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Alzheimer’s-inflammation link strengthened
A study reported at the first Alzheimer's Association International Conference on Prevention of Dementia, held in Washington, DC from June 18 to 21 found that early life inflammation is associated with four times the risk of developing Alzheimer’s disease than that experienced by individuals not similarly exposed.
Lead author Margaret Gatz, who is a professor of psychology at the University of Southern California College of Letters, Arts and Sciences, presented the findings of a study of 109 pairs of identical twins, one of each who had dementia, who participated in the Swedish Twin Registry. Previous research by Dr Gatz and other scientists concluded that Alzheimer’s disease has a strong genetic component. An identical twin has a significantly increased chance of developing the disease if the other twin has it.
For the current research, Dr Gatz was inspired by the work of Caleb Finch and Eileen Crimmons, whose 2004 paper published in Science proposed an association between longer life spans and a reduced incidence of childhood infectious diseases. Gatz and colleagues at the Karolinska Institute in Stockholm used surveys completed by the participants in the 1960s to obtain information concerning the subjects’ health history and education. They found that stroke and not having a long formal education increased the risk of dementia but not Alzheimer’s disease. However, an early history of periodontal disease, indicating inflammation, quadrupled Alzheimer’s disease risk. Dr Gatz explained, "We're talking about gum disease, but it was measured by teeth lost or loose. It's not perfect. Given it's not perfect, it's even more striking that it's such a solid risk factor . . . If what we're indexing with periodontal disease is some kind of inflammatory burden, then it is probably speaking to general health conditions. There was in our twins quite a lot of periodontal disease, and at that time in Sweden there was a lot of poverty."
Additionally, the study failed to find a strong association between increased mental activities and education and Alzheimer’s disease risk.
The message of the current study is not necessarily that improved oral health prevents Alzheimer’s disease, but that early life inflammation may have dire effects later on. Dr Gatz added, "People can plan a life span that will alter dementia risk. And these aren't risk factors that are unique to dementia. Many of these are also risk factors for other disorders. This is good news."
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A letter published in the June 2005 Journal of the American Geriatrics Society (http://www.blackwell-synergy.com/loi/jgs) reported an increase in the white matter lesions in Alzheimer's disease patients associated with reduced levels of vitamin B6. Lesions in the white matter of the brain are associated with brain aging and may reflect chronic cerebral ischemia, although their role in Alzheimer's disease has not been defined.
The most characteristic features of Alzheimer's disease are senile plaques of beta-amyloid peptide, neurofibrillary tangles involving tau protein, loss of synapses, and (ultimately) the death of neurons. Although neurofibrillary tangles are more closely associated with neuronal death than beta-amyloid, the evidence is becoming convincing that beta-amyloid is the factor most responsible for starting the degenerative processes of Alzheimer's disease.
In Alzheimer's disease, an inflammatory cascade begins in response to beta-amyloid. The inflammatory response, involving cytokines and prostaglandins, occurs around beta-amyloid in the neuron. This inflammatory process continues and accelerates the loss of neurons.
The mechanism of inflammation is a complex interaction of chemical messengers. Arachadonic acid, via 5-lipoxygenase, forms leukotrienes that cause vasoconstriction, bronchospasm (i.e., asthma), and increased permeability. Alternatively, arachadonic acid can form, via cyclooxygenase, prostaglandins, which have similar actions and cause pain. Aspirin and indomethican inhibit cyclooxygenase which results in pain relief, but does not address the underlying cause of the inflammation or stop the actions of the leukotrienes.
Inflammation can be acute, as occurs after a physical injury, or chronic. There are several causes of chronic inflammation, including:
Inflammation is considered to be an underlying cause of Alzheimer's disease, primarily