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Please try again, the name must be unique Only letters and numbers accepted. There is an additional concern about the ACH: The theory's prediction that reducing brain amyloid might improve cognitive performance or diminish the risk of AD has been tested with trials of medications that do indeed reduce amyloid in the blood and brain.

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So far, clinical trial results have been negative for many of these medications and the small number of positive findings have been of limited magnitude. Among the most encouraging sources of evidence in support of the ACH are the genetic findings that link amyloid-related gene problems to the development of early-onset AD. Down syndrome, in which there is an extra copy of the chromosome that contains genes coding for amyloid precursor protein APP , is associated with early and severe development of AD.

These gene mutations can be inherited and greatly increase the risk of developing early-onset AD, but in families like Jennifer's, where onset of AD occurred after age 60, other factors play a role, in addition to genetics. Neurofibrillary tangles reflect a problem with tau protein, a microscopic component of brain cells that is essential to their survival. The clumping and spread of chemically altered tau protein molecules follows a spatial and temporal pattern that is different from that of APs, so some researchers continue to look for a theory that includes problems with tau protein, not just amyloid.

Recent research, too, has raised the possibility that NFT can spread, almost like an infection, from one affected brain cell to those nearby. The importance of this finding is still being investigated. Normal aging is associated with brain changes such as tissue loss and degeneration of the synapse, which is the part of the nerve cell that is involved in passing an electrical or chemical signal to another nerve cell.

What Causes Alzheimer's Disease?

Plaques and sometimes tangles are known to develop in cognitively normal older adults. These changes occur more frequently and severely in people with advanced vascular disease, suggesting that reduced blood flow to brain cells may be important in the development of AD. Many cognitively normal older adults show no NFTs, suggesting that AD is more than just normal aging of the brain.

The loss of brain cells that produce acetylcholine, a neurotransmitter that is active in the transmission of nerve impulses was an early finding in AD research. Unfortunately, these medications are symptomatic treatments at best and often achieve only a limited benefit. The loss of these particular brain cells, therefore, is thought by many to be an effect rather than a cause of AD.

In support of that idea is the finding that cell loss includes not only cholinergic cells but other cell types as well. Other neurotransmitters such as serotonin are also reduced in AD. Some scientists believe that exposure of the brain to a harmful influence is what causes AD. There is evidence for toxic effects of aluminum on the brain, for example, though an actual link to AD is considered unlikely by leading researchers. Head injury is known to result in the appearance of plaques and tangles as well as clinical symptoms of cognitive impairment.

Alzheimer’s Reality Check: Debunking Myths and Conspiracy Theories – Livpact

AD, however, develops in many people who have not sustained head injuries. Head injury, therefore, cannot be a necessary step in the development of AD. Other theories of AD question whether an immune system run amok or a misguided inflammatory reaction might be significant. These theories continue to be explored. What about nutrition? We have seen recent reports linking prolonged cognitive health with adherence to a brain-healthy diets, such as the so-called Mediterranean-style diets, which emphasize fresh fruits and vegetables, nuts, healthy fats rather than saturated ones, and fiber.