New di­ag­no­sis for Alzheimer’s

A new blood-based method de­vel­oped to de­tect de­men­tia

The McGill Daily - - Contents - Tai (Ritchie) Vinh Truong Sci+tech Writer

An ag­ing pop­u­la­tion has be­come an un­avoid­able trend amongst de­vel­oped coun­tries. For the first time ever, in 2016, se­niors made up a higher per­cent­age of the Cana­dian pop­u­la­tion than chil­dren. Ad­vances in health­care have sig­nif­i­cantly im­proved qual­ity of life and length­ened life­span. How­ever, with this im­prove­ment comes the in­creas­ing preva­lence of neu­rode­gen­er­a­tive dis­eases. More and more peo­ple ex­pe­ri­ence im­paired move­ment and loss of men­tal func­tion­ing (de­men­tia) as they ap­proach old age. Neu­rode­gen­er­a­tive dis­eases all share a com­mon root in pro­tein mis­fold­ing. As a re­sult, ag­gre­ga­tion ac­cu­mu­lates and leads to loss of neu­ronal func­tion­ing.

Alzheimer’s dis­ease (AD) is the most com­mon cause of de­men­tia. While the causes of AD have not been de­ter­mined, its pathol­ogy is be­lieved to be driven by the ex­ces­sive ac­cu­mu­la­tion of pro­teins that are found nat­u­rally in our body such as amy­loid plaques and tau tan­gles. Out­side the cells, amy­loid bunches dis­rupt sig­nal­ing be­tween neu­rons and trig­ger in­flam­ma­tion, which can dam­age sur­round­ing neu­rons. As op­posed to amy­loid plaques, tau tan­gles are found in­side the cells. Mod­i­fied tau pro­teins form neu­rofib­ril­lary tan­gles, dam­ag­ing neu­ronal cy­toskele­ton, and even­tu­ally leads to pro­grammed cell death.

The ma­jor­ity of brain pro­cesses such as mem­ory and learn­ing de­pend on com­mu­ni­ca­tions be­tween neu­rons. In AD pa­tients, neu­rons lose the ca­pac­ity to re­lay in­for­ma­tion and de­cay over time. At early stages, com­pli­ca­tions such as wan­der­ing, get­ting lost, dif­fi­culty un­der­stand­ing ques­tions, and slight be­hav­ioral and per­son­al­ity changes dras­ti­cally af­fect qual­ity of life. As the dis­ease pro­gresses, pa­tients grad­u­ally have prob­lems rec­og­niz­ing friends and fam­ily mem­bers, lose the abil­ity to multi-task, and of­ten ex­pe­ri­ence hal­lu­ci­na­tions, delu­sions, and para­noia.

Cur­rent treat­ments aim at main­tain­ing men­tal func­tion, man­ag­ing be­hav­ioral symp­toms, and im­ped­ing the dis­ease’s pro­gres­sion. While AD’S pro­gres­sion can­not be stopped or cured, early di­ag­no­sis al­lows pa­tients and their fam­i­lies to seek pro­fes­sional help when the dis­ease is at pre-clin­i­cal stage be­fore the symp­toms are ev­i­dent. They can start cop­ing and plan­ning for the fu­ture by learn­ing about the dis­ease and de­vel­op­ing sup­port groups. In some cases, early in­ter­ven­tion may po­ten­tially re­verse some of the im­pair­ments. Un­for­tu­nately, most pa­tients are not di­ag­nosed un­til signs of cog­ni­tive deficits be­come ap­par­ent and ir­re­versible. Fur­ther­more, cur­rent di­ag­no­sis tests are of­ten ei­ther in­va­sive or ex­pen­sive and time con­sum­ing. Due to the in­con­ve­niences, sus­cep­ti­ble pa­tients may be dis­cour­aged from tak­ing the as­sess­ments. These prob­lems call for a new di­ag­nos­tic test that is less ex­pen­sive, and min­i­mally in­va­sive, but that re­mains as ac­cu­rate as the es­tab­lished ones.

