While Aβ peptides of 39–42 amino acids are the primary component of protein aggregates found in senile plaques of Alzheimer’s disease and impaired mitochondrial electron transport along with exposure to metal ions can lead to Aβ aggregation and subsequent activation of PARP1, which is closely linked to several neurological diseases (74), our focus remains on ARL2’s potential influence on neuroinflammatory processes in brain regions such as the cerebral cortex and hippocampus in the context of sleep disorders and stroke. The gene discussed is PARP1; the disease is early-onset autosomal dominant Alzheimer disease.