Re­searchers find patho­log­i­cal signs of whose brains are much like hu­mans’

Malta Independent - - WORLD - Univer­sity of Florida Maria Carolina Gal­lego-Iradi,

A team of sci­en­tists in the United Kingdom and the U.S. re­cently re­ported the dis­cov­ery of patho­log­i­cal signs of Alzheimer’s dis­ease in dol­phins, an­i­mals whose brains are sim­i­lar in many ways to those of hu­mans.

This is the first time that these signs – neu­rofib­ril­lary tan­gles and two kinds of pro­tein clus­ters called plaques – have been dis­cov­ered to­gether in marine mam­mals. As neu­ro­science re­searchers, we be­lieve this dis­cov­ery has added sig­nif­i­cance be­cause of the sim­i­lar­i­ties be­tween dol­phin brains and hu­man brains.

The new find­ing in dol­phins sup­ports the re­search team’s hy­poth­e­sis that two fac­tors con­spire to raise the risk of de­vel­op­ing Alzheimer’s dis­ease in dol­phins.

Those fac­tors are: longevity with a long post-fer­til­ity life span – that is, a species liv­ing, on av­er­age, many years af­ter the child-bear­ing years are over – and in­sulin sig­nal­ing.

Gal­lego-Iradi, one of the au­thors of the pa­per, be­gan the study on the dol­phins’ brains more than a decade ago on the shores of Spain. It took sev­eral more years for other re­searchers to estab­lish the con­nec­tion be­tween meta­bolic dys­func­tion and in­sulin re­sis­tance in dol­phins and hu­mans. This re­cent study also did that.

To­gether, the in­sight into the sim­i­lar­i­ties be­tween dol­phins and hu­mans has led us to hy­poth­e­size that Alzheimer’s and di­a­betes are dis­eases not of old age but of a long post-fer­til­ity life span.

A dis­as­trous dis­easeAlzheimer’s is a progressive brain dis­ease that leads to mem­ory loss and changes in cog­ni­tive abil­ity. There is no cure, and the dis­ease ul­ti­mately leads to death.

It is hard to over­state the bur­den of the dis­ease, both on those who are di­ag­nosed with it and their fam­i­lies. It is the sixth-lead­ing cause of death in the U.S. Deaths from the dis­ease in the U.S. rose 55 per­cent from 1999 to 2014.

Alzheimer’s dis­ease has two ma­jor patho­log­i­cal hall­marks: The de­vel­op­ment of clus­ters of a pro­tein called beta-amy­loid out­side the cells and tan­gles of an­other pro­tein called tau inside the cell.

The pro­tein clus­ters out­side the cells are called se­nile plaques. The tan­gles inside are called neu­rofib­ril­lary tan­gles.

We saw both of these in the brains of the de­ceased dol­phins.

The big brain the­o­ryDol­phins be­long to an order of mam­mals called cetaceans that have adapted to live in the wa­ter.

Al­though dol­phins live in wa­ter and hu­mans live on Earth, dol­phins and hu­mans are very much alike in some key ways. In the last 50-60 mil­lion years, the brains of dol­phins and other cetaceans, in­clud­ing por­poises and whales, have hy­per­ex­panded. So have hu­man brains. This is a process called enchep­hal­iza­tion.

Also, as do hu­mans, dol­phins have a highly evolved brain de­vel­op­ment and a very com­plex so­cial re­la­tion­ship. This brain sim­i­lar­ity with hu­mans sug­gests the pos­si­bil­ity that dol­phins, as hu­mans, have de­vel­oped sim­i­lar molec­u­lar ma­chiner­ies and patho­log­i­cal char­ac­ter­is­tics, in­clud­ing sim­i­lar neu­rode­gen­er­a­tive dis­eases.

And, cetaceans and hu­mans live long. This is im­por­tant, as longevity is one of the most rel­e­vant fac­tors in neu­rode­gen­er­a­tive dis­eases. Cetaceans have longevity ranges be­tween 20-100 years, which is enough time to de­velop brain amy­loid de­posits.

Some as­pects of Alzheimer’s pathol­ogy have been re­ported in a wide range of other an­i­mals. Our evo­lu­tion­ary rel­a­tives, such as apes and mon­keys, and our pets, dogs and cats, de­velop one of the patholo­gies, the amy­loid pathol­ogy. Amy­loid plaques also have been de­scribed in cap­tive wild an­i­mals such as bears.

But to see both plaques and tan­gles in an­other species is rare.

We be­lieve this makes our find­ings in dol­phins of both neu­ritic plaque and tan­gle pathol­ogy in dol­phins all the more re­mark­able.

Stranded dol­phins led to the first dis­cov­eryCe­taceans be­come stranded many times each year all over the world. This strand­ing gen­er­ates alarm, and sci­en­tists study to un­der­stand why it hap­pens. Some of the fac­tors in­clude poor wa­ter qual­ity; an­i­mals liv­ing in very deep wa­ter who de­tect the shore too late; un­bal­ance and con­fu­sion cre­ated by Earth’s mag­netic field changes; con­tam­i­na­tion by heavy me­tals such as mer­cury, cad­mium or zinc; or con­tam­i­na­tion by com­pounds such as PCBs and DDTs. Other pos­si­ble causes are viruses and par­a­sites, trau­matic death, pre­da­tion or fish­ing mu­ti­la­tion, or ship sonars in­ter­fer­ing with an­i­mal echolo­ca­tion.

Dol­phins stranded in Spain be­tween 2003 and 2006 led to Gal­lego Iradi’s find­ings about the Alzheimer’s pathol­ogy.

The sam­ples rep­re­sented three dif­fer­ent species of dol­phins (bot­tlenose, striped and Risso’s) stranded on the coasts of Spain. Their brains all had the same twisted strands and pro­tein clus­ters in their brain as hu­man pa­tients with Alzheimer’s dis­ease. They also had neu­ronal loss, strength­en­ing the idea that dol­phins and hu­mans could have the same Alzheimer’s pathol­ogy.

Years af­ter those find­ings, other sci­en­tists be­gan to ex­plore a pos­si­ble con­nec­tion be­tween a fail­ure in in­sulin sig­nal­ing and Alzheimer’s.

Hu­mans, at some point in our evo­lu­tion­ary his­tory, ac­quired a trait along the in­sulin sig­nal­ing path­way. They do not im­ply that in­sulin sig­nal­ing af­fects only longevity, that the ef­fects of in­sulin sig­nal­ing on me­tab­o­lism, longevity and de­men­tia are nec­es­sar­ily me­di­ated through a sin­gle mech­a­nism and even that de­fects in in­sulin-like growth fac­tor sig­nal­ing in­evitably re­sult in de­men­tia.

Dr. Si­mon Love­stone at the Univer­sity of Ox­ford and Dr. Frank Gunn-Moore at the Univer­sity of Saint An­drews be­gan to de­velop a hy­poth­e­sis that this fail­ure in in­sulin sig­nal­ing in hu­mans, re­lated to post­fer­til­ity longevity, could be a cause of Alzheimer’s in hu­mans. And here’s an­other con­nec­tion. Cetaceans are uniquely prone to a pre­di­a­betes state and are one of the few an­i­mals, other than hu­mans, with a nat­u­rally long post-fer­til­ity life span.

We pos­tu­lated a linked mech­a­nism that led us to hy­poth­e­size that an­i­mals with a long post-fer­til­ity life­span would be at risk for both in­sulin re­sis­tance and Alzheimer’s. This hy­poth­e­sis led us to the pre­dic­tion that cetaceans and other an­i­mals with un­usual longevity would be at risk for both in­sulin re­sis­tance and would have Alzheimers’ pathol­ogy – a pre­dic­tion for which we have pro­vided some proof in our re­cent ar­ti­cle.

This ar­ti­cle was orig­i­nally pub­lished on The Con­ver­sa­tion. Read the orig­i­nal ar­ti­cle here: http://the­con­ver­sa­tion.com/re­searchers­find-patho­log­i­cal-signs-of-alzheimersin-dol­phins-whose-brains-are-much-like -hu­mans-86741.

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