Background: Developmental dyslexia is a common specific learning disorders and is characterized by persistent difficulties in reading decoding and automatization. Although single-deficit theories, particularly the phonological deficit theory, have provided evidence for explaining specific components of dyslexia, substantial heterogeneity in the cognitive, neural, and behavioral profiles of individuals with dyslexia challenges the adequacy of a single mechanism to account for the full phenotype.

Objective: This study critically examined the evolution of explanatory accounts of developmental dyslexia, from single-deficit models to multifactorial, multilevel, interactive, and network-based frameworks, and to consider the implications of this shift for assessment and intervention.

Method: This study employed a critical review with an analytical, thematic approach. Relevant literature was identified through searches of PubMed, Google Scholar, and ScienceDirect, supplemented by screening the reference lists of key studies. Publications from 2000 onward were examined alongside foundational sources addressing the theoretical foundations of dyslexia. Selected sources included empirical, longitudinal, neuroimaging, and intervention studies, as well as systematic reviews and meta-analyses. The literature was synthesized according to the explanatory scope of the theoretical accounts, their capacity to explain cognitive and behavioral heterogeneity, and their ability to establish links across biological, neural, cognitive, environmental, and behavioral levels of analysis.

Results: The findings indicate that single-deficit theories can account for important mechanisms, including phonological processing, temporal processing, visual–attentional processes, working memory, and automatization; however, none can, on its own, fully account for the heterogeneity observed in dyslexia. In contrast, multifactorial and interactive models suggest that different individuals may arrive at similar reading difficulties through different combinations and interactions of cognitive and neuropsychological vulnerabilities. Evidence from network analyses and neuroimaging further supports the involvement of multiple networks and distinct cognitive–neural pathways, although the causal relationships across these levels remain incompletely understood.

Conclusion: Developmental dyslexia cannot be reduced to a single deficit. Multifactorial, multilevel, and interactive frameworks offer greater potential for explaining individual differences and may provide a conceptual basis for profile-based assessment and interventions tailored to individual needs. Nevertheless, further longitudinal and intervention research is required to establish the validity and causal explanatory power of these approaches.