Experimental Drug A Cure To Alzheimer’s Disease?

Alzheimer’s disease is a progressive disorder that causes brain cells to waste away (degenerate) and die. It is the major cause of dementia – a continuous decline in thinking and other abilities.

The early signs of the disease may be forgetting recent events or conversations. As the disease progresses a person with Alzheimer’s disease will develop severe memory impairment and lose the ability to carry out everyday tasks.

Symptoms Include;


The memory loss associated with Alzheimer’s disease persists and worsens, affecting the ability to function at work or at home.

Thinking and reasoning

Alzheimer’s disease causes difficulty concentrating and thinking, especially about abstract concepts such as numbers.

Changes in personality and behavior

Brain changes that occur in Alzheimer’s disease can affect moods and behaviors. 

Preserved skills

Many important skills are preserved for longer periods even while symptoms worsen. Preserved skills may include reading or listening to books, telling stories and reminiscing, singing, listening to music, dancing, drawing, or doing crafts.


  • There are several factors that has been noted as the causes of the disease;
  • Age
  • Genetics
  • Hereditary
  • Down syndrome
  • Poor sleep patterns
  • And a few others.

Scientist however are currently developing a treatment for stroke survivor but may also stave off Alzheimer’s disease.


This drug is a modified version of activated C protein, which protects brain cells and blood vessels from damage due to inflammation.

The drug is currently under development to treat brain bleeds in people who have experienced a stroke. So far, the drug seems to reduce bleeding in the brain with few side effects or safety concerns.

As a result of 3K3A-APC’s positive performance in other trials, the authors of the current study decided to pit it against Alzheimer’s.

The scientists carried out their study using mice with a number of genetic mutations that research has shown to increase Alzheimer’s risk. These animals produce high levels of beta-amyloid and demonstrate both cognitive decline and neuroinflammation.

As the researchers had theorized, 3K3A-APC reduced the buildup of toxic protein in the brains of these mice.

Also, the mice did not demonstrate the expected memory deficits that protein buildup produces, and cerebral blood flow was normal. In Alzheimer’s disease, signs of inflammation in the brain are common. In mice that received 3K3A-APC, the team noted significantly reduced inflammation.

They found that 3K3A-APC reduced the amount of an enzyme called beta-secretase 1 (BACE1), which nerve cells create. BACE1 is necessary for the formation of beta-amyloid; without it, plaques cannot form.

This current medication uses a slightly different approach as it blocks the production of the enzyme rather than blocking the enzyme itself.

As ever, before a new treatment can make it to market, much more research will be necessary in other animal models and, eventually, humans.

As Alzheimer’s is currently untreatable, finding a new way to approach the disease is invaluable. These results are exciting and, no doubt, follow-up work will be underway shortly.

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