Converging evidence suggests that developmental dyslexia is a neurobiological disorder, characterized by deficits in the auditory, visual, and linguistic domains. In the longitudinal project of the Dutch Dyslexia Programme, 180 children with a familial risk of dyslexia (FR) and a comparison group of 120 children without FR (noFR) were followed from the age of 2 months up to 9 years. Children were assessed on (1) auditory, speech, and visual event-related potentials every half year between 2 and 41 months; (2) expressive and receptive language, motor development, behaviour problems, and home-literacy environment by questionnaires at the age of 2 and 3; (3) speech-language and cognitive development from 47 months onwards; and (4) preliteracy and subskills of reading, and reading development during kindergarten and Grades 2 and 3. With regard to precursors of reading disability, first analyses showed specific differences between FR and noFR children in neurophysiological, cognitive, and early language measures. Once reading tests administered from age 7 to 9 years were available, the children were divided into three groups: FR children with and without dyslexia, and controls. Analyses of the differences between reading groups yielded distinct profiles and developmental trajectories. On early speech and visual processing, and several cognitive measures, performance of the non-dyslexic FR group differed from the dyslexic FR group and controls, indicating continuity of the influence of familial risk. Parental reading and rapid naming skills appeared to indicate their offspring's degree of familial risk. Furthermore, on rapid naming and nonverbal IQ, the non-dyslexic FR group performed similarly to the controls, suggesting protective factors. There are indications of differences between the FR and control groups, irrespective of reading outcome. These results contribute to the distinction between the deficits correlated to dyslexia as a manifest reading disorder and deficits correlated to familial risk only. Copyright © 2013 John Wiley & Sons, Ltd.