Parkinson's Disease and Alzheimer's Disease Similarities Lead to Potential Drug Discovery

For many years scientists and doctors have been constantly spotting the similarities between Alzheimer’s and Parkinson’s. Both conditions attack neurons directly, one focuses more on the processes related to movement and the other on the cognitive part, affecting memory and mental activities. Another relevant similarity between these two conditions is an increase shown in the % of people suffering from dementia. Being dementia only one of many secondary effects that may be triggered by these Alzheimer’s and Parkinson’s.

However, similarities between them have led to researches on what kind of treatment may be useful for both. It is easy to spot how important it is to focus on brain cells recovery and regeneration in order to stop or even think about reverting possibilities against neuron destruction.

Aging also modifies cognitive abilities, reducing the processing speed and making difficult to focus on many tasks at the same time. Nevertheless, aging is only one of the factors that contribute in the process of neurons deterioration and progressive destruction. Actually, a big percentage of the population that suffers from dementia suffer from Alzheimer. Right now Alzheimer represents a 75% of all dementia diagnoses.

Undeniable similarities between both conditions

These two conditions have always been compared. Reasons are yet to be revealed on why people suffering from Parkinson’s are prone to develop Alzheimer’s as well. Thus, taking into account that both conditions affect brain cells, one directly destroying the ones in charge of cognitive processes and the other one mostly destroying cells related to movement and motor skills.

A curious fact about both conditions is how people with Parkinson’s that are not taking any kind of medication may see themselves affected at a cognitive level as well. This is possible because even though both conditions are not similar in a physical way (they attack different parts of the brain and have distinct genetic and environmental risk factors), at a biochemical level both conditions can be very similar.

In both conditions, Alzheimer’s disease and Parkinson’s disease, it is a common factor the appearance of protein forms in the way of toxic clumps that affect the brain cells. These abnormal aggregates of protein change their name depending on the condition. For Parkinson’s disease they are called Lewy bodies, they develop inside the nerve cells as accumulations of a sticky protein called alpha-synuclein. While in Alzheimer’s disease these cells are called tau and they are more like neurofibrillary tangles instead of mini accumulations.

Potential drug discoveries

Having present this similarity during researches led scientists to an important discovery. A group of scientists led by Keqiang Ye have targeted this fact as a way to attack both conditions. In previous works, Ye and his team had identified an enzyme that was able to trim tau. The result for this trimming was that it turned into a stickier and toxic protein clump. The next step was to develop a drug that was able to inhibit this trimming process. The enzyme responsible of the trimming process is called asparagine endopeptidase, and a drug that counters its effects has already been tested in animals with beneficial results.

Even though, the drug against asparagine endopeptidase was designed and developed in order to inhibit the trimming process in tau, they have also shown to have beneficial effects and actually act the exact same way toward alpha synuclein that forms Lewy bodies (Parkison’s disease).

Similarities in the behavior of both toxic proteins, tau and Lewy bodies,  are undeniable and it is not strange that a drug that can have good effects on one of them couldn’t affect the other one in the same way. Ye states that reasoning about AEP cuts it is very likely that if it has worked with Tau, it should also work it alpha-synuclein because they behave in a very similar way.

During testing processes a particular chunk of alpha-synuclein can be found in the samples of brain tissues taken from patients with Alzheimer’s and Parkinson’s disease. Apparently the chunk is produced by asparagine endopeptidaseand is the beginning of a new toxic process that extends all around the brain, however, samples taken from brain tissues treated with the drug have not shown the same.

Needs to be upgraded yet

In said samples, asparagine endopeptidase was confined to lysosomes. Lysosomes are parts of the cell that serve as garbage disposers. However, it seems like in samples of patients with Parkinson’s the asparagine endopeptidase had started leaking through the lysosomes. The behavior of asparagine endopeptidase is key in order to develop a complete cure for the symptom, therefore if the main goal is to have it as a solid treatment against Parkinson’s it has yet to be fully developed.

Nevertheless, the drug is still being tested and there is still some time left before it comes out with a marketable presentation. Therefore there are many other aspects that need to be tested, as an example, for Parkinson’s maybe the drug will need a higher dose, or even an extra component that helps alleviate those small differences between Lewys bodies and Tau. Whatever is the case, there is a ray of hope regarding effective treatments against these conditions that been regarded as impossible to cure for so long.

How this discovery affects future research in the fields of Parkinson’s and Alzheimer’s

This is surely a big discovery that will affect all future researches regarding Alzheimer’s and Parkinson’s diseases. Notwithstanding, doctor Ye has advised asparagine endopeptidase is not the only enzyme causing trimming and therefore toxic reproduction of the brain cells. Furthermore, the entire enzyme is still capable of segregating and destroy other brain cells.

But despite all the cons that this drug still has to face and resolute, it is a very promising start and the community is looking forward to have it tested in humans to see if it works as it has worked in animals. This enzyme inhibitor is nothing but the first step to a plethora of researches focusing on different ways to stop both conditions from appearing in the first place.