours to 1%/h in the subsequent 5 hours
“Comparing these data, it appears reasonable to conclude that the rate of loss of axonal terminals is not linear: it is about 7%/h within the first 4 h after the first MPTP injection and 1%/h during the next 5 h.”
Nomifensine administration maintained striatal dopamine concentration at control levels and significantly protected axonal terminals from MPTP toxicity
“Administration of nomifensine was shown to maintain the striatal DA concentration at the control level upon MPTP treatment and significantly protect axonal terminals (Fig. 3 A,B).”
SEMAX administered 12 hours before MPTP increased striatal dopamine, suggesting an effect via endogenous neurotrophic factor secretion rather than antioxidant activity
“An increase in DA was observed only in the group receiving SEMAX 12 h before MPTP (Fig. 3 C,D).”

Limitations stated by the authors

The study was conducted in an animal model, and the authors note that previous drugs effective in animal models have not passed clinical trials
“Indeed, drugs with neuroprotective properties, which have shown high efficiency in animal models of Parkinsonism, have not passed clinical trials [2, 3].”

Source: PubMed 34707903 · DOI 10.32607/actanaturae.11433 · all study summaries

Reported findings

The rate of dopaminergic axonal terminal degeneration is nonlinear, decreasing from approximately 7%/h in the first 4 hours to 1%/h in the subsequent 5 hours

“Comparing these data, it appears reasonable to conclude that the rate of loss of axonal terminals is not linear: it is about 7%/h within the first 4 h after the first MPTP injection and 1%/h during the next 5 h.”

Nomifensine administration maintained striatal dopamine concentration at control levels and significantly protected axonal terminals from MPTP toxicity

“Administration of nomifensine was shown to maintain the striatal DA concentration at the control level upon MPTP treatment and significantly protect axonal terminals (Fig. 3 A,B).”

SEMAX administered 12 hours before MPTP increased striatal dopamine, suggesting an effect via endogenous neurotrophic factor secretion rather than antioxidant activity

“An increase in DA was observed only in the group receiving SEMAX 12 h before MPTP (Fig. 3 C,D).”

Limitations stated by the authors

The study was conducted in an animal model, and the authors note that previous drugs effective in animal models have not passed clinical trials

“Indeed, drugs with neuroprotective properties, which have shown high efficiency in animal models of Parkinsonism, have not passed clinical trials [2, 3].”