The mechanism is unclear but some studies suggest a potential effect of the treatments on brain connectivity,20 with recent research identifying an association between NPS and dementia subtypes based on patterns of brain connectivity.21 Therapeutic interventions with secretase or BACE1 inhibitors, which shut down the production of native Aβ, may be detrimental due to the blockade of Aβ-associated compensatory brain network changes.22 Collectively, these data support testing whether therapeutic strategies aimed at increasing CSF Aβ42 levels could also improve NPS. The gene discussed is BACE1; the disease is dementia.