Alzhiemers disease essay

They gain access in a number of ways: HSV-1 infects the cornea of the eye and then invades cells in the trigeminal nerve, which travels to the brain. The parasite Toxoplasma gondii , which has been shown to infect nearly one-quarter of the US population, sneaks into the brain via endothelial cells. And some oral bacteria — those implicated in cavities and gingivitis — sneak in via the olfactory bulb, a highly innervated area adjacent to the brain. In a letter to the editor of the Journal of the American Medical Association in , MacDonald, then at Southampton Hospital in Long Island, described discovering the bacteria that cause Lyme disease inside the brains of two deceased dementia patients.

Most people who contract this bacteria develop chronic latent infections in which the microbes hide silently, often for years, inside their cells. Yet some studies do suggest that infections come first. They instead argue that infections — perhaps a number of different types — can spark a cascade of events that, over time, can culminate in the disease. The process could start like this: the brain gets injured or infected and then responds by accumulating beta-amyloid plaques to repair the problem.

The idea that beta-amyloid might be protective was first proposed in a paper by the Australian neurologists Stephen Robinson and Glenda Bishop, who noted, among other things, that amyloid plaques accumulate after serious brain injury. The beta-amyloid peptide also has not changed much over the past million years and is found in most vertebrates, which further supports the idea that it has an important job. Within hours of injecting salmonella into mouse brains, Moir and his colleagues saw widespread beta-amyloid plaques appear.

The blood-brain barrier becomes more permeable with age; maybe microbes have an easier time crossing it later in life. When enough beta-amyloid plaques accumulate after an infection, though, they start creating their own problems. Some microbes might trigger the activation of immune molecules outside the brain that then travel into the brain, influencing it; others might cause the body to create self-attacking antibodies that damage brain cells.

Microglia also become more overzealous with age, making inflammatory responses more potent and dangerous. Certainly, the pathogen hypothesis has only limited, correlative evidence in its support. But the amyloid cascade hypothesis has some compelling direct evidence against it. It tells a different story. They found that one key difference between the resilient brains and the diseased brains was that the former had much fewer activated microglia.

The result is a dangerous circular logic that is holding back the field.

Genetics of Alzheimer's disease.

Why do researchers reject the pathogen hypothesis for a lack of evidence yet support a theory that lacks supporting data too? There might be deeper psychological barriers to accepting the pathogen hypothesis as well. Time and time again, scientists have had trouble accepting that microbes can cause common diseases. One particularly famous example involves gastric ulcers: although the internist Barry Marshall and the pathologist Robin Warren had isolated H.

Marshall eventually convinced the world by drinking a concoction of the bacteria himself, which gave him gastritis, the precursor to an ulcer, which he then cured with antibiotics. H istory and bias aside, though, the pathogen hypothesis certainly prompts more questions than it provides answers.

How Coco Connects Legacy and Alzheimer's Disease - Video Essay

But HSV-1 re-activates only sporadically, so the viruses are circulating in the brain only during short windows. Even when viruses are definitely there, they are still tough to isolate. Of course, the right drug would have to be given at the right time, which complicates the picture.

Still, Itzhaki, for one, has been advocating for a clinical trial involving antiviral drugs for years. It has yet to happen. Indeed, funding has been a major issue among researchers trying to investigate the pathogen hypothesis. The vast majority of funds, Robinson says, continue to be spent on research and trials related to the amyloid cascade hypothesis. Still, Moir says he senses that the research community is slowly becoming more receptive to the idea.

Sarah Stein Lubrano. Exp Neurol.

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Hammond, C. Latest view on the mechanism of action of deep brain stimulation.

Hedges, L. Hill, N. Computerized cognitive training in older adults with mild cognitive impairment or dementia: a systematic review and meta-analysis. Hoeppner, J. Huntley, J. Do cognitive interventions improve general cognition in dementia? A meta-analysis and meta-regression. BMJ Open 5 , e Ibarria, M. Khedr, E. Kimbrell, T.

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  7. Left prefrontal-repetitive transcranial magnetic stimulation rTMS and regional cerebral glucose metabolism in normal volunteers. Psychiatry Res. Kuhn, J. Psychiatry 20 , — Laxton, A. Deep brain stimulation for the treatment of Alzheimer disease and dementias. World Neurosurg.

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