This is a longitudinal study that aims to identify potential neural oscillatory deficits in neonates associated with genetic and familial risk of dyslexia. Poor awareness of speech sounds (phonology) is the hallmark of dyslexia, across all languages studied so far. Despite the identification of several dyslexia susceptibility genes, little is known about the mechanisms by which genetic abnormalities give rise to neural deficits and how these in turn generate phonological deficits. Here, we hypothesised that common genetic polymorphisms in major dyslexia susceptibility genes (which are involved in developmental processes in-utero), are associated with abnormalities in the cortical microcircuitry, as hence in the functional connectivity and brain-to-speech (B2S) synchrony at birth. Identifying potential neonatal neural markers in association with dyslexia would be important for the understanding and supporting phonological development as it occurs during early infancy. One hundred infants (49 at high familial dyslexia risk) were assessed at birth, and half of them were followed up longitudinally at 7.5, 15 and 24 months of age. The current dissertation is focused on the neonatal dataset only. Previously reported single nucleotide polymorphisms (SNPs) – single base alterations in individual nucleotides within a gene - across major dyslexia susceptibility loci were analysed (DCDC2, KIAA0319, ROBO1 and DYX1C1) based on the neonatal blood-spot samples. Electroencephalography (EEG) was used to assess the new-born infants’ channel-to-channel network coherence and their neuronal oscillatory processing of prosodically enhanced speech. We predicted lower network coherence, as well as a reduced and delayed B2S synchrony (measured as phase-locking values - PLV) in infants at high familial risk of dyslexia, and in those carrying the less common variants of the tested SNPs. We found evidence for a reduced left hemispheric directed coherence in infants with the rarer ROBO1 and DCDC2 genotypes, independent of their familial risk. In contrast, we found that high familial risk was the strongest indicator of a significant delay in the PLV peak to the onset of speech, despite a similar PLV peak strength between the risk groups. The effect was driven by the infants with dyslexic mothers. Finally, the less common variants of two ROBO1 SNPs were associated with a delayed PLV peak beyond the infant’s familial risk. Although not directly tested, we can hypothesise that delays in peaks synchrony can be theoretically related to less synchronised or noisier internal neural environment in relation to dyslexia, which could result in less efficient synchronisation to external stimuli. Together, the neonatal results point toward a measurable dyslexia-risk related neural endophenotypes present at birth. They indicate a possible distinction between the effects of the at-risk genotype on the network coherence measures, and of the familial risk on the efficiency of the brain-to-speech synchrony. The developmental trajectories of these neonatal effects, and their significance over early phonological development and later dyslexia outcomes remain to be investigated. These results, however, present a potential mechanism for the emergence of an early neurobiological dyslexia-risk profile, which is yet to undergo the developmental, environmental, and experiential influences that would later shape language acquisition and reading skill.