Quite some time ago during my internal medicine residency, articles began to appear in medical journals advancing the idea that stomach ulcers might be caused by bacteria. Mainly, I remember how dismissive most gastroenterologists were of this idea. \u201cIt is utterly impossible,\u201d said one lecturer, \u201cthat any bacteria could survive in the intense acidity of the stomach.\u201d<\/p>\n\n\n\n
And then, in an effort to prove his point, the extremely dedicated Australian researcher Barry Marshall, MD<\/a>, drank a petri dish filled with the bacterium Helicobacter pylori<\/em> (H. pylori<\/em>) and did indeed develop ulcers. Buried in the ulcers were colonies of H. pylori<\/em>, thriving in the acid environment. Ugh, you might be thinking, but at least Marshall received a Nobel Prize for his efforts.<\/p>\n\n\n\n Almost 40 years later, we now know several illnesses are linked to chronic infections. For example, chronic lung disease and asthma are frequently associated with smoldering mycoplasma<\/em> and chlamydia<\/em> infections. The potpourri of bacteria in untreated chronic gum disease slowly generates a widespread inflammation in your arteries that leads to deposits of cholesterol and significantly increases your chances of heart disease and strokes.<\/p>\n\n\n\n In the 21st<\/sup> century, we don\u2019t see the vast numbers of people with chronic syphilis who filled the asylums of the 19th<\/sup> century. Instead, we\u2019re battling a cousin of the syphilis bacterium (Treponema pallidum<\/em>) in the form of Borrelia burgdorferi<\/em>, the cause of chronic Lyme disease.<\/p>\n\n\n\n The current controversy over whether or not Alzheimer\u2019s disease (AD) could possibly be triggered by a chronic infection<\/a> sounds very similar to Dr. Marshall and his struggles with H. pylori<\/em>. When you read the editorials by researchers making a case for AD as an infection, you sense they\u2019re battling vested interests to get funding for research. Their ideas are too far out of the box and the pharmaceutical industry is preoccupied with developing useless and expensive drugs (Namenda, Aricept) that neither cure nor stop the progress of AD and are meant to be taken for years and years.<\/p>\n\n\n\n Wouldn\u2019t it be a game-changer if you could get tested for your personal susceptibility to AD and, if positive, be prescribed a generic antibiotic or antiviral and know your AD risks had plummeted dramatically?<\/p>\n\n\n\n This next section, in which I\u2019ll attempt to explain the mechanics behind this astonishing news, is a little complicated. If you haven\u2019t yet had your coffee, you can stop reading now with the take-away that \u201cscientists are working on it.\u201d Add this Health Tip to your Facebook page and get on with your eggs. Or just keep reading.<\/p>\n\n\n\n Risk #1 is genetic Risk #2 is plaque build-up in your brain Risk #3 is an infection Because the organisms causing these infections are very tiny, they can pass through the protective shield called the blood-brain barrier and enter the brain. Although the idea of any infection entering your brain does sound spooky, if you’re either APOE-2 or APOE-3, you have a powerful defense system that clears the infection away without any permanent damage. The only symptom you might notice is a headache or some temporary difficulties with concentration.<\/p>\n\n\n\n Risk #4 is the important part: how you clear infection from your brain This research is highly controversial because scientists have been able to duplicate all this only in mice. And even though we all like baked brie, we are not mice. The process of the research went like this: they took groups of APOE-4-positive and APOE-4-negative mice and infected them with chlamydia<\/em>. Later, they examined the mouse brains and found Alzheimer plaques only in the APOE-4-positive group. The APOE-4-negative mice showed normal brain tissue.<\/p>\n\n\n\n If you\u2019ve stayed with me this long you\u2019re undoubtedly asking \u201cWhat does this mean for me?\u201d and \u201cIf I\u2019m at risk, is there anything I can do to reduce my Alzheimer chances?\u201d<\/p>\n\n\n\n Controversial again. Doctors definitely do not agree on this:<\/p>\n\n\n\n I know I\u2019ve thrown a lot at you for a Tuesday morning. Here\u2019s what I personally would do:<\/p>\n\n\n\nAlzheimer\u2019s and bacteria<\/strong><\/h3>\n\n\n\n
<\/u>AD undeniably runs in families. We all carry two copies of the APOE gene<\/a> (\u201cE\u201d is for epsilon<\/em>, not the letter \u201cE\u201d), one from each parent. There are three different APOE genes: e2, e3, and e4. It\u2019s APOE-4, present in 20% of the population, that not only increases the risk of developing AD, but also increases your risk for atherosclerosis, heart disease, stroke, and macular degeneration.<\/p>\n\n\n\n
<\/u>If you\u2019ve read anything about AD, you\u2019ve come across the words \u201cplaque\u201d and \u201camyloid.\u201d These are terms used by pathologists to describe what they see under the microscope in the brains of those who had Alzheimer\u2019s<\/a> before death. The depositing of plaques made up of the protein amyloid (a distant cousin to starch) interferes with brain function. As more and more amyloid gets deposited in the brain, mental function declines until an Alzheimer\u2019s patient enters a vegetable-like state and eventually dies.<\/p>\n\n\n\n
<\/u>Here\u2019s where it gets interesting. Throughout our lives, there are many bacterial infections we acquire and rid ourselves of without any complications. One large group of these is called community-acquired pneumonia (as opposed to pneumonia acquired in a hospital or other institution) and the most common causes are mycoplasma<\/em> (M. pneumoniae<\/em><\/a>) and chlamydia<\/em>. You can also get herpes (a virus), Lyme disease, mononucleosis (a virus), and a bunch more. We find evidence of previous infection via blood tests, looking for the antibodies our immune system create against the infection.<\/p>\n\n\n\n
<\/u>If you\u2019ve got the APOE-4 gene, when the infection moves through the blood-brain barrier your brain responds differently and starts forming the amyloid plaque of Alzheimer\u2019s. In other words, Alzheimer\u2019s develops from your brain\u2019s inability to clean up an otherwise relatively innocuous infection.<\/p>\n\n\n\nCan you say controversial?<\/strong><\/h3>\n\n\n\n