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Researchers analyzed 212 cognitively unimpaired, self-identified white adults ages 55 to 90 from the Alzheimer’s Disease Neuroimaging Initiative (ADNI). Participants’ ADHD polygenic risk scores (ADHD-PRS) were measured to determine their genetic liability for ADHD. However, none of the participants had a clinical ADHD diagnosis.

A series of cognitive imaging tests and assessments were performed at the baseline of the study (then six months later, one year later, and annually after that) to track cognitive decline and AD pathology.

These tests included:

• Amyloid-β positron emission tomography (Aβ-PET) scans to detect deposits of Aβ (a key peptide in the pathogenesis of AD) in the brain
• Levels of phosphorylated tau (p-tau) in cerebrospinal fluid (CSF)—the accumulation of which leads to synaptic impairment and neuronal dysfunction
• Brain magnetic resonance imaging (MRI) scans to visually inspect gray matter probability maps
• Clinical and neuropsychological assessments to test cognitive functions—such as logical memory, word recall, executive function, and auditory verbal learning

The study found that higher ADHD-PRS (i.e., a higher genetic liability for ADHD) was associated with decreased cognitive performance and memory over time.

The combination of a high genetic liability to ADHD and brain Aβ deposition was more significant on cognitive deterioration than either factor alone.

In Aβ-positive individuals, higher ADHD-PRS was also associated with increased CSP p-tau levels, reduced gray matter density, and atrophy in the frontal and parietal regions. No significant association was observed between high genetic liability to ADHD and neurodegeneration in Aβ-negative individuals.

Though this research indicates associations between the genetic risk of ADHD to Alzheimer’s disease, lead study author and psychiatry resident at UPMC, Douglas Leffa, M.D., Ph.D., says more work is needed to link a confirmed ADHD diagnosis to the risks of Alzheimer’s disease.

“We believe the next step will be to measure biomarkers of Alzheimer’s pathology in older individuals that were diagnosed with ADHD in childhood. By following these individuals over time, we will be able to confirm the association between ADHD and late-onset Alzheimer’s disease, as well as better comprehend the mechanisms behind it,” he explains.

Additionally, Leffa points out that studies on the genetic risk of ADHD (including this one) and most of the Alzheimer’s literature have been conducted in individuals that self-identify as white. “Future research should definitely focus on recruiting a more diverse population in order to answer how race plays into the genetic association between ADHD and Alzheimer’s disease,” he says.

As we’ve seen in the results of this study, genetic liability for ADHD itself does not lead to neurodegeneration. Rather, a high ADHD-PRS puts Aβ-positive (but not Aβ-negative) individuals at a higher risk of cognitive decline.

As such, the advice for taking care of your cognitive well-being as you age is the same for individuals with and without ADHD: