Research has shown that nearly two-thirds of dementia cases of patients over 60 in the Western Hemisphere are cases caused by Alzheimer’s disease.  This correlation with age continues as the frequency of Alzheimer’s nearly doubles by five year increments after the age of 65.To gain a better understanding of this prevalence, scientists are looking into the amyloid-b precursor protein (APP) gene which has shown to have a significant effect in those with Alzheimer’s disease.  Through their research, derived from 1,795 Icelandic citizens, scientists have discovered a mutation in the APP gene that safeguards individuals from cognitive deterioration and Alzheimer’s disease. Because mutations on this site (A673T allele) also prevents cognitive decline in patients without Alzheimer’s, this suggests that the two conditions may be controlled by or related through the same mechanisms. 

Patients enrolled in this study were registered through the Memory Clinic at Landspitali University Hospital and the cognitive condition was assessed through the Minimum Data Set (MDS) for nursing homes.  Genotypic data was then collects for the APP site A673T for all 1,763 patients.  This data reveals that this site on APP is vital to the production of amyloid plaque, making it able to protect patients from the cognitive decline seen in Alzheimer’s and non-Alzheimer’s patients.  These results make this mutation the first genetic variant discovered that can create a strong shield from Alzheimer’s disease.  It also confirms  the hypothesis that the pathogenesis of regular cognitive deterioration and Alzheimer’s disease may be partially related, suggesting that Alzheimer’s disease may be the driving force of the correlation between age and decline in cognitive function.

By Alec Waid, Intern Roskamp Institute
 


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