Putting the Pieces Together On How to Cure Alzheimer’s
By S. Brachmann; ipwatchdog.com; 3/27/16

The National Institute on Aging estimates that there are more than five million Americans who may suffer from Alzheimer’s, which accounts for anywhere from 60 percent to 80 percent of all cases of dementia in the U.S. Alzheimer’s causes the buildup of amyloid plaques and tau tangles in the brain tissue of an affected individual, killing off brain cells for years before symptoms of memory loss start to occur.

Alzheimer’s disease is such a difficult medical problem to answer in part because the damage is irreversible, but also because there are so many scientific unknowns involved in the process. Researchers still have very little understanding of the underlying causes for Alzheimer’s, which is a major reason why no cure exists yet. An editorial published in a recent issue of the Journal of Alzheimer’s Disease theorizes that microbes in the brain could be a contributing factor, but this theory has proven to be controversial in the past. The major risk factors for Alzheimer’s are related to aging and genetics, factors which cannot be changed through conventional medicine. Regular physical exercise, challenging mental activity and overall diet are thought to help improve overall health and thus the risk of developing Alzheimer’s, but it’s not known what can be done to directly prevent the formation, or slow the progression, of the damage once it starts.

A good attention to proper oral care and hygiene may be another way to encourage the best possible prognosis for Alzheimer’s patients, according to a study published in the peer-reviewed open access scientific journal PLOS ONE. Researchers from the University of Southampton and King’s College London contributing to the study found a steep decline in the mental activity of Alzheimer’s patients among those who had gum disease. The findings support the notion that the immune system response triggered by bacteria reaching the brain, including certain inflammatory effects, may be strongly linked to the progression of Alzheimer’s disease.

Computer usage may also be an indicator of Alzheimer’s in people of advanced age, according to research performed at Oregon Health and Science University and also published in the Journal of Alzheimer’s Disease. A demonstrated link between computer use and hippocampal volume, which is a major factor affecting human memory, was found in healthy adults of at least 65 years of age. Smaller hippocampal volume is thought to be an indicator of Alzheimer’s.

Early Diagnosis of Alzheimer’s

Earlier diagnoses can give Alzheimer’s patients more time to plan for their long-term care and explore treatment options. A new type of blood test developed by German scientists could increase the maximum amount of time for early detections up to 15 years before clinical symptoms begin to appear. The study results, published in a March issue of Biophotonics, discuss a test involving an infrared sensor which is able to detect the misfolding of amyloid-beta peptides which gradually form into amyloid plaques, causing brain damage. The earlier detections could help doctors prescribe medications that would delay the onset of brain damage; once clinical symptoms appear, a great deal of irreversible damage has already been done.

Early detection of Alzheimer’s could also be bolstered by innovative medical science research taking place at the University of Southern California. A study published in the scientific journal Trends in Cognitive Science identifies the locus coeruleus as the first part of the human brain which is affected by the onset of Alzheimer’s. The locus coeruleus regulates blood vessel interactivity throughout the brain and releases norepinephrine, a neurotransmitter which affects attention, cognition and memory. The way that the locus coeruleus interacts with the rest of the brain makes it more susceptible to toxins as well as infections in other areas of the brain, the researchers found.

Research into Alzheimer’s

A new defense against the formation of amyloid-beta into hardened plaques could have come from a team of Swiss scientists working at the École Polytechnique Fédérale de Lausanne. A study published in the neurology journal Brain discusses an implantable capsule containing cells which have shown themselves to be effective at counteracting the process by which amyloid-beta uses to clump together. The researchers have been able to produce the amyloid-beta countering effects by implanting the capsule into mice. The semi-permeable capsule, which measures 27 millimeters (mm) long by 12 mm wide by 1.2 mm thick, includes a hydrogel shielding the cells from the body’s immune system while allowing the cells to draw nutrients from the body.

Snake venom could prove to be an unlikely source for an Alzheimer’s treatment, but that could be the case thanks to research taking place at Australia’s Monash University. Scientists at that institution were able to isolate a molecule from the venom of a poisonous snake, Bothrops asper, which stimulated enzymes helping to fight the plaque created by amyloid-beta deposits. The compound has also shown some effectiveness in being used to treat bleeding caused by wounds.

Techniques for unraveling the tau tangles which are another element of Alzheimer’s progression in patients could be coming if a drug developed by a Singapore-based pharmaceutical firm continues to have successful trials. TauRx Pharmaceuticals, founded in 2002, has produced a drug called LMTX which helped to produce better cognitive scores in Alzheimer’s patients in early trials. The results are based on three decades of research performed by Claude Wischik, currently a professor at the University of Aberdeen in Scotland.

The brain damage caused by Alzheimer’s might be irreversible, but a study produced by researchers at the Massachusetts Institute of Technology (MIT) and published in Nature gives rise to the notion that a person’s memories could still be retrieved even after Alzheimer’s has damaged brain tissues. The researchers identified dentate gyrus (DG) neurons which, when activated, were able to retrieve memories in mice which were formed during contextual fear conditioning. Researchers also ablated the DG neurons using diphtheria toxin and found that the mice couldn’t retrieve the same memories. There are likely differences in the brain functions of human Alzheimer’s patients and engineered mice, researchers warn, but this finding would provide further evidence of the important role played by the hippocampus, where the DG neurons are located.

Future developments that could link vascular disease to the development of Alzheimer’s could come from Emory University in the coming years. The academic institution recently received a five-year, $5.2 million grant for greater exploration into any possible connection between the regulation of blood pressure and Alzheimer’s. It’s hoped that the research will lead to potential new treatments for the disease, specifically ones which may target the renin-angiotensin system and endothelial cells.

 

 

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