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The true cause of Alzheimer’s finally discovered?

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Despite decades of research dedicated to Alzheimer’s disease, we are still far from having identified the exact biomolecular mechanisms, which turned out to be much more complex than we thought. In the last five years, this complexity has called into question the famous “amyloid cascade theory”, which has become increasingly controversial as treatments based on it show little efficacy. Recently, Yale researchers discovered that dementia caused by the disease could be caused by a “swelling” of axons, caused by a buildup of lysosomes (cell organelles) around amyloid plaques. Will this discovery finally provide a better clue to treat the disease?

For a long time, it was widely accepted that the main cause of Alzheimer’s disease was the accumulation of amyloid plaques in neurons. However, research has recently revealed that this accumulation is only one of the characteristics of the disease and therefore many other mechanisms remain to be discovered. In question, some researchers have incriminated autoimmune diseases, while others have suggested that the symptoms of the disease are caused rather by the reduction of the soluble form of the amyloid protein.

In addition, given the low efficacy of currently available treatments, scientists are forced to look at other avenues in the hope of developing potentially more suitable treatments. Most of the approved treatments focus in particular on the removal of amyloid plaques. And despite its ability to reduce buildup, dementia symptoms improve little or not at all in patients with the disease.


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The new study, detailed in the journal Nature, suggests that the buildup of lysosomes, the organelles responsible for dissolving cellular debris, may be the cause of Alzheimer’s dementia symptoms. In fact, another study has already evoked a more or less similar theory, according to which lysosomes would become unable to properly digest cell debris, which accumulates and swells in patients. This study also suggested that by “exploding” from overload, these lysosomes eventually burst and release toxic compounds that kill the cell, as well as amyloid proteins, which accumulate and solidify.

The Yale researchers suggest, on the other hand, that these lysosomal inflammations, detected around areas of amyloid plaque accumulation, impede the flow of electrical signals through neurons, leading to dementia. ” We have identified a potential Alzheimer’s disease signal that has functional implications for brain circuitry, and each spheroid has the potential to disrupt the activity of hundreds of neural axons and thousands of interconnected neurons. “, explain the authors of the new study.

Swelling caused by a specific biomarker

Using a mouse model in which Alzheimer’s disease was previously induced, the researchers found that each amyloid plaque formation was surrounded by an accumulation of small spherical grains along the axons, which were abnormally swollen. These grains were mainly composed of lysosomes that, when accumulated, prevent the circulation of electrical signals at the level of the axons.

Using a cell imaging technique, the researchers showed that the disruption of electrical signals from interneurons was strongly related to the size of the granules accumulated along the axons. The number of these spheroids would also be involved, according to postmortem analysis of the brains of Alzheimer’s disease patients, and each spheroid would disrupt the connection between thousands of neurons.

The Yale researchers also discovered that a protein called PLD3 induces the growth and clumping of lysosomes, leading to widespread inflammation of the axons. By genetically engineering mice to remove the biomarker, they found a significant reduction in axonal inflammation in diseased mice. The latter’s neural functions also improved significantly.

Furthermore, high levels of PLD3 would induce an excessive accumulation of lysosomes and hypertrophy of axons, even in healthy mice. Thus, ” it might be possible to eliminate this degradation of electrical signals in axons by targeting PLD3 or other molecules that regulate lysosomes, regardless of the presence of plaques said Jaime Grutzendler, professor of neurology and neuroscience at Yale and lead author of the study.

However, lysosome hypertrophy is equally more important near amyloid plaques. Therefore, therapeutic targeting of PLD3 could be a promising avenue for potentially effective treatments, as well as tools for early diagnosis. But more research is still needed before PLD3’s involvement in disease can be confirmed.

Source: Nature

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