While research has identified hundreds of genes required for normal memory formation, genes that suppress memory are of special interest because they offer insights into how the brain prioritizes and manages all of the information, including memories, that it takes in every day. These genes also provide clues for how scientists might develop new treatments for cognitive disorders such as Alzheimer\u2019s disease.<\/p>\n
Scientists from the Florida campus of The Scripps Research Institute (TSRI) have identified a unique memory suppressor gene in the brain cells of Drosophila, the common fruit fly, a widely recognized substitute for human memory studies.<\/p>\n
The study, which was led by Ron Davis, chair of TSRI\u2019s Department of Neuroscience].<\/p>\n
Davis and his colleagues screened approximately 3,500 Drosophila genes and identified several dozen new memory suppressor genes that the brain has to help filter information and store only important parts. One of these suppressor genes, in particular, caught their attention.<\/p>\n
\u201cWhen we knocked out this gene, the flies had a better memory\u2014a nearly two-fold better memory,\u201d said Davis. \u201cThe fact that this gene is active in the same pathway as several cognitive enhancers currently used for the treatment of Alzheimer\u2019s disease suggests it could be a potential new therapeutic target.\u201d<\/p>\n
When the scientists disabled this gene, known as DmSLC22A, flies\u2019 memory of smells (the most widely studied form of memory in this model) was enhanced\u2014while overexpression of the gene inhibited that same memory function.<\/p>\n
\u201cMemory processes and the genes that make the brain proteins required for memory are evolutionarily conserved between mammals and fruit flies,\u201d said Research Associate Ze Liu, co-first author of the study. \u201cThe majority of human cognitive disease-causing genes have the same functional genetic counterparts in flies.\u201d<\/p>\n
The gene in question belongs to a family of \u201cplasma membrane transporters,\u201d which produce proteins that move molecules, large and small, across cell walls. In the case of DmSLC22A, the new study indicates that the gene makes a protein involved in moving neurotransmitter molecules from the synaptic space between neurons back into the neurons. When DmSLC22A functions normally, the protein removes the neurotransmitter acetylcholine from the synapse, helping to terminate the synaptic signal. When the protein is missing, more acetylcholine persists in the synapse, making the synaptic signal stronger and more persistent, leading to enhanced memory. <\/p>\n
\u201cDmSLC22A serves as a bottleneck in memory formation,\u201d said Research Associate Yunchao Gai, the study\u2019s other co-first author. \u201cConsidering the fact that plasma transporters are ideal pharmacological targets, drugs that inhibit this protein may provide a practical way to enhance memory in individuals with memory disorders.\u201d<\/p>\n
The next step, Davis added, is to develop a screen for inhibitors of this pathway that, independently or in concert with other treatments, may offer a more effective way to deal with the problems of memory loss due to Alzheimer\u2019s and other neurodegenerative diseases.\nScripps Florida<\/link>\n","protected":false},"excerpt":{"rendered":"
While research has identified hundreds of genes required for normal memory formation, genes that suppress memory are of special interest because they offer insights into how the brain prioritizes and manages all of the information, including memories, that it takes in every day. These genes also provide clues for how scientists might develop new treatments […]<\/p>\n","protected":false},"author":2,"featured_media":0,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_monsterinsights_skip_tracking":false,"_monsterinsights_sitenote_active":false,"_monsterinsights_sitenote_note":"","_monsterinsights_sitenote_category":0,"footnotes":""},"categories":[35],"tags":[],"_links":{"self":[{"href":"https:\/\/clinlabint.com\/wp-json\/wp\/v2\/posts\/1237"}],"collection":[{"href":"https:\/\/clinlabint.com\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/clinlabint.com\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/clinlabint.com\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/clinlabint.com\/wp-json\/wp\/v2\/comments?post=1237"}],"version-history":[{"count":0,"href":"https:\/\/clinlabint.com\/wp-json\/wp\/v2\/posts\/1237\/revisions"}],"wp:attachment":[{"href":"https:\/\/clinlabint.com\/wp-json\/wp\/v2\/media?parent=1237"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/clinlabint.com\/wp-json\/wp\/v2\/categories?post=1237"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/clinlabint.com\/wp-json\/wp\/v2\/tags?post=1237"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}