Alzheimer’s gene `starts` changing brain patterns early in life
Washington – A new study from the Centre for Addiction and Mental Health has suggested that people who are more prone to developing Alzheimer’s disease later in life show changes in their brains from childhood.
The gene, called SORL1, is one of a number of genes linked to an increased risk of late-onset Alzheimer’s disease, the most common form of the illness.
SORL1 carries the gene code for the sortilin-like receptor, which is involved in recycling some molecules in the brain before they develop into beta-amyloid a toxic Alzheimer protein.
SORL1 is also involved in lipid metabolism, putting it at the heart of the vascular risk pathway for Alzheimer’s disease as well.
To understand SORL1’s effects across the lifespan, Dr. Aristotle Voineskos, head of the Kimel Family Translational Imaging-Genetics Laboratory at CAMH, along with Daniel Felsky, studied individuals both with and without Alzheimer’s disease.
Their approach was to identify genetic differences in SORL1, and see if there was a link to Alzheimer’s-related changes in the brain, using imaging as well as post-mortem tissue analysis.
In each approach, a link was confirmed.
In the first group of healthy individuals, aged 8 to 86, researchers used a brain imaging technique called diffusion tensor imaging. Even among the youngest participants, those with a specific copy of SORL1 showed a reduction in white matter connections in the brain important for memory performance and executive function.
The second sample included post-mortem brain tissue from 189 individuals less than a year old to 92 years, without Alzheimer’s disease. Among those with that same copy of the SORL1 gene, the brain tissue showed a disruption in the process by which the gene translated its code to become the sortilin-like receptor.
Finally, the third set of post-mortem brains came from 710 individuals, aged 66 to 108, of whom the majority had mild cognitive impairment or Alzheimer’s. In this case, the SORL1 risk gene was linked with the presence of amyloid-beta, a protein found in Alzheimer’s disease.
The study is published online in Molecular Psychiatry.