The key to diagnosing a brain disease earlier than ever

Earlier this year, Parkinson’s disease research (PD) entered a new era when the Michael Jay Fox Foundation announced an important scientific progress – discovering a marker for PD. This meant that, for the first time, we can now identify the first known symptoms of the disease in Parkinson’s patients.

This new method is called the “alpha synchlin” (SAA) method, and is capable of detecting inaccurate alpha sinoclin in the spine-conventional spine fluid, which is clearly associated with Parkinson’s. With the 90 % stunning feature, those who evidence of PD pathology in their cells are separated from those who do not do so. This is done even before the symptoms appear, such as how to use hypertension or cholesterol levels to detect cardiovascular risk long before a heart attack someone in the ER.

It is difficult to make the consequences of this progress over too hard for people with their alpha syncline disorders. From one thing, we never have a way to know who these people are – to the moment of diagnosis, where constant damage to brain cells is underway. In the case of self-diagnosis, which is created for most people as a screw of blue, it is always mentally disappointing and basically looking for a short time in the doctor’s office-is not very useful for providing medical care, let alone the development of biomedical medicine.

The new SAA experiment is currently in drug tests as the first step that can identify the biology we are targeting – to ensure that they are experimenting with the appropriate population by using pharmacies. For biophama companies who decide to enter or stay in a risky neurological environment, this offer changes the value of investment in its face. In 2024, we will see the sloping new potential drugs entering the pipeline and progressing them towards pharmaceutical shelves.

The important thing is how to achieve SAA success. Searching for a marker need to find “needle in alfalfa”: People without traditional PD and unwanted symptoms of life increased by increasing the risk of the disease. It was important to understand what biology would separate them from those who do not receive Parkinson. But how do you find someone who doesn’t know who was looking for?

As it turns out, your smell is a good predictor of brain disease. (We are not talking here, not about losing the short-term odor associated with Coveid-19, but to lose the remarkable and lasting odor that continues over the years.) For some time, researchers consider the link between smell loss and nerve production, especially if there are some other risk factors, such as diagnosing RM (RBD). Research shows that half of people over the age of 60 lives with some loss of smell, but the majority do not notice it until they were tested. If you marry this with the fact that all major brain diseases – Alzheimer’s, Parkinson’s, Als, Huntington – are accompanied by some smelling, this is astonishing.

Michael Jay Fox’s large -scale observation study uses Parkinson’s to use poor odor as one of its criteria to find and register people at risk. (It should be noted that, for this risk group, it is still unclear If Or Kay This disease may eventually be shown.) Highly advanced screening machine? A humble scratch and sniff test, though scientifically valid.

Unless the SAA marker is approved, a decline in odor cannot be objectively associated with the biology of Parkinson’s disease. But now we can report that the experiment is accurately diagnosed in 99 % of people with a weak and so -called Parkinson’s scattered odor (in other words, those who do not have genetic mutations).

In 2024, we will see a change in sea facilities around PD screening and forecasting and possibly other aging diseases. The annual scratch and snack test may soon be as common as your mammography or colonoscopy. In 2024, with widespread acceptance, this simple, inexpensive and accessible mechanism fundamentally changes what may change in Parkinson’s research and care.