Re­searchers from Lan­caster Univer­sity ad­dressed these con­cerns in the re­cent edi­tion of the jour­nal Pro­ceed­ings of the Na­tional Academy of Sciences of the United States of Amer­ica. In this study, blood plasma from 549 in­di­vid­u­als with var­i­ous neu­rode­gen­er­a­tive dis­eases as well as age- matched healthy in­di­vid­u­als were col­lected and an­a­lyzed with Fourier- trans­formed in­frared spec­troscopy (FTIR). FTIR is an an­a­lyt­i­cal tech­nique that mea­sures the ra­di­a­tions ab­sorbed by dif­fer­ent chem­i­cal struc­tures. It pro­vides in­for­ma­tion about the unique molec­u­lar com­po­si­tion, and struc­tures within each sam­ple. “In­ter­ro­ga­tion of these sam­ples with spec­tro­scopic tech­niques al­lows for the gen­er­a­tion of a spec­tral fin­ger­print, which sub­se­quently fa­cil­i­tates the dis­crim­i­na­tion of the dif­fer­ent pop­u­la­tions and iden­ti­fi­ca­tion of po­ten­tial biomark­ers,” re­marked Maria Paraske­vaidi, the study’s lead au­thor. Us­ing clas­si­fi­ca­tion al­go­rithms, the re­searchers were able to dif­fer­en­ti­ate be­tween AD and healthy in­di­vid­u­als with the ac­cu­racy reach­ing 86 per­cent. This is as ac­cu­rate as cur­rent di­ag­nos­tic tests in the clin­ics but costs less money. In ad­di­tion, dif­fer­en­ti­a­tion of AD from other neu­rode­gen­er­a­tive dis­eases was achieved with sat­is­fac­tory se­gre­ga­tion and clas­si­fi­ca­tion re­sults. No­tably, de­men­tia caused by AD was distin­guished from de­men­tia linked to Lewy bod­ies (DLB), the sec­ond most com­mon cause of de­men­tia, with an ac­cu­racy of 90 per­cent. De­spite their sim­i­lar­i­ties in symp­toms, AD and DLB have been shown to re­spond dis­tinc­tively to dif­fer­ent med­i­ca­tion. Cor­rectly iden­ti­fy­ing AD and DLB can help a doc­tor de­vise ap­pro­pri­ate clin­i­cal man­age­ment, which will in turn im­prove the pa­tient’s qual­ity of life.

This study in­tro­duces a new, con­ve­nient, and highly ac­cu­rate test for di­ag­nos­ing AD. Cur­rent tests in­volve the la­bo­ri­ous process of col­lect­ing cere­brospinal fluid or the ex­pen­sive and time­con­sum­ing brain imag­ing. Other blood- based tech­niques fo­cus­ing on mea­sur­ing lev­els of amy­loid beta and tau pro­teins have yielded con­tentious re­sults; the plasma level of amy­loid beta was re­ported to in­crease in some stud­ies and de­crease in oth­ers. In fact, a re­cent meta- anal­y­sis of 231 stud­ies has come to the con­clu­sion that level of plasma amy­loid beta is not strongly cor­re­lated with AD, and should not be used in clin­i­cal prac­tice for di­ag­no­sis. Sim­i­larly, the level of plasma tau has been in­ves­ti­gated as biomarker for AD. While the level of plasma tau is in­creased in AD pa­tients com­pared to healthy con­trols was a con­sen­sus view among re­searchers, the find­ing needs fur­ther ver­i­fi­ca­tions in larger co­horts. At the present, “there is no sin­gle de­fin­i­tive med­i­cal test for di­ag­nos­ing AD,” said Paraske­vaidi. How­ever, with in­cred­i­ble ef­forts like the one in this study, we are get­ting closer to a test that would al­low for early and ac­cu­rate di­ag­no­sis of AD. I feel more hope­ful as I re­flect upon Alois Alzheimer’s say­ing “Ex­ces­sive reser­va­tions and par­a­lyz­ing de­spon­dency have not helped the sciences to ad­vance nor are they help­ing them to ad­vance, but a healthy op­ti­mism that cheer­fully searches for new ways to un­der­stand, as it is con­vinced that it will be pos­si­ble to find them.”

Claire Gre­nier | The Mcgill Daily

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