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Telomere length (TL) is highly heritable, and a shorter telomere at birth may increase the risk of age-related problems. Additionally, a shorter TL may represent a biomarker of chronic stress and has been associated with psychiatric disorders. However, no study has explored whether there is an association between TL and the symptoms of one of the most common neurodevelopmental disorders in childhood: Attention Deficit/Hyperactive Disorder (ADHD). We evaluated 61 (range, 6–16 years) ADHD children and their parents between 2012 and 2014. TL was measured with a quantitative polymerase chain reaction method with telomere signal normalized to the signal from a single copy gene (36B4) to generate a T/S ratio. Family data was processed through a generalized estimated equations (GEE) model to determine the effect of parental TL on children TL. Inattentive and hyperactive-impulsive symptoms were also evaluated in relation to TL. For the first time, we found general heritability to be the major mechanism explaining interindividual TL variation in ADHD (father-child: 95% CI = 0.35/0.91, p < 0.001; mother-child: 95% CI = 0.38/0.74, p < 0.001). The hyperactive-impulsive dimension of ADHD was related with children’s TL (r = −339, p = 0.008) and maternal TL (r = −264, p = 0.047), but not with paternal TL (p > 0.05). The ADHD inattentive dimension was not significant associated with TL in this study (p > 0.05). TL was shown to be a potential biomarker of the ADHD symptoms burden in families affected by this neurodevelopmental disorder. However, it is crucial that future studies investigating the rate of telomere attrition in relation to psychiatric problems to consider the strong determination of TL at birth by inheritance.

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Signaling pathways play important roles in the coordination and integration of a myriad cellular functions. Because of widespread interest in the dopaminergic pathways, the protein dopamine and cyclic adenosine 3',5'-monophosphate-regulated phosphoprotein with molecular weight of 32 kDa, known by the acronym DARPP-32, occupies a central role in the biology of dopaminoceptive neurons in the central and peripheral nervous system (PNS). Its involvement has been demonstrated in many neural phenomena, including physiologic and pathologic neuroplasticity to drug effects and cognition. However, DARPP-32 has also been identified in non-neuronal tissues and its level of expression has been associated with the malignant level of some types of cancer, via modulation of cell survival and differentiation. This review considers some of these apparently compartmentalized functions of DARPP-32 and its potential as a therapeutic target.