The Asian Age - - D C Discourse -

We have made g r e a t strides in t r e a t i n g heart dis­eases, can­cer and such cat­a­strophic ill­nesses, but the dis­eases of the brain still be­long to the realm of rel­a­tively un­solved mys­ter­ies. This is not sur­pris­ing con­sid­er­ing that the brain and its mech­a­nism are the most com­plex en­ti­ties in a body. Yet, our cred­i­bil­ity of the un­der­stand­ing of hu­man phys­i­ol­ogy is ques­tioned by “how much we know about the mam­malian brain and its func­tions?”

A mother re­turns dis­heart­ened from a neu­rol­o­gist as she hears “No” for an an­swer to whether there’s a cure for her child’s cere­bral at­ro­phy. Fur­ther­more, Alzheimer and de­men­tia are treated symp­tomat­i­cally.

A re­cent re­port states that the preva­lence of de­men­tia is some­where be­tween five per cent and seven per cent glob­ally among peo­ple aged over 60. Over the age of 85, be­tween 25 per cent and 50 per cent of peo­ple are es­ti­mated to have symp­toms of de­men­tia, such as Alzheimer’s.

World­wide, the eco­nomic im­pact of de­men­tia is al­most a tril­lion dol­lars a year. Not in­cluded here is the crush­ing emo­tional toll th­ese dis­eases take on fam­ily mem­bers as they watch loved ones slowly fade away and be­come al­most strangers. In view of the great toll neu­rode­gen­er­a­tive dis­eases are taking on our pop­u­la­tion and our health­care bud­get, it is vi­tal that we gain greater un­der­stand­ing of th­ese dis­ease pro­cesses, es­pe­cially of the changes oc­cur­ring at the molec­u­lar level in cru­cial re­gions like the synapses. ( Sy­napse is the junc­tion be­tween two nerve cells, con­sist­ing of a minute gap across which im­pulses pass by dif­fu­sion of a neu­ro­trans­mit­ter.)

My collaborator neu­ro­sur­geon, Dr Eti­enne, calls such an un­der­stand­ing “an im­por­tant step to un­ravel the mech­a­nisms un­der­ly­ing neu­rode­gen­er­a­tive dis­eases like Parkin­son’s dis­ease, mo­tor neu­ron dis­ease ( Amy­otrophic Lat­eral Scle­ro­sis), Prion dis­eases, Hunt­ing­ton’s dis­ease, Alzheimer’s dis­ease and other de­men­tias.”

The patho­logic changes that oc­cur in th­ese dis­eases are, of course, a lot more com­plex than just what oc­curs at the synapses. A re­search team at the pres­ti­gious Mas­sachusetts Gen­eral Hospi­tal states: “In Alzheimer’s dis­ease, glial cells ( cells sur­round­ing neu­rons) de­rived from meso­derm ( one of the three pri­mary germ lay­ers in the very early em­bryo) func­tion as scav­engers in the ner­vous sys­tem. Th­ese cells ac­cu­mu­late near amy­loid with mu­ta­tions in them en­hanc­ing the dis­ease.

“The in­abil­ity to scavenge the pro­duced amy­loid plaques causes events that fur­ther af­fect the cells, lead­ing to dam­ag­ing in­flam­ma­tion; in Parkin­son’s dis­ease, ac­ti­vated mi­croglia are stated to be high in the dam­aged brain struc­ture.”

Scans have been re­ported to show se­ri­ous “in­flam­ma­tory mi­croglia early in the course of the dis­ease, and ev­i­dence sug­gests that the same sort of ‘ dou­ble- edged sword’ sit­u­a­tion seen in Alzheimer’s dis­ease also oc­curs in Parkin­son’s.”

Though much of this may sound like Greek to those who are not di­rectly in the field, this should give us an in­di­ca­tion of the tremen­dous com­plex­ity of the chal­lenges fac­ing med­i­cal re­searchers in this field. No one fully un­der­stands what causes the dreaded neu­rode­gen­er­a­tive dis­eases like Alzheimer’s. It is be­lieved that there may well be a ge­netic com­po­nent to it. A com­bi­na­tion of ge­netic, en­vi­ron­men­tal and lifestyle fac­tors has all been sug­gested as con­trib­u­tors to the on­set of this ill­ness.

The ques­tion is why Alzheimer’s strikes older peo­ple more. Age- re­lated changes have been re­ported to in­clude the shrink­ing of parts of the brain, in­flam­ma­tion, un­sta­ble free rad­i­cals, and a break­down of en­ergy pro­duc­tion within a cell. Un­der­stand­ing how one goes from this to the dra­matic changes that oc­cur in a beloved rel­a­tive, to ul­ti­mately los­ing her/ him while be­ing still phys­i­cally present, is the great chal­lenge fac­ing re­searchers in the field of Alzheimer’s dis­ease. Spec­tac­u­lar ad­vances have been achieved in this field in re­cent years. One of the most prom­i­nent find­ings in Alzheimer’s dis­ease is the de­vel­op­ment of aber­rant pro­teins as plaques and tan­gles. Ad­vances in brain imag­ing tech­niques al­low re­searchers to see the de­vel­op­ment of ab­nor­mal pro­teins in the brain. Sci­en­tists are also ex­plor­ing the very ear­li­est steps in the dis­ease process by study­ing the changes in the brain and body flu­ids that can be de­tected years be­fore symp­toms of the dis­ease ap­pear. Find­ings from th­ese stud­ies could not only make di­ag­no­sis eas­ier, but even help un­der­stand the cause of the dis­ease, the Holy Grail for re­searchers on any ill­ness.

An­other ap­proach to un­der­stand­ing com­plex dis­ease pro­cesses has been to try to gain an in­sight into how an­i­mal ner­vous sys­tems evolved from sim­ple struc­tures to be­come a com­plex net­work, trans­mit­ting sig­nals be­tween dif­fer­ent parts of the body.

A promis­ing ex­am­ple is a new study at the Univer­sity of Ex­eter, us­ing sim­ple multi- cel­lu­lar or­gan­isms to re­veal the be­gin­nings of the ner­vous sys­tems found in more com­plex an­i­mals.

With the BRAIN ( Brain Re­search through Ad­vanc­ing In­no­va­tive Neuro t e chnolo g i e s ) Ini­tia­tive in var­i­ous coun­tries, we are mak­ing progress, though in re­al­ity, we may still know only a small per­cent­age of the brain’s com­plex chem­istry. A very hope­ful sign has been the in­creas­ing in­ter­est stu­dents in uni­ver­si­ties have been show­ing in pur­su­ing neu­ro­science as a ca­reer.

What is re­quired is ac­tive sup­port from the govern­ment for con­tin­ued re­search in the neu­ro­sciences.

( The au­thor is Lon von Dud­dle­son Krumb Pro­fes­sor of Mineral En­gi­neer­ing at Columbia Univer­sity. He heads a team do­ing re­search on brain dis­eases us­ing elec­tron spin res­o­nance.)

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