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Developing a new preclinical pipeline using humanized mice and advanced biomarkers improves the accuracy of drug discovery for synucleinopathies like Parkinson's disease (PD). This approach enhances the prediction of treatment outcomes for neurodegenerative diseases.

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Area of Science:

  • Neuroscience
  • Pharmacology

Background:

  • The global population of senior citizens is growing, leading to an increased prevalence of neurodegenerative diseases, including synucleinopathies (Parkinson's disease, Lewy Body Dementia, Alzheimer's disease).
  • Drug development for synucleinopathies faces challenges due to poor animal model translatability and limited cognitive biomarkers for predicting treatment success.
  • Current research aims to create a comprehensive preclinical drug discovery pipeline integrating humanized mice, neurochemical, imaging, and cognitive biomarkers to improve predictive accuracy.

Purpose of the Study:

  • To develop and validate a preclinical drug discovery pipeline for synucleinopathies.
  • To enhance the predictive accuracy of therapeutic efficacy and adverse effects using integrated biomarkers.
  • To improve the translation of preclinical findings to clinical success for neurodegenerative disease treatments.

Main Methods:

  • Utilized preformed fibril (PFF) injections of human synuclein in humanized mouse models.
  • Employed high-throughput touchscreen-based cognitive tasks to assess cognitive deficits.
  • Integrated fiber photometry for dopamine dynamics, immunofluorescence, lightsheet microscopy, and MRI for pathological and anatomical assessments.
  • Initiated experiments to test therapeutic interventions including drugs, genetic manipulations, and vaccines against alpha-synuclein (a-Syn) toxicity.

Main Results:

  • PFF-injected mice showed significant cognitive deficits in visual discrimination and conditional learning tasks prior to motor impairments.
  • Altered dopamine dynamics were observed in freely behaving PFF-injected mice.
  • Cognitive and neurochemical changes correlated with increased phosphorylated a-Syn spread through cortical-striatal-thalamic networks.
  • MRI revealed spatial atrophy patterns mimicking human synucleinopathy.
  • Preliminary data suggest treatments can mitigate a-Syn toxicity and improve cognitive deficits.

Conclusions:

  • Established a preclinical pipeline integrating humanized mice, cognitive tasks, neurochemical monitoring, and imaging.
  • The pipeline demonstrates potential for improved prediction of therapeutic efficacy and adverse effects in synucleinopathies.
  • Aims to accelerate the development of effective treatments for synucleinopathies and reduce late-stage drug failures.