Synapse loss is the principal cause of cognitive decline in Alzheimer’s disease (AD) and related disorders ( LBD, ADRD). Many, if not all patients experience a “mixed-dementia”, caused by multiple toxic oligomers such as amyloid beta, tau, and alpha-synuclein in the brain, but also now being documented throughout the body. These individuals experience an accelerated disease. The first study [Kuhn, 2024] reports that RAP-103, a CCR5 antagonist, at exceedingly low concentrations, prevents amyloid beta destruction of synapses in cultured rodent and human neurons. A further study [Liz, 2024] showed that RAP-103 blocks the effects of alpha-synuclein on hippocampal neurons, spines, and synapses via CCR5 dependent pathways. These effects, if translated to people, are expected to slow, prevent, even reverse cognitive decline in multiple dementias, especially those with significant mixed etiologies.