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NEURODEVELOPMENTAL BIOMARKER NDEL1 ACTIVITY IS DECREASED IN BLOOD SERUM OF PATIENTS WITH MENTAL DISORDERS BUT INCREASED IN PATIENTS WITH DEPRESSION AND DEPRESSIVE BIPOLAR DISORDER
Mirian Hayashiand 2 co-authors
UNIFESP
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS02-07PM-249
Presentation
Date TBA
Board: PS02-07PM-249
Event Information
Poster Board
PS02-07PM-249
Poster
View posterAbstract
Background Mood disorders like Major Depressive Disorder (MDD) and Bipolar Disorder (BD) lack validated biomarkers, and traditional monoaminergic therapies often face challenges regarding resistance and delayed efficacy. This study investigated Ndel1—an oligopeptidase that cleaves neurotensin and regulates neurite outgrowth—as a potential pathophysiological factor and treatment response biomarker.
Methods & Results Researchers evaluated Ndel1 activity and cellular integrity in cultured neurons treated with serum from MDD and BD patients, as well as with standard psychotropic medications. The study found that serum from patients with depression exerted neurotoxic effects, reducing cell viability and altering neuronal morphology, particularly in MDD samples. However, serum exposure alone did not significantly alter Ndel1 activity. Conversely, direct treatment with fluoxetine or quetiapine significantly reduced intracellular Ndel1 (iNdel1) activity and neurite density, recapitulating the morphological alterations observed after exposure to patient serum. Ex vivo assays also revealed that while psychotropics and patient serum both reduced neurite density - indicating circulating neurotoxic factors - intracellular responses differed. Indeed, MDD serum uniquely upregulated neuronal intracellular Ndel1 (iNdel1) activity, suggesting a disorder-specific compensatory mechanism against serum-induced neuronal stress.
Conclusion These findings suggest that while peripheral factors in mood disorders compromise neuronal integrity, antidepressants and antipsychotics specifically modulate intracellular Ndel1 function. This implicates the enzyme in the mechanism of action for these treatments and highlights the potential of Ndel1 as a biomarker and/or target for treatment response in affective disorders.
Methods & Results Researchers evaluated Ndel1 activity and cellular integrity in cultured neurons treated with serum from MDD and BD patients, as well as with standard psychotropic medications. The study found that serum from patients with depression exerted neurotoxic effects, reducing cell viability and altering neuronal morphology, particularly in MDD samples. However, serum exposure alone did not significantly alter Ndel1 activity. Conversely, direct treatment with fluoxetine or quetiapine significantly reduced intracellular Ndel1 (iNdel1) activity and neurite density, recapitulating the morphological alterations observed after exposure to patient serum. Ex vivo assays also revealed that while psychotropics and patient serum both reduced neurite density - indicating circulating neurotoxic factors - intracellular responses differed. Indeed, MDD serum uniquely upregulated neuronal intracellular Ndel1 (iNdel1) activity, suggesting a disorder-specific compensatory mechanism against serum-induced neuronal stress.
Conclusion These findings suggest that while peripheral factors in mood disorders compromise neuronal integrity, antidepressants and antipsychotics specifically modulate intracellular Ndel1 function. This implicates the enzyme in the mechanism of action for these treatments and highlights the potential of Ndel1 as a biomarker and/or target for treatment response in affective disorders.
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