New Treatment for Alzheimer’s Disease (Everything You Need to Know)
Treatments for Alzheimer’s temporarily improve symptoms of memory loss and thinking difficulties. Alzheimer’s treatments boost the transmission of information between brain cells by enhancing the performance of chemicals in the brain. The treatments, however, do not stop the underlying decline and death of brain cells. The death of more cells fuels the progression of Alzheimer’s disease.
There is cautious optimism about finding treatments that will delay Alzheimer’s progression or stop it altogether new treatment for Alzheimer’s As we learn more about how Alzheimer’s affects the brain, we are able to develop treatments that short-circuit the basic processes that cause the disease.
In the future, Alzheimer’s treatments may include a combination of medications, just as many cancer treatments or HIV/AIDS treatments. Some of the treatment options currently being studied include the following.
New Treatment for Alzheimer’s: A Disease Guide
Some new Alzheimer’s treatments in development target microscopic clumps of beta-amyloid (plaques). The presence of plaques is a characteristic sign of Alzheimer’s disease. There are several strategies to combat beta-amyloid, including:
- Activating The Immune System:
Drugs called monoclonal antibodies may prevent beta-amyloid from clumping into plaques or remove beta-amyloid plaques that have formed and help the body remove beta-amyloid from the brain. As your immune system responds to foreign invaders or vaccines, monoclonal antibodies mimic your body’s naturally produced antibodies.
An aducanumab drug was approved for treating some cases of Alzheimer’s disease by the Food and Drug Administration (FDA) in June 2021. It is the first and only drug approved in the United States to target and remove amyloid plaques from the brain, which are the underlying causes of Alzheimer’s.
The drug is a monoclonal antibody against the protein amyloid-beta (Aβ), which accumulates in the brains of people with Alzheimer’s disease. The FDA approval was based on two clinical trials involving nearly 2,000 patients, one of which was a phase III trial with a total of 1,143 participants. In this study, the investigational drug aducanumab reduced both the rate of cognitive decline and the progression of Alzheimer’s disease.
- Protecting Against Destruction
The drug saracatinib, originally developed as a cancer treatment, is now being tested for Alzheimer’s.
A protein that allowed synapses to work again was blocked in mice with the drug, and some memory loss was reversed. Researchers are now testing saracatinib for its possible effectiveness in treating Alzheimer’s disease in humans.
“The results are promising, but more work is needed to see if this could be a viable treatment for Alzheimer’s,” said study leader Dr. Michael Weiner, an associate professor of neurology at Johns Hopkins University School of Medicine. The findings appear in the journal Neuron. Researchers had previously found that when the nerve cells of mice with Alzheimer’s were treated with a protein called amyloid beta, which is believed to play a role in the disease, their brains seemed to clear out the plaque deposits.
- Production Blockers
The use of these therapies may reduce the amount of beta-amyloid in the brain. Researchers have found that beta-amyloid is made in two steps by different enzymes.
Several experimental drugs aim to inhibit the activity of these enzymes. Inhibitors of beta- and gamma-secretases are known as beta- and gamma-secretase inhibitors. There is less enthusiasm for beta-secretase inhibitors due to recent studies showing they do not slow down cognitive decline in those with mild or moderate Alzheimer’s and that they cause significant side effects.
Alzheimer’s disease affects more than 5 million Americans and is a leading cause of death in older adults. It causes progressive memory loss and other cognitive impairments that are often associated with Alzheimer’s-related neuropathology, such as the accumulation of insoluble amyloid-beta peptide (Aβ) and neurofibrillary tangles. Aβ is formed by cleavage of the amyloid precursor protein (APP) by beta-secretase (BACE) and gamma-secretase.