Scientists Now Identify How the Brain Links Memories

Our brain usu­al­ly stored mem­o­ries into groups so that the rec­ol­lec­tion of one sig­nif­i­cant mem­o­ry trig­gers the recall of oth­ers con­nect­ed by time and they rarely record sin­gle mem­o­ries. But, as we age our brains grad­u­al­ly lose this abil­i­ty to link relat­ed memories.

In such, UCLA researchers have recent­ly dis­cov­ered a key mol­e­c­u­lar mech­a­nism behind mem­o­ry link­ing. They’ve also iden­ti­fied a way to restore this brain func­tion in mid­dle-aged mice — and an FDA-approved drug that achieves the same thing.

The find­ings, which are pub­lished in Nature, sug­gest a new method for strength­en­ing human mem­o­ry in mid­dle age and a pos­si­ble ear­ly inter­ven­tion for dementia.

Alci­no Sil­va, an author of the research and a dis­tin­guished pro­fes­sor of neu­ro­bi­ol­o­gy and psy­chi­a­try at the David Gef­fen School of Med­i­cine at UCLA said that our mem­o­ries are a huge part of who we are and the abil­i­ty to link relat­ed expe­ri­ences teach­es how to stay safe and oper­ate suc­cess­ful­ly in the world.

Accord­ing to the researchers, cells are stud­ded with recep­tors. To enter a cell, a mol­e­cule must latch onto its match­ing recep­tor, which oper­ates like a door­knob to pro­vide access inside.

The UCLA team said they focused on a gene called CCR5 that encodes the CCR5 recep­tor — the same one that HIV hitch­es a ride on to infect the brain cell and cause mem­o­ry loss in AIDS patients.

Sil­va’s lab demon­strat­ed in ear­li­er research that CCR5 expres­sion reduced mem­o­ry recall.

In the ongo­ing study, Sil­va and his work­mates dis­cov­ered a cen­tral mech­a­nism under­ly­ing mice’s abil­i­ty to link their mem­o­ries of two dif­fer­ent cages. A tiny micro­scope opened a win­dow into the mice’s brain. This enabled the sci­en­tists to observe neu­rons fir­ing and cre­at­ing new memories.

The mem­o­ry link­ing was inter­fered by boost­ing CCRS gene expres­sion in the brains of mid­dle-aged mice. The mice for­got the con­nec­tion between the two cages.

When the sci­en­tists delet­ed the CCR5 gene in the ani­mals, the mice were able to link mem­o­ries that nor­mal mice could not.

Sil­va had pre­vi­ous­ly stud­ied mar­avi­roc (a drug). This drug was approved by the U.S. Food and Drug Admin­is­tra­tion in 2007 for the treat­ment of HIV infec­tion. Sil­va’s lab dis­cov­ered that mar­avi­roc also sup­pressed CCR5 in the brains of mice.

Sil­va said, “When we gave mar­avi­roc to old­er mice, the drug dupli­cat­ed the effect of genet­i­cal­ly delet­ing CCR5 from their DNA.” The old­er mice were able to link mem­o­ries again.

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The find­ing sug­gests that mar­avi­roc could be used off-label to help restore mid­dle-aged mem­o­ry loss, as well as undo the cog­ni­tive deficits caused by HIV infection.

He also states, “Our next step will be to orga­nize a clin­i­cal tri­al to test mar­avi­roc’s influ­ence on ear­ly mem­o­ry loss with the goal of ear­ly inter­ven­tion.” “Once we ful­ly under­stand how mem­o­ry declines, we pos­sess the poten­tial to slow down the process.”

Which begs the ques­tion, why does the brain need a gene that inter­feres with its abil­i­ty to link memories?

Also Read:Is the soul more real than neu­rons and synapses?

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