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Alzheimer’s “vaccine” seen to help mice

Nov. 13, 2007
Courtesy Oklahoma Medical Research Foundation
and World Science staff

A vac­cine might blunt or even pre­vent the dead­ly, mem­o­ry-robbing dev­asta­t­ion of Alz­heim­er’s dis­ease, a study has found.

Sci­en­tists im­mu­nized mice with a mol­e­cule thought to play role in the ill­ness. The treated mice, they said, showed bet­ter cog­ni­tive per­for­mance than un­vac­ci­nat­ed mice, and a sig­nif­i­cant re­duc­tion in the build-up of pro­tein plaques be­lieved to cause brain cell death and dys­func­tion in Alz­hei­m­er’s.

Courtesy USDA


“These re­sults are ex­tremely ex­cit­ing,” said Jor­dan Tang of the Ok­la­ho­ma Med­i­cal Re­search Founda­t­ion, a non­prof­it re­search in­sti­tute, who led the stu­dy. The find­ings ap­pear in The Jour­nal of the Federa­t­ion of Amer­i­can So­ci­eties for Ex­pe­ri­men­tal Bi­ol­o­gy.

Alzheimer’s grad­u­ally rav­ages vic­tims’ mem­o­ries and per­son­al­ities by kill­ing brain cells. The dis­ease af­fects more than 5 mil­lion Amer­i­cans, in­clud­ing near­ly half the popula­t­ion over 85, ac­cord­ing to the Alz­hei­mer’s As­socia­t­ion.

Tang and col­leagues pre­vi­ously had iden­ti­fied a mol­e­cule—an en­zyme called me­map­sin 2—that cuts a pro­tein in­to frag­ments which, in turn, are be­lieved to cause Alz­heim­er’s. In the new stu­dy, the group used me­map­sin 2 as a vac­cine for mice ge­net­ic­ally en­gi­neered to de­vel­op Alz­hei­mer’s symp­toms. The mice “de­vel­oped 35 per­cent few­er plaques,” said Tang. 

Tang’s previous work al­so has led to the crea­t­ion of an ex­pe­ri­men­tal drug that would treat Alzheimer’s by in­hibit­ing me­map­sin 2. Hu­man clin­i­cal tri­als on that be­gan last sum­mer. Tang said a vac­cine would be a sup­ple­ment to, not a sub­sti­tute for, oth­er treat­ments of this na­ture. “Alz­hei­mer’s is a com­pli­cat­ed, mul­ti­faceted dis­ease,” he said. “We can­not rely on a ‘one-size-fits-all’ strat­e­gy, be­cause what works in one pa­tient will not nec­es­sarily work in anoth­er.”

Vac­cina­t­ion strate­gies, de­signed to stim­u­late the im­mune sys­tem to fight the plaques, have been con­sid­ered a prom­is­ing way for­ward, but their suc­cess has been lim­it­ed, Tang said. In 2002, for ex­am­ple, the phar­ma­ceu­ti­cal com­pa­ny Elan halted tri­als of a dif­fer­ent vac­cine af­ter 15 pa­tients suf­fered swell­ing of the cen­tral nerv­ous sys­tem.

But the new vac­cine “stim­u­lates the im­mune sys­tem more gently than pre­vi­ous Alz­hei­mer’s vac­cines, so we are op­ti­mis­tic about its prospects,” said Ste­phen Pres­cott, pres­ident of the founda­t­ion in Ok­la­ho­ma ­city. The next step, said Tang, will be to prog­ress to­ward hu­man tri­als. “There cur­rently is no ef­fec­tive treat­ment for Alz­heim­er’s dis­ease,” he not­ed, “so we must ex­plore eve­ry pos­si­ble op­tion.”


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A vaccine might blunt or even prevent the deadly, memory-robbing devastation of Alzheimer’s disease, a study has found. Scientists immunized mice with a molecule thought to play role in the illness. The treated mice, they said, showed and better cognitive performance than unvaccinated mice, and a significant reduction in the build-up of protein plaques believed to cause brain cell death and dysfunction in Alzheimer’s. “These results are extremely exciting,” said Jordan Tang of the Oklahoma Medical Research Foundation, a nonprofit research institute, who led the study. The findings appear in The Journal of the Federation of American Societies for Experimental Biology. Alzheimer’s is a disorder that gradually kills brain cells, devastating a victim’s memory and personality. According to the Alzheimer’s Association in the United States, the disease affects more than 5 million Americans, including nearly half the population over 85. Tang and colleagues previously had identified a molecule—an enzyme called memapsin 2—that cuts a protein into fragments which, in turn, are believed to cause Alzheimer’s. In the new study, the group used menapsin 2 as a vaccine for mice genetically engineered to develop Alzheimer’s symptoms. The mice “developed 35 percent fewer plaques,” said Tang. Tang’s work with memapsin 2 also has led to the creation of an experimental drug that would treat Alzheimer’s by inhibiting menapsin. Human clinical trials on that began last summer. Tang said a vaccine would be a supplement to, not a substitute for, other treatments of this nature. “Alzheimer’s is a complicated, multi-faceted disease,” he said. “We cannot rely on a ‘one-size-fits-all’ strategy, because what works in one patient will not necessarily work in another.” Vaccination strategies, designed to stimulate the immune system to fight the plaques, have been considered a promising way forward, but their success has been limited, Tang said. In 2002, for example, the pharmaceutical company Elan halted trials of a different vaccine after 15 patients suffered swelling of the central nervous system. But the new vaccine “stimulates the immune system more gently than previous Alzheimer’s vaccines, so we are optimistic about its prospects,” said Stephen Prescott, president of the foundation in Oklahoma City. The next step, said Tang, will be to progress toward human trials. “There currently is no effective treatment for Alzheimer’s disease,” he noted, “so we must explore every possible option” to stop it.