A pattern of epigenetic alteration of genes involved in Alzheimer's disease has been discovered.
Researchers found that a type of epigenetic change called histone acetylation was associated with several genes known to play a role in the formation of the proteins beta-amyloid and tau. A progressive build-up of these proteins is linked to disrupted neural function, leading to the symptoms of Alzheimer's.
'Changes influencing the activity of many genes were found to be robustly associated with the pathological hallmarks of Alzheimer's disease,' said Dr Sarah Marzi, from King's College London and Queen Mary University of London, part of the research team.
The research, published in Nature Neuroscience, was the first genome-wide study investigating histone acetylation in Alzheimer's. Histone acetylation acts as a marker to alter how much genes in the region are expressed.
The researchers analysed histone modification in brain tissue from patients who had died from Alzheimer's, comparing it with tissue from those who had died from other causes. The researchers found a total of 4162 locations in the genome where histone acetylation of Alzheimer's patients differed significantly from the controls.
There were similar differences in patients who had isolated cases of Alzheimer's without a history of the condition, as with those who had forms that were inherited. This suggests that 'there are common mechanisms both hereditary and isolated forms of this terrible illness', said Dr Marzi.
It is not yet clear whether this epigenetic signature of Alzheimer's is a cause or effect of the disease. However, Professor Jonathan Mill of the University of Exeter Medical School, who co-led the study, noted that drugs to modify histone acetylation are at present 'among the most promising new treatments for Alzheimer's disease'.