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Untangling Alzheimer’s

Vizamyl Neg+Pos scan (3)

The brain is arguably the most vital of organs. It is the source of everything we do, everything we think and everything we feel. It processes the cacophony of stimuli from the world around us into a coherent landscape we can see, touch, hear, smell and taste.

So when the brain goes wrong, lives are indelibly marred by the confusing and seemingly inexplicable breakdown in a loved one’s personality, their potential, and their defining traits.

This is why it is as important as ever to take stock of how far we have come in our pursuit of better understanding and treatment for brain diseases.

The Pulse spoke with Dr Ben Newton, Director of PET (Positron Emission Tomography) Neurology for GE Healthcare, about neurodegeneration, Alzheimer’s disease, and how close we are to finding a cure.

The astronomical numbers involved in explaining the brain are difficult to wrap one’s head around: scientists say our understanding of it is roughly half a century behind our understanding of the rest of the body.

The brain is a dense network of cells containing more connections than there are stars in our entire galaxy, in constant communication via chemical signals called neurotransmitters. While it makes up around 3 percent of our body mass, the brain consumes 20 percent of our oxygen and glucose. It is made up of 75 percent water, but can hold 1,000 TB of information.

While Alzheimer’s disease is the most common form of dementia – accounting for around 70 percent of cases – modern medicine remains ill-prepared for it. Most diagnoses are only confirmed once the disease has taken a toll on a patient, and all current treatments address the symptoms rather than the causes of Alzheimer’s. This is because there are several theories about the disease process, and Alzheimer’s disease is probably the result of a combination of them all.

“The symptoms are caused by a number of different pathologies or problems. Nobody really knows the precise cause,” said Dr Newton. “In simple terms, Alzheimer’s disease is the most common cause of dementia.”

What we do know, from post-mortem observations in Alzheimer’s patients but also by using PET imaging, is that abnormal proteins build ups up. The most widely studied of these proteins is called Amyloid Beta, which forms plaques in certain areas of the brain and either scrambles or cuts off communication signals between the cells  in the brain, explaining the symptoms of memory loss and changing behavior.

“We think that when those signals are interrupted, brain cells start to die. Over time, the death of brain cells can be detected as a shrinkage in the brain,” said Dr Newton. “Death of brain cells, loss of nerve tissue, and shrinkage of the brain results in cognitive dysfunction, thinking difficulties, memory loss and so on.”

“The area of obvious shrinkage is the cortex, the main part of the brain responsible for thinking and language,” he added. “But there are also other parts, like the amygdala and hippocampus (which are deep in the brain and are involved in integration of emotions / emotional behavior and memory and spatial awareness) which can also see a buildup of these abnormal proteins.”

Alzheimer’s reputation as an insidious disease comes from the fact that it is only diagnosed once it has firmly taken hold of the brain. Amyloid plaques can in fact start to accumulate in brain tissue about ten years before any symptoms occur, but knowing who to screen and when to screen them, while also staying within PET amyloid imaging ‘appropriate use’ criteria, poses a big challenge.

“A lot of the damage to the brain may have already occurred well before the patient experiences the memory loss and behavioral problems which are typical of dementia,” said Dr Newton.

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“The idea is that, with PET scanning, you could detect the disease at a very early stage. The problem of course is: how do you select patients for PET scanning when they don’t necessarily show any outward signs of cognitive dysfunction?”

The Mini Mental State Examination, or MMSE is the most commonly used test for complaints of memory problems. In this test a neurologist asks a series of questions to asses a patients mental abilities, including memory, attention and language. If any memory or cognitive problems are apparent from their MMSE score, a patient could in theory  be referred for a PET Amyloid scan.

To Dr Newton and his colleagues, with whom he is collaborating on several clinical trials of potential Alzheimer’s drugs (that treat the disease itself rather than just the symptoms), the future may be brighter than the current situation in our battle against Alzheimer’s may suggest.

“There are two major approaches that pharma companies are taking at the moment,” said Dr Newton. “One approach is to block the production of the abnormal proteins that build up in the brains of patients with dementia.” This would essentially prevent the toxic effect they have on the nerve cells in the brain, and stop them dying.

“The other approach is to, through antibody treatment, get the abnormal protein that’s already built up to be cleared out -basically removed from the brain.”

“Some companies have used this approach, some have used the other, and a couple have tried to combine the two,” added Dr Newton. Some of the trials testing these new approaches are already in or about to enter phase III, meaning that tangible data could be available within a couple of years. In any case, some peace of mind can be gained from knowing that the cutting edge of healthcare technology is being invested in one day making Alzheimer’s a distant memory.