Scientists have come a step closer to finding out what the causes of Alzheimer’s disease are.
Recently the number of genes known to be associated with Alzheimer”s disease has increased from four to eight, including the MS4A gene cluster on chromosome 11.
New research has expanded on this using a genome-wide association study (GWAS) to find a novel location within the MS4A gene cluster, which is associated with Alzheimer”s disease.
Alzheimer”s disease is the most common cause of dementia in the developed world. It irrevocably destroys cells in the brain that are responsible for intellectual ability and memory.
Despite continued investigation, the causes of Alzheimer”s disease are not yet fully understood but they are thought to be a mixture of genetic and environmental factors.
Alzheimer’s disease
Several studies have used GWAS to search the entire human genome for genes, which are mutated in Alzheimer”s sufferers in the hope of finding a way to treat or slow down the disease.
A team of researchers across Spain and USA sponsored by non-profit Fundacion Alzheimur (Comunidad Autonoma de la Region de Murcia) and Fundacio ACE Institut Catala de Neurociencies Aplicades performed their own GWAS study using patients with Alzheimer”s disease, and non-affected controls, from Spain and then combined their results with four public GWAS data sets.
“Combining these data sets allowed us to look more accurately at small genetic defects,” Dr Agustin Ruiz said.
“Using this technique we were able to confirm the presence of mutations (SNP) known to be associated with Alzheimer”s disease, including those within the MS4A cluster, and we also found a novel site.
“Several of the 16 genes within the MS4A cluster are implicated in the activities of the immune system and are probably involved in allergies and autoimmune disease.
“MS4A2 in particular has been linked to aspirin-intolerant asthma. Our research provides new evidence for a role of the immune system in the progression of Alzheimer”s disease,” he concluded.
The findings have been published in BioMed Central”s open access journal Genome Medicine.
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For years, scientists and doctors have believed that protein aggregates called amyloid fibrils found in the brain were the culprit behind Alzheimer”s disease.
But now, a new research suggests that protein molecules are constantly attaching and detaching from the fibrils, in a recycling process that could be manipulated to yield new treatments for Alzheimer”s and other diseases.
In a study that focused on the fibrils associated with AD, Natàlia Carulla and colleagues used laboratory techniques to detail molecular recycling within fibrils formed by two proteins, Aß40 and Aß42, which are most associated with AD.
After monitoring recycling for 40 days, they found that both Aß40 and Aß42 molecules recycle within the fibril population, although to different extents. After 40 days, 80 percent of the molecules making up Aß40 fibrils underwent recycling while only 30 percent did so in Aß42 fibrils. These observations imply that Aß42 recycles more slowly.
“It will be important to address if differences in the recycling species within Aß40 and Aß42 fibrils are relevant in the development of Alzheimer”s disease. We are now working towards this aim. Once we have this information, we will be in a position to devise new therapeutic strategies that can modulate recycling,” said Carulla.
The study has been reported in the Journal of the American Chemical Society.