You may already know someone who suffered from Alzheimer\u2019s disease. It is the most common form of dementia, according to the United States\u2019 Centers for Disease Control and Prevention (CDC). Additionally, according to websites Alzheimer\u2019s News Today and Alzheimer\u2019s Disease International, there are around 44 million people around the world who suffer from this degenerative disease, and that on average someone somewhere around the globe gets the disease every three seconds.<\/p>\n\n\n\n
Studies over the decades have arrived at the hypothesis that Alzheimer\u2019s disease is mostly caused by the build-up of amyloid<\/em> proteins in the brain. These amyloid proteins form what are called plagues, and they usually form in the gaps between nerve cells. Once they set themselves between nerve endings, the cells then struggle to send signals to each other, prompting loss of brain function.<\/p>\n\n\n\n While doubts are present on whether or not this \u201camyloid hypothesis\u201d truly holds up as the explanation for the disease, the noticeable build-up of plaques in the brain is still one of the most prominent\u2014if not the most prominent\u2014sign of the onset of Alzheimer\u2019s disease. There is, however, one more hypothesis out there that strives to explain how this disease hits us\u2014and according to what its proponents propose, it may come from an unlikely place.<\/p>\n\n\n\n Curtin University researcher John Mamo was set to address this second hypothesis: that Alzheimer\u2019s disease is actually mostly caused by amyloid coming from the liver<\/em> instead. Thing is, amyloid is also produced by the brain, hence why most people believe the origins of the disease are from the brain rather than any other organ below it. Mamo and team wanted to find out just how it sets in, so in their landmark study published in the journal PLOS Biology<\/em>, they modeled the disease on mice to study its effects.<\/p>\n\n\n\n The majority of mouse models concerning research on the disease involves the overproduction of amyloid in the mouses\u2019 brains, which according to the team only corresponds to the hereditary form of the disease known as early-onset Alzheimer\u2019s<\/em>. To them, the form of Alzheimer\u2019s brought about by old age, known as sporadic Alzheimer\u2019s<\/em>, remains unaddressed. This form is not associated with familial or genetic history, and is thus nonhereditary.<\/p>\n\n\n\n In an effort to address sporadic Alzheimer\u2019s, Mamo and the team proceeded to engineer mice in such a way that they can only produce amyloid through the liver and not the brain. The evidence they obtained seems to corroborate what they believe to be amyloid trekking the \u201cblood-to-brain pathway<\/em>\u201d from the liver to the brain. And true enough, they found that mice who had no capacity to produce amyloid in the brain still developed inflammation up in the brain, which the team considers a positive result corresponding with their radical hypothesis.<\/p>\n\n\n\n \u201c[T]he study found that mouse models producing lipoprotein-amyloid in the liver suffered inflammation in the brain, accelerated brain cell death and memory loss,\u201d according to Mamo. \u201cThis [pathway] is significant because if we can manage the levels in blood of lipoprotein-amyloid and prevent their leakage into the brain, this opens up potential new treatments to prevent Alzheimer\u2019s disease and slow memory loss.\u201d<\/p>\n\n\n\n This, of course, may mean that early detection and prevention of this degenerative disease may take on radically new methods should their hypothesis be proven true. For one, a person\u2019s propensity to generate amyloid in the liver may then be used as an early marker to determine how likely a person is to develop Alzheimer\u2019s at an older age. Also, dietary restrictions may be deployed to preserve liver health, potentially also delaying the onset of the disease long before the patient reaches the age commonly associated with the said onset.<\/p>\n\n\n\n Mamo added: \u201cWhile further studies are now needed, this finding shows the abundance of these toxic protein deposits in the blood could potentially be addressed through a person\u2019s diet and some drugs that could specifically target lipoprotein amyloid, therefore reducing their risk or slowing the progression of Alzheimer\u2019s disease.\u201d<\/p>\n\n\n\n The team is now preparing to move on to human clinical trials; in it, they plan to make use of a drug used primarily for cholesterol management. This drug, called probucol<\/em>, can also suppress amyloid production in the liver. The trial, which had already begun this year, needs about 300 subjects with mild dementia related to the onset of Alzheimer\u2019s. In it, they plan to observe whether or not a daily dosage of probucol for two years can decelerate cognitive decline.<\/p>\n\n\n\n (To find out more about how our brain is involved with our body, check out this piece where we report on the effects histamine may have on depressive episodes<\/a>.)<\/p>\n\n\n\nReferences<\/h2>\n\n\n\n