Researchers from University of Kentucky reveal why Alzheimer's drung keep failing despite years of effort and investment
Alzheimer’s is the most common cause of dementia, which accounts for 50 to 70 percent of all cases of dementia. Each year, more than 5 million Americans are affected by Alzheimer’s disease and the number is projected to rise even more in the next few decades. But the disease is still untreatable. No treatment can currently halt the progression of the disease, despite the fact that many drugs have been tested in clinical trials every year and few have been approved as well but all result in minimal to no effect.
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Now, researchers from University of Kentucky Sanders-Brown Center on Aging hint at why Alzheimer’s drugs keep on failing. New research suggests that treatment targeting Alzheimer’s patients may be ineffective if the patient also has Vascular Cognitive Impairment and Dementia or VCID, the second most common cause of dementia.
“These finding are important in that they provide a possible explanation for why clinical trials of anti-Aβ immunotherapy for Alzheimer's disease are historically unsuccessful,” said lead author Donna Wilcock from University of Kentucky.
“If up to 40 percent of people with Alzheimer’s also have VCID, treatment candidates that target only the AD physiology won't be effective in those patients. It’s like treating only half the disease.”
Alzheimer’s has become a graveyard for many drugs. Many of those drugs show promising results in early trials or when they are tested on animals but failed to show the same effectiveness in human patients. Study suggests that researchers probably require a drug that can target both VCID and Alzheimer’s disease. Moreover, they need a suitable animal model to assess the impact of their drug.
“There has been one failure after another in clinical trials, which has been really disheartening for the scientific community and for patients. My work might shed some early light on why they failed and eventually open the door for a combination treatment for VCID and AD.”
To evaluate the ability of anti-Aβ immunotherapy on Alzheimer’s disease, researchers developed an innovative mouse model and used it both with combined AD/VCID and without ACID. Researchers found that therapeutic anti aβ antibody improved cognitive capabilities in the group with ACID but not against combined AD and VCID.
“The failure of anti-Aβ immunotherapy in the mixed AD-VCID model suggests that both disease processes have to be treated to have a successful outcome," said Wilcock. "The missing link has been that our animal models usually possess the hallmarks of only one disease, which has led to failure of successful translation to clinic.”
The findings of the study could lead to more improved treatments and approaches for Alzheimer’s disease in the future.