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Abstract

Background: Neonatal brain development is a highly dynamic process characterized by rapid neuronal growth, synaptogenesis, and myelination. Protein homeostasis during this critical period is essential to maintain cellular function and prevent pathological protein aggregation. Alpha-synuclein, a presynaptic neuronal protein, has been implicated in various neurodegenerative disorders, particularly Parkinson's disease and related synucleinopathies.
Methods: This review explores the intersection of neonatal brain development and protein aggregation, focusing on alpha-synucleinopathy and its implications for neurodegenerative diseases.
Results: Recent evidence suggests that early-life protein aggregation may have long-term consequences on neurodegeneration. Dysregulation of proteostasis mechanisms in the neonatal brain may predispose individuals to early alpha-synuclein aggregation, which could act as a priming event for later-life neurodegeneration.
Conclusion: Understanding the developmental origins of alpha-synucleinopathies may aid in identifying early biomarkers and developing neuroprotective strategies to mitigate long-term neurological consequences.