2 types of Alzheimer’s, part III

Serious memory loss problems experienced in the senior years come under one umbrella term: “dementia.”

These frustrating situations have a plethora of causes, too. These include bad drug reactions, depression, inadequate diet, consuming too much alcohol, blood clots or tumors in the brain, head injuries, and thyroid, kidney, or liver problems, as well as vascular dementia.

The diagnosis of mild cognitive impairment (MCI) should be followed up by visits to a medical specialist every 6-12 months due to the fact that this problem might be an early sign of the much more serious Alzheimer’s Disease.

The National Institute on Aging tells us that Alzheimer’s Disease is indeed a complex disease, scientists and doctors do not yet know its cause. Nevertheless, “Having certain genes is a risk factor for Alzheimer’s.”

The two types of Alzheimer’s Disease (AD) are late-onset and early-onset, each of which carry different genetic risk factors. Most people show first signs of late-onset in their mid-60s or later. The risk for this form of AD increases with age. While not fully known, causes involve a mix of genes, lifestyle, and environment. One form of gene called APOE4 can increase the chance for late-onset AD, but this isn’t true of everyone who has this late form of dementia. People with early-onset Alzheimer’s type begin to show signs between the age of 30 and age 60. This form of AD is, however, very rare. Known as familial AD or FAD, some types of this dementia are caused by a permanent change in one or more genes passed down from a parent to a child. But some people with early-onset Alzheimer’s do not have FAD; their reason for getting the disease is unknown. Meeting with a genetic counselor may lead to the possibility of testing for FAD.

New research has determined that women have a greater chance of developing AD than men due to women’s longer life expectancy. The odds for men is 1 in 11, compared with 1 in 6 for women. According to Alzheimer’s Research Review (Spring 2017), a particular gene, USP9, seems to provide protection against AD through its interaction with another gene regulating tau proteins found in abnormally high numbers in the affected female patients’ brains.

The newsletter states, “The team found that blocking the USP9 gene significantly reduced the activity of the tau gene.”

Another possibility currently explored by researchers, according to the ADR Review, is the current hypothesis of inflammatory activity in the brain, thus increasing the production of (beta) amyloid, killing healthy neurons, and ultimately reducing the ability of the brain’s security system to remove amyloid plaques. Until now, the history of AD drug research has been marked by failed late-stage clinical trials. But recently, The Wall Street Journal (April 24, 2017) explains that Novartis AG, a Swiss drug giant, “thinks its best bet for testing two new Alzheimer’s drugs is on people who don’t actually have Alzheimer’s.” They propose two trials for this year, one including people with two copies of the APOE4 gene and one including people with one copy of the APOE4 gene.

In this way, the company hopes to find a successful medicine to deter the advancement of late-onset Alzheimer’s.

Comments are closed.