A recent study by the Tanz Center for Research in Neurodegenerative Diseases at the University of Toronto has challenged existing theories about the hormone somatostatin’s role in the early stages of Alzheimer’s disease.
Co-author Gerold Schmitt-Ulms indicates that this research, for the first time, provides substantial evidence that somatostatin plays a significant role in Alzheimer’s disease.
Although it doesn’t prevent the clumping of the amyloid-beta protein – a characteristic feature of Alzheimer’s – it does slow the process down.
According to the dominant hypothesis, Alzheimer’s disease is triggered by an overproduction of amyloid-beta protein, leading to small clumps known as oligomers.
Over time, these oligomers accumulate and form larger plaques, causing damage to neurons.
Since the 1970s, researchers noticed that individuals with Alzheimer’s had lower levels of somatostatin than healthy individuals and that amyloid-beta plaques tend to form near neurons that produce somatostatin.
In the early 2000s, Japanese researchers found that somatostatin increases the production of an enzyme called neprilysin, which can degrade amyloid beta.
Thus, if somatostatin levels were decreased, the lack of neprilysin would allow plaques to continue growing, exacerbating Alzheimer’s disease.
New Findings about Somatostatin
Schmitt-Ulms and his team decided to investigate somatostatin and its relationship with the toxic oligomeric forms of amyloid-beta.
Interestingly, they found that somatostatin only interacts with these oligomers, preventing their formation.
This groundbreaking discovery suggested that somatostatin could have a more direct role in the early stages of Alzheimer’s disease than previously thought.
The researchers then used genetically modified mice to further understand the role of somatostatin.
They found that, in the absence of somatostatin, there were more amyloid-beta aggregates, similar to what is observed in human Alzheimer’s disease.
However, this did not seem to be related to an effect of somatostatin on neprilysin levels, contrary to previous understanding.
Instead, it suggested that somatostatin can block the formation of oligomers by interacting directly with amyloid-beta.
Implications and Future Steps
This new understanding of the role of somatostatin in Alzheimer’s disease provides crucial insights, although it is yet unclear what it means for treatment.
Somatostatin has several crucial roles in the body, making it difficult to augment its production selectively to prevent amyloid aggregation.
Moreover, it is not certain whether boosting somatostatin and thus halting amyloid-beta aggregate growth would be beneficial.
Nonetheless, these findings have invigorated Alzheimer’s research and challenged conventional understanding, even if the implications for therapeutics remain unclear.
The study highlights that somatostatin – one of the earliest molecules biochemically linked to Alzheimer’s – might play a different role in the disease’s onset than previously thought.
If you care about Alzheimer’s, please read studies about Vitamin D deficiency linked to Alzheimer’s, vascular dementia, and Oral cannabis extract may help reduce Alzheimer’s symptoms.
For more information about brain health, please see recent studies about Vitamin B9 deficiency linked to higher dementia risk, and results showing flavonoid-rich foods could improve survival in Parkinson’s disease.
The study was published in Scientific Reports. Follow us on Twitter for more articles about this topic.
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