LAUSR

Intact memory function is critical for carrying out daily life activities, such as managing finances, remembering to take medications, d r i v i n g i n f a m i l i a r e n v i r o n m e n t s , remembering a grandchild’s birthday, and learning to use a new computer. However, memory defic its not only accompany normal ag ing but are a lso comorbid with many psychiatric, neurological, and neurodegenerative diseases. Intellectual disability, autism, attention deficit disorder, learning disabil ity, schizophrenia, and de press io n a l l have memo r y d ef i c i t components, as do Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and other neurodegenerative diseases (Khan et al., 2014). Therefore, a large proportion of the human population is affected by this brain disorder. In addition, according to the US Census Bureau and Eurostat estimations, the aged population (individuals over the age of 65 years) will double within three decades. Thus, the number of persons with memory deficits is expected to increase drastically, as is the social and economic burden associated with their treatment and care. Cognition-enhancing pharmacological agents are viewed as a strategy for treating memory deficits or slowing the effects of aging on memory function. Some of the most thoroughly studied examples of memory enhancers are partial agonists of the N-methyl-D-aspartic acid receptor, D-cycloserine and D-serine; synthetic ampakines that allow glutamate to exert a prolonged effect on α-amino-3-hydroxy-5methyl-4-isoxazole-propionicacid receptors; and stimulant drugs that inhibit monoamine r e u p t a ke , i n c l u d i n g a m p h e t a m i n e s (Adderall), methylphenidate (Ritalin) and modafinil (Provigil); and donepezil (Aricept), which was designed to inhibit the enzyme acetylcholinesterase, which is responsible for degrading acetylcholine. These agents and other memory enhancers that have been studied to date have failed to produce consistent and invariable effects across various types of memory and have shown limited to no effect on memory deficits. Recently, we discovered that the expression of regulator of G protein signaling 14 of 414 amino acids (RGS14414) in the brain not only induced memory enhancement of multiple types of memory but also was sufficient for the rescue of recognition, spatial, and temporal memory, which are kinds of episodic memory that are primarily affected in patients or individuals with memory dysfunctions, in rodent models of aging and Alzheimer’s disease (LópezAranda et al., 2009; Masmudi-Martín et al., 2019; Navarro-Lobato et al., 2021). This RGS14414-mediated memory enhancement was facilitated through an increase in 14-33ζ activity (Navarro-Lobato et al., 2021).