2025-04-07
MoCA boosted, brain relieved!
Neurology
#Parkinson #Cognition #Inflammation #IL6 #Entacapone #MoCA
Parkinson’s disease (PD) is a progressive neurodegenerative disorder primarily characterized by motor symptoms such as tremors, rigidity, and bradykinesia. However, in moderate to advanced stages, non-motor symptoms—particularly cognitive impairments—become increasingly common, affecting memory, attention, executive function, and information processing speed. These cognitive issues significantly impact quality of life, reduce independence, and complicate overall disease management.
Traditional dopaminergic treatments, particularly the combination of levodopa and carbidopa (LC), help control motor symptoms in the short term. However, their effectiveness tends to diminish over time, and their impact on cognition remains limited. Given these therapeutic limitations, new strategies are being explored to address the non-motor dimensions of PD.
In this context, the addition of entacapone—a catechol-O-methyltransferase (COMT) inhibitor—to the LC combination has attracted particular interest. This triple combination, known as levodopa-carbidopa-entacapone (LCE), extends the effect of levodopa by reducing its peripheral degradation, thereby ensuring better dopamine availability in the brain. Beyond its motor benefits, this prolonged dopaminergic modulation may also have positive effects on certain brain functions, especially cognitive ones.
This study explores the impact of LCE on cognitive function and systemic inflammation, particularly using the MoCA score and IL-6 levels, in patients with moderate to advanced Parkinson’s disease.
Eighty patients with moderate to advanced Parkinson’s disease were enrolled in the study and randomly assigned to one of two groups:
All participants underwent a comprehensive evaluation at the beginning and end of the study, including motor tests, cognitive assessments (notably the MoCA score), emotional assessments (anxiety, depression), and biological analyses (pro-inflammatory cytokine levels).
The results show a significant cognitive improvement in the LCE group, with an average increase of 1.5 points in the MoCA score (p < 0.001). No significant change was observed in the LC group. On the biological level, patients treated with LCE also showed a marked reduction in serum interleukin-6 (IL-6) levels, a pro-inflammatory cytokine involved in neurodegeneration (p = 0.002). A negative correlation was observed between the drop in IL-6 levels and the improvement in cognitive performance, suggesting a potential link between peripheral inflammation and brain function in Parkinson’s patients.
No significant differences between the two groups were found in terms of motor symptoms, anxiety, or depression. These findings suggest that adding entacapone may specifically target cognitive and inflammatory components of the disease, without affecting other clinical dimensions in the short term.
Parkinson’s disease is a progressive neurological condition often associated with tremors and motor impairments. In more advanced stages, cognitive disorders become common and severely affect patients' independence and quality of life. A major challenge lies in the lack of effective treatments to slow down or reverse this cognitive decline. While dopaminergic therapies such as levodopa-carbidopa (LC) relieve motor symptoms, their effect on cognition remains limited.
This study explores whether the combination of levodopa-carbidopa-entacapone can improve cognitive function in patients with Parkinson’s disease. It also examines its biological impact, focusing on IL-6 levels—a pro-inflammatory cytokine potentially linked to cognitive decline.
These findings support the hypothesis of an indirect therapeutic effect of LCE on cognition, potentially mediated by an anti-inflammatory action. They suggest a connection between improved cognitive function and reduced systemic inflammation, notably through IL-6 modulation. However, several limitations remain, and further clinical trials are needed to confirm these initial observations and better define responder profiles.
This study lays the groundwork for a new strategy: targeting inflammation to protect cognitive function. What if, in Parkinson’s disease, preserving the mind also meant acting on the immune system?
Parkinson’s disease (PD) is a progressive neurodegenerative disorder primarily characterized by motor symptoms such as tremors, rigidity, and bradykinesia. However, in moderate to advanced stages, non-motor symptoms—particularly cognitive impairments—become increasingly common, affecting memory, attention, executive function, and information processing speed. These cognitive issues significantly impact quality of life, reduce independence, and complicate overall disease management.
Traditional dopaminergic treatments, particularly the combination of levodopa and carbidopa (LC), help control motor symptoms in the short term. However, their effectiveness tends to diminish over time, and their impact on cognition remains limited. Given these therapeutic limitations, new strategies are being explored to address the non-motor dimensions of PD.
In this context, the addition of entacapone—a catechol-O-methyltransferase (COMT) inhibitor—to the LC combination has attracted particular interest. This triple combination, known as levodopa-carbidopa-entacapone (LCE), extends the effect of levodopa by reducing its peripheral degradation, thereby ensuring better dopamine availability in the brain. Beyond its motor benefits, this prolonged dopaminergic modulation may also have positive effects on certain brain functions, especially cognitive ones.
This study explores the impact of LCE on cognitive function and systemic inflammation, particularly using the MoCA score and IL-6 levels, in patients with moderate to advanced Parkinson’s disease.
What if we boosted memory too?
Eighty patients with moderate to advanced Parkinson’s disease were enrolled in the study and randomly assigned to one of two groups:
- Standard treatment: levodopa + carbidopa (LC)
- Triple combination: levodopa + carbidopa + entacapone (LCE)
All participants underwent a comprehensive evaluation at the beginning and end of the study, including motor tests, cognitive assessments (notably the MoCA score), emotional assessments (anxiety, depression), and biological analyses (pro-inflammatory cytokine levels).
The results show a significant cognitive improvement in the LCE group, with an average increase of 1.5 points in the MoCA score (p < 0.001). No significant change was observed in the LC group. On the biological level, patients treated with LCE also showed a marked reduction in serum interleukin-6 (IL-6) levels, a pro-inflammatory cytokine involved in neurodegeneration (p = 0.002). A negative correlation was observed between the drop in IL-6 levels and the improvement in cognitive performance, suggesting a potential link between peripheral inflammation and brain function in Parkinson’s patients.
No significant differences between the two groups were found in terms of motor symptoms, anxiety, or depression. These findings suggest that adding entacapone may specifically target cognitive and inflammatory components of the disease, without affecting other clinical dimensions in the short term.
Read next: IL6 receptor inhibitors: exploring the therapeutic potential of several diseases using Mendelian randomisation of drug targets
LCE: An unexpected cognitive boost?
Parkinson’s disease is a progressive neurological condition often associated with tremors and motor impairments. In more advanced stages, cognitive disorders become common and severely affect patients' independence and quality of life. A major challenge lies in the lack of effective treatments to slow down or reverse this cognitive decline. While dopaminergic therapies such as levodopa-carbidopa (LC) relieve motor symptoms, their effect on cognition remains limited.
This study explores whether the combination of levodopa-carbidopa-entacapone can improve cognitive function in patients with Parkinson’s disease. It also examines its biological impact, focusing on IL-6 levels—a pro-inflammatory cytokine potentially linked to cognitive decline.
These findings support the hypothesis of an indirect therapeutic effect of LCE on cognition, potentially mediated by an anti-inflammatory action. They suggest a connection between improved cognitive function and reduced systemic inflammation, notably through IL-6 modulation. However, several limitations remain, and further clinical trials are needed to confirm these initial observations and better define responder profiles.
This study lays the groundwork for a new strategy: targeting inflammation to protect cognitive function. What if, in Parkinson’s disease, preserving the mind also meant acting on the immune system?
Read next: The impact of loneliness on Parkinson’s Disease
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