From a molecular neuroscience perspective, for both ADHD and ASD (autism) you're unlikely to find any pure biomarkers as clean as a disease like huntingtons disease whose mechanism is clearly understood as extra CAG repeats on the HTT gene (a clean mendelian disorder). ADHD is defined by behavior/cognitive symptoms and most all behavior/cognitive diseases are multifactoral, which ADHD is. WES/WGS and GWAS has been done and for familial ADHD and unlike ASD there is mostly no clear monogenic mutation (a single gene that would explain the phenotype) [note monogenic mutations are usually a very small subset of cases but give scientists a look into what pathway/mechanism is causing a multifactoral disease]. Thus it is not for a lack of looking classically, and deficit is speculated to likely manifest as a neural circuit organization or synaptic issue (though the latter is more closely linked to ASD). This is currently impossible (basically) to measure in alive human brain as it requires nanoscopic imaging, note how challenging the fly map was (incomplete IMO as well).