New Treatments in Alzheimer’s Disease
Researchers at the University of Southern California Keck School of Medicine are beginning human trials to test two treatments that may help prevent or delay the onset of Alzheimer’s disease.
Alzheimer’s disease is the sixth-leading cause of death in the United States, and the condition affects over 47 million people around the world. According to the Mayo Clinic, the average age of diagnosis is 65, but in recent years, the number of individuals diagnosed in their 40s and 50s is on the rise.
The new treatments are a vaccine and an oral medication that target beta-amyloid proteins that harden to form insoluble plaques in the brain. These plaques, known as beta-amyloid plaques, are thought to be one of the main contributors to the development of Alzheimer’s disease.
A Preventative Approach
Researchers believe that beta-amyloid plaques contribute to the development of Alzheimer’s disease because they develop on the synapses and block cells from communicating with each other. Beta-amyloid plaques also increase inflammation that destroys brain cells.
If these treatments prove successful, they could stop the disease before it starts or delay its onset.
The USC scientists’ take on preventative treatment is a relatively new approach to Alzheimer’s treatment. Many Alzheimer’s studies focus on treating individuals who already have the disease.
Participants in the study are randomly assigned a form of therapy: a vaccine, an oral medication, a placebo vaccine or a placebo oral medication. Patients will take the treatment for five to eight years.
Participants in the study must also undergo genetic testing to identify if they have an inherited predisposition to developing the condition.
Both the vaccine and the oral medication target beta-amyloid plaques, but in two different ways. The vaccine treatment provokes the body to produce beta-amyloid antibodies. The oral version of the treatment is designed to block the enzymes that cause beta-amyloid proteins to develop.
The Role of Genes
Genetics plays an integral part in the development of beta-amyloid proteins and Alzheimer’s disease.
Some genetic mutations, like the amyloid precursor protein, cause beta-amyloid plaques to develop. Researchers first identified the APP mutation on chromosome 21 in 1987 as a contributor to the development of Alzheimer’s disease. The APP mutation is said to be a determinant genetic mutation, which means individuals who have the variation are guaranteed to develop the disease.
Another genetic mutation, the APOE4 mutation, also contributes to the development of beta-amyloid plaques. Nearly half of the people diagnosed with Alzheimer’s disease have this variation. This genetic mutation is a risk genetic mutation; having it increases the risk of developing Alzheimer’s disease but does not guarantee it.
One copy of the APOE4 gene increases the risk of developing Alzheimer’s disease by two or three times. Around 3 percent of the population has two copies of the gene, which increases their risk of developing the disease by 12 times.
APOE4 also causes earlier onset of the disease.
“Being able to prevent or even delay the onset of Alzheimer’s disease would significantly improve the quality of life for many individuals,” said Dr. Bill Johnson, M.D.
Johnson is a Dallas, Texas, physician who treats individuals with Alzheimer’s disease and other cognitive conditions with adipose fat stem cell therapy.
“Stem cells have a potent anti-inflammatory property that helps reduce the damage caused by brain plaques,” Johnson said.
When inflammation is reduced, normal cell function and communication can resume, slowing the progression of the disease.
Medical News Today. Alzheimer’s: Targeting ApoE gene may ‘stop the disease’. Medical News Today. 20 September 2017.