Ebixa – In a class of its own to treat Alzheimer's disease

Growing old can bring with it many health problems - and not just physical ones. One of the sure signs of aging is a decline in our mental capabilities. Fortunately for many of us age only brings with it a little forgetfulness and perhaps we also find that we’re just not quite as mentally alert as we once were.

So just what exactly is Alzheimer’s disease? In very basic terms Alzheimer’s disease is an irreversible, progressive, terminal brain disease that slowly destroys a person’s memory and thinking skills. Eventually someone suffering from Alzheimer’s disease will not be able to carry out even the simplest of tasks and will require round the clock care. Life expectancy often depends on how quickly symptoms progress. For some the time between diagnosis and death can be as little as 18 months, for others as long as 15 years - the average time is about 7 to 10 years with most people requiring full time round the clock care after about 5 years although this again depends upon the speed of progression of the disease.

Memory problems usually appear as the first symptoms of Alzheimer’s disease. Other common behavioural symptoms include sleeplessness, agitation, wandering, anxiety, anger, and depression. Although it’s unusual for any symptoms to manifest themselves before the age of 60, the destructive processes in the brain that cause the disease may have begun 10 or even 20 years earlier.

Unfortunately scientists don’t yet fully understand what triggers these damaging processes and more than one theory exists as to what actually causes Alzheimer’s disease. What is known for sure is that when someone suffers from Alzheimer’s disease their brain tissue becomes irreparably damaged.

By the 1990’s the amyloid hypothesis, which is now perhaps the most widely accepted theory, had been proposed. In an Alzheimer’s patient bundles of fibres known as neurofibrillary tangles begin to develop in the entorhinal cortex which is hidden deep inside the brain. This part of the brain plays a crucial role in memory formation. Deposits known as amyloid plaques also begin to appear in other parts of the brain. As more tangles and plaques develop healthy brain tissue becomes affected and is unable to function properly. Connections between nerve cells (neurons) break down and eventually the neurons die. Crucially, the hippocampus, which is also essential in forming memories and lies near to the entorhinal cortex, becomes affected by these destructive changes.

As the death of neurons increases, affected brain regions begin to shrink. By the final stage of Alzheimer’s, damage is widespread and brain tissue has shrunk significantly.

It’s impossible to under-estimate the effects of Alzheimer’s disease - not just on the sufferer but on those around them who care for them. It’s a devastating disease that robs family and friends of their loved one well before they eventually die.

By now you are probably thinking that the situation is hopeless. Alzheimer’s disease is a complex disease and although it cannot be cured, there are treatments available that aim to treat the symptoms or reign in the progression of this devastating condition for as long as possible. The majority of the currently available drugs work by stopping the action (inhibiting) an enzyme called acetylcholinesterase. Acetylcholinesterase breaks down acetylcholine - a neurotransmitter chemical found in the brain. Neurotransmitters act as the brain’s messenger service enabling neurons (nerve cells) to communicate with one another.

These types of medications were developed in response to the cholinergic hypothesis as to what causes Alzheimer’s disease. This hypothesis proposes that Alzheimer’s disease is caused by the reduced production of acetylcholine. By inhibiting acetylcholinesterase and stopping it from breaking down acetylcholine, acetylcholine levels are temporarily boosted. Unfortunately these medications are no longer that popular mainly because they have not been overly effective in treating acetylcholine deficiencies.

Ebixa (also known as Memantine is entirely different and is the first in a new class of therapies aimed at treating the moderate to later stages of Alzheimer’s disease. Instead of trying to prevent acetylcholinesterase from working, its target is another neurotransmitter - glutamate. Glutamate is the most common neurotransmitter in the brain and is always excitatory. This means that once released by a neuron (called the presynaptic neuron) glutamate always triggers a nerve impulse in the receiving neuron (the postsynaptic neuron). Inhibitory neurotransmitters, on the other hand, act to prevent further transmission of nerve impulses.

Glutamate plays a pivotal role in learning and memory formation. Every neuron has a specific set of neuro-receptors. These act like docking sites and are responsible for receiving neurotransmitters released by neighbouring cells. Only certain neurotransmitters trigger certain receptor sites and, in the case of glutamate, it triggers specific N-methyl-D-aspartate (NDMA) receptor sites on the postsynaptic neuron.

Glutamate binds with the NDMA receptors and this action allows calcium ions to flow into the neuron. This, in turn, creates the right chemical environment for information to be processed, stored and retrieved.

The problem is that if there is an excess of glutamate NMDA receptors become “overexcited” and allow too much calcium into neurons. If this happens the functioning of the neurons is disrupted and ultimately it leads to cell death. Unfortunately, glutamate is released in excessive amounts by cells damaged by Alzheimer’s disease and certain other neurological disorders. With sustained elevation of glutamate levels, the neurons in the brain of someone suffering from Alzheimer’s disease are subjected to chronic calcium overexposure which inevitably leads to cell degeneration.

By filling NDMA receptor sites, Ebixa is able to partially block NDMA receptors so that they cannot bind with any excess glutamate. In doing so, Ebixa protects cells against the destructive force of excess glutamate which, in turn, may slow down the progression of symptoms in the middle and later stages of Alzheimer’s disease.

The effects of Ebixa are not just confined to improving cognitive performance. Certainly for those taking Ebixa not only are they likely to notice an overall global improvement in their cognition, function and behaviour, e.g. they may find it easier to remember routines and find their way around, but they may also notice real improvements in their abilities to carry out everyday daily activities such as getting up, washed and dressed - all of which eases the burden not just on the patient but on their carers as well. And anything that can improve the quality of life for all those affected by this cruellest of diseases has to be something to shout about.