Abstract: Alzheimer’s disease (AD) is the sixth leading cause of death in the United States with approximately 5.8 million Americans currently living with AD. Due to the lack of a disease modifying treatment for AD and the aging baby boomer generation, this number is pro- jected to grow to 13.8 million by 2050 (Gaugler et al., 2019). Amy- loid-beta (Aβ) plaque accumulation, one of the major pathological hallmarks of AD, can begin > 20 years before clinical symptoms of AD. By the time AD is clinically diagnosed, neuronal loss and neu- ropathological lesions (Aβ plaques and tau tangles) have already occurred in many brain regions (Gaugler et al., 2019). AD demen- tia correlates highly with neuronal loss, and therefore, reduction of neuropathological lesions in the AD brain at the time of clinical diagnosis alone cannot reverse AD dementia. We propose that a therapy that combines a reduction of neuropathological lesions of AD along with neuronal repair and neurogenesis may be required to treat AD dementia.