The study was done by 2 big research teams -- one from the U.S., the other from Europe.
It revealed variations in the genes ABCA7, MS4A, CD2AP, CD33 and EPHA1 which can increase susceptibility to the disease.
"This is the culmination of years of work on Alzheimer's disease by a large number of scientists, yet it is just the beginning in defining how genes influence memory and intellectual function as we age," Gerard Schellenberg, leader of the University of Pennsylvania study, said in a statement.
The U.S. study, which was carried out by researchers from 44 universities and research institutions across the country, involved genetic analysis of more than 11,800 people with Alzheimer's disease and almost 11,000 elderly people who were "cognitively normal."
The discovery is an important step in a long journey toward new treatments for the neurodegenerative disease that impairs memory and cognition.
Alzheimer's disease is the leading cause of dementia and the sixth leading cause of death in the U.S., according to the Centers for Disease Control and Prevention. Although specific genetic mutations are known to cause the early onset form of the disease, the late onset form is thought to arise from a complex interaction of susceptibility genes and other risk factors.
It's been nearly two decades since the first major Alzheimer's disease susceptibility gene -- apolipoprotein E, or APOE -- was reported. But it only explained one part of the genetic contribution to a disease marked by several abnormal features, including plaques of a protein called amyloid, tangles of a different protein called tau and inflammation.
Researchers say the newly found genes reveal three new pathways involved in breaking down the neurons in the brain's memory center.
