Alzheimer’s is a debilitating mental illness that affects more than 6 million Americans of all ages. The condition is especially prevalent among the elderly, with an estimated 6.5 million Americans aged 65 and older living with Alzheimer’s last year. Some figures show that 73% of the people living with Alzheimer’s are 75 years old and older.
Alzheimer’s usually occurs when amyloid proteins build up abnormally in and around brain cells and form deposits of plaque, causing a reduction in neurotransmitter activity. The plaque buildup causes parts of the brain to shrink over time, usually beginning with the regions in charge of retaining memory.
However, a new study from USC Leonard Davis School of Gerontology challenges the long-thought notion that Alzheimer’s is caused by the buildup of certain proteins in the brain Although prior research has associated amyloid beta (Aβ) protein buildup with the development of Alzheimer’s, we don’t actually know what causes this buildup. The senior author of the study, Caleb Finch, who is also a professor at USC Leonard Davis, stated that little was also known about the connection between this protein and normal brain aging.
Researchers from the university set out to determine Aβ levels in human brains by analyzing tissue samples provided by healthy patients and patients living with dementia. They found that older, cognitively healthy patients exhibited roughly the same amounts of dissolvable, nonfibrillar amyloid protein as people with Alzheimer’s. However, Alzheimer’s patients had much higher amounts of the insoluble Aβ fibrils, which came together and built up to form the brain plaque usually associated with the neurological disease.
According to the first author of the study, Max Thorwald, and Finch, study findings challenge the notion that the underlying cause of Alzheimer’s disease is the simple presence of high amyloid protein levels. They explained that the rise in soluble Aβ levels may be due to age-related changes in the brain rather than Alzheimer’s. The researchers believe that Alzheimer’s may occur due to a diminished ability to clear the protein from brain cells, not the overproduction of Aβ.
Thorwald added that their findings supported the use of “aggregated or fibrillary amyloid” as biomarkers for patients with Alzheimer’s. Furthermore, he noted that the site where amyloid processing happens tends to have fewer enzymes and precursors for processing, indicating that the removal of amyloid protein, not overproduction, is associated with Alzheimer’s.
In their report, the researchers emphasized the need for more studies to explore this connection, highlighting that future studies needed to leverage positron emission tomography (PET) imaging in both Alzheimer’s patients and healthy individuals to analyze how processing and removal of amyloid cause changes in the brain over time.
As researchers dig more into the reasons why Alzheimer’s develops and how it progresses, patients and their caregivers can continue to rely on the wearable devices made by manufacturers such as MetAlert Inc. (OTC: MLRT) so that the effects of memory loss don’t result in something worse, such as a patient wandering away from home to an unsafe environment.
NOTE TO INVESTORS: The latest news and updates relating to MetAlert Inc. (OTC: MLRT) are available in the company’s newsroom at https://ibn.fm/MLRT
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