Two independent studies publish in the journalNature Neurosciencehave found compelling grounds that epigenetic changes in the brainiac are involved in Alzheimer ’s disease . While it is difficult at this degree to bang whether these alterations to DNA are affect in the onset of disease or occur as a result of the disease , the finding are important because they may help our reason of the impact of environmental risk of exposure factors and lifestyle on Alzheimer ’s .

Alzheimer’sis the most common form of dementia , affecting over 26 million people worldwide . Thediseaseinvolves the progressive degeneration of sure regions of the brain , in particular the cerebral cortex , which results in a mixed bag of symptoms such as memory loss and behavioural changes . While much is know about the encephalon changes that occur as a result of the disease , trivial is recognise about the cause and why it seems to leave some areas of the brain whole .

so as to shed light on this poorly understood area , two team of researchers , one from theUSand the other from theUK , investigate post - mortem brain tissue and looked for modifications to the DNA that do n’t involve change to the episode itself . These changes , known as epigenetic change , can alter gene expression , for example by switch gene on or off in certain tissue .

“ The epigenome is malleable and may harbour traces of life issue that influence disease susceptibleness , such as smoking , depression and climacteric , which may influence susceptibleness to Alzheimer ’s and other diseases , ” lead author of one of the study Philip De Jager aver in anews - release .

For the UK - basedstudy , researchers from the University of Exeter and King ’s College London examined the genius of342 patientsthat had died of Alzheimer ’s . They looked at 3 areas of the learning ability that suffer important wrong in Alzheimer ’s : the prefrontal pallium , the entorhinal pallium and the worldly convolution . They then compared this with stemma samples and tissue from the cerebellum as this is usually unaffected in Alzheimer ’s patients .

For the US - basedstudy , Brigham and Women ’s Hospital and Rush University Medical Center researchers analyzed prefrontal cortex tissue paper from 708 mass , 60 % of whom had Alzheimer ’s when they died .

Both studies identify genes that displayed significant changes in methylation levels . deoxyribonucleic acid methylationswitches genes off through the addition of a chemical called a methyl group group . The UK team distinguish 7 genes that showed increased levels of methylation , whereas the US team discover 11 . However , 4 of these cistron werecommonto both studies . Furthermore , both teams identified one special cistron that seemed to be importantly affect : ANK1 .

The research worker find thatANK1washypermethylatedin the area that suffer significant wrong in Alzheimer ’s patient , but not in the blood or the cerebellum which is largely protect from degeneration . moreover , these changes seem to occur early on in the disease , meaning that they could potentially do as marker to predict patient outcome .

These findings are important because they may help us understand some of the mechanisms need in the onrush of Alzheimer ’s , which could eventually be overwork in the development of novel intervention . Indeed , epigenetic changes are potentiallyreversible , therefore one day it may be potential to target the genes identify in this study to slow down disease progress . However , it is currently too early to tell whether these epigenetic change hasten disease or are a result of the disease itself . Further research is therefore justify to clarify this .

[ ViaNew ScientistandNature Neuroscience ]