

Far too many have witnessed the devastating effects of Alzheimer’s disease on loved ones. The slow and uncontrollable deterioration into someone unlike the person once known is chilling, but it happens to more than 5.5 million Americans.
A study by the Society for Neuroscience found that accumulation of the protein beta-amyloid begins to slow by the time the patient is considered to have preclinical Alzheimer’s disease (AD). As a result, scholars advise conducting anti-amyloid therapy before the onset of symptoms to prevent the growth of the molecules. However, some scientists argue that the procedure will produce inconsequential outcomes.
What is Beta – Amyloid?
According to the Mayo Clinic, Alzheimer’s is the most common cause of dementia in individuals over 65 years of age. Progressive declines in memory, cognition, and social skills characterize the illness.
The symptoms result from the degeneration of neurons, which send signals throughout the nervous system. The trigger of the issue is currently unknown, but whatever it is, it leads to brain shrinkage and altered connections.
Two hallmark signs of the disease have been the target of research for decades, beta-amyloid plaques and neurofibrillary tangles.
As explained by the National Institute on Aging, the plaques form from the breakdown of precursor proteins, which are naturally occurring substances in the brain. Abnormal levels inhibit neuronal communication and spur cell death.
Development of anti-amyloid therapy has been the subject of an extensive investigation, but to little avail. Such methods will unlikely remedy the illness. Various studies instead argue that the accumulation is the result of brain damage and not the culprit of AD development.
That is not to say that scientists are incompetently performing their duties. Rather, they are passionately attempting to uncover the details of one of the trademarks of the disease in an attempt to find a cure. Nevertheless, a mass movement towards examining other aspects of Alzheimer’s seems long overdue.
Other Causes and Treatments
Some have changed focus to neurofibrillary tangles, which are excessive accruals of the protein tau inside neurons. During healthy functioning, tau works to strengthen the support system of brain cells. However, they may undergo unusual chemical changes, sticking to other tau molecules and forming tangles.
They especially gather in the hippocampus, which is the area of the brain responsible for memory formation, generating the characteristic loss of remembrance experienced by patients. Adopting sufficient methods for restoration in this region is challenging.
The hippocampus contains pyramidal neurons. Damage to these cells initiates immune responses and scar formation that produce shielding, as reported by the Alzheimer’s Association. Due to the shielding, regeneration fails following injury, as nutrients and other substances cannot pierce the area.
Present studies have focused on injecting stem cells before scar formation to enable rejuvenation. Although this procedure proves promising, early detection is necessary to treat the patient adequately.
As millions currently suffer from the debilitating effects of Alzheimer’s, researchers are passionately working to uncover the disease’s secrets. The origins are unknown, but scientific progress moves closer to a cure with each passing day.
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