Alzheimer’s disease is a progressive brain disorder that has a gradual onset, mostly undetected at first since the condition is marked with memory loss that is linked from the so-called senior moments typical of normal aging. As the disease progress, it causes an increasing decline in functioning, including loss of speech, loss of motor function, and profound personality and behavioral changes. The person with Alzheimer’s has been observed to display paranoia, delusions, hallucinations, inattention to hygiene, and belligerence.
After its discovery more than a century ago, no cure has been discovered to stop this memory-robbing disease. There isn’t even a definitive test to identify the disease in its early stages. As a matter of fact, the only way to diagnose a person with Alzheimer’s is after performing an autopsy of brain tissue to examine its hallmark lesions – atrophy of cerebral neurons, senile plaque deposits, and enlargement of the third and fourth ventricles of the brain.
For so many years, the attempts to curtail its tracks had left scientists in frustration and despair. In 2002, a promising vaccine was tested, but instead of protecting the brain from the deleterious effect of Alzheimer’s, it even caused dangerous inflammation in the brain and spinal column and had to be abandoned after years of research. Last August of this year, a highly anticipated drug worsened rather than improved cognitive symptoms.
So, are we losing the fight against this much feared condition among our senior citizens? Has medical science surrendered in finding the cure or even protecting those at risk to develop Alzheimer’s? Time magazine has described that research on finding the drug to cure Alzheimer’s is the cold fusion of medical research: everyone agrees it would be great, and everyone who tries it fails.
To fully understand how this condition can easily wipe out stored precious memories created over a lifetime, it is better to identify the main players, or so to speak, the thieves behind the crime.
Just like other degenerative disorders, Alzheimer’s has a genetic component. Research has shown linkages to chromosomes 21, 14, and 19 (APA, 2000). The disease is caused by buildup of protein-based plaques in the brain identified as amyloid. What triggered the research community to know more about these protein-plaques is that amyloid in living patients does not necessarily indicate the disease. Is there more to this than meets the eye?
Investigators are working very hard to identify additional sources of the plaque formation. They came up with apolipoprotein E (ApoE), which in certain forms can promote the formation of amyloid. In addition to this, a neural protein known as tau, which stabilizes axons, was also implicated to the process of amyloid build-up.
Putting all of these components together, researchers have traced how neurons gradually die among Alzheimer’s patients:
- · Amyloid initially forms as amyloid precursor protein (APP)
- Enzymes break APP into short fragments.
- The fragments clump together, forming plaques.
- Once plaques form, tau, may start to break down.
- When tau no longer stabilizes the axons, the neuron shrivels and dies, leaving behind its tangled carcass.
As the neural debris accumulates, the immune system’s inflammatory response is then activated to remove it. In time, this will develop to neural connection shutdown that leads to a drop in cognitive function.
Setting up the Alarm
One way to catch a thief is to set up a security alarm. But this is not a piece of cake for the medical researchers in stopping Alzheimer’s from snuffing out the essence of the affected person. Drugs that were designed to target amyloid plaques affect other processes in the body too, including those that regulate how cells communicate as well as the development of heart, pancreas, and immune system cells. In addition, when scientists examined the autopsied brains of patients in the failed vaccine, they noted that the subjects had fewer plaques than before they received the vaccine but still had shown no improvement on tests of mental function.
With these futile steps, the old adage “an ounce of prevention is better than a pound of cure” may have lost its significance in dealing with persons at risk to develop Alzheimer’s. Nevertheless, a glimmer of hope is still on the horizon. In 2004, the U.S. National Institute on Aging (NIA) partnered with pharmaceutical companies to create the Alzheimer’s Disease Neuroimaging Initiative, a $60 million project tasked to identify between Alzheimer’s patients and unaffected individuals. Once identified, the persons at risk may be tested with drugs whose brains are just beginning to accumulate amyloid.
Lessons Learned
Optimism to treat the disease is still present. From the mistakes committed in the past, experts are now holding two essential lessons that empower the future of Alzheimer’s research:
- Timing. It is crucial to treat Alzheimer’s patients as early as possible, perhaps even before they show signs of memory loss or cognitive decline, rather than attempt to improve a brain already scourged by the disease.
- Scope of medical assault. Adopting a multipronged approach that address as many of the disease’s complex abnormalities as possible may improve the chances that new therapies used early on will not only delay symptoms but also reverse them.
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