Age-related cognitive decline tied to immune-system molecule

A blood-borne molecule beta-2 microglobulin, or B2M that increases in abundance as we age blocks regeneration of brain cells and promotes cognitive decline suggests a new study in Nature Medicine.
Researchers showed that B2M levels steadily rise with age in mice, and are also higher in young mice in which the circulatory system is joined to that of an older mouse. These findings were confirmed in humans, in whom B2M levels rose with age in both blood and in the cerebrospinal fluid (CSF) that bathes the brain.
When B2M was administered to young mice, either via the circulatory system or directly into the brain, the mice performed poorly on tests of learning and memory compared to untreated mice, and neurogenesis was also suppressed in these mice.
The group also bred mice missing the gene for B2M itself. These mice performed better than their normal counterparts on learning tests well into old age, and their brains did not exhibit the decline in neurogenesis typically seen in aged mice.
Authors emphasized that the effects on learning observed in the B2M-administration experiments were reversible: 30 days after the B2M injections, the treated mice performed as well on tests as untreated mice, indicating that B2M-induced cognitive decline in humans could potentially be treated with targeted drugs.