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Age at onset (AAO) has frequently been a key indicator in delineating disorder subtypes leading to gene identification. Thus far, differences in AAO have helped to separate genetic from sporadic cases in common illnesses such as breast cancer.¹ Differences in AAO may also be used to identify different vulnerability genes, as in Alzheimer disease,² or different mutations in the same gene, as in Duchenne-Becker muscular dystrophy.³ More recent findings have shown that AAO may also reflect differential expansion of an unstable DNA region at or near the disease locus, as in myotonic dystrophy⁴ and Huntington disease.

In bipolar I affective disorder (BPAD), clinical, familial, and biological differences have been reported according to AAO. Early-onset BPAD is associated with (1) higher frequency of affective disorders in relatives^{5, 6, 7}; (2) higher rates of comorbid conditions such as psychotic symptoms during affective episodes,^{7, 8, 9} lifetime panic disorder,^{9, 10} or conduct disorder, alcohol abuse, and drug . . . [Full Text of this Article]

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