The importance of the SorLA or LR11 receptor in braking Alzheimer’s was originally defined here at Emory by Jim Lah and Allan Levey’s labs. Japanese researchers recently determined the structure of SorLA and published the results in Nature Structural and Molecular Biology. Their findings point toward a direct role for SorLA in binding toxic circulating beta-amyloid and transporting it to the lysosome for degradation. Hat tip to Alzforum.
If youâ€™ve been paying attention to Alzheimerâ€™s disease research, youâ€™ve probably read a lot about beta-amyloid. Itâ€™s a toxic protein fragment that dominates the plaques that appear in the brains of people with Alzheimerâ€™s. Many experimental therapies for Alzheimerâ€™s target beta-amyloid, but so far, they’ve not proven effective.
That could be for several reasons. Maybe those treatments started too late to make a difference. But an increasing number of Alzheimerâ€™s researchers are starting to reconsider the field’s emphasis on amyloid. Nature News has a feature this week explaining how the spotlight is shifting to the protein ApoE, encoded by the gene whose variation is responsible for the top genetic risk factor for Alzheimerâ€™s.
In line with this trend, Emoryâ€™s Alzheimer’s Disease Research Center recently received a five-year, $7.2 million grant to go beyond the usual suspects like beta-amyloid. Emory will lead several universities in a project to comprehensively examine proteins altered in Alzheimerâ€™s. Youâ€™ve heard of the Cancer Genome Atlas? Think of this as the Alzheimerâ€™s Proteome Atlas, potentially addressing the same kind of questions about which changes are the drivers and which are the passengers.
Emoryâ€™s back-to-basics proteomics approach has already yielded some scientific fruit, uncovering changes in proteins involved in RNA splicing and processing. Also, the Nature feature also has some background on a clinical trial called TOMMORROW, which Emoryâ€™s ADRC is participating in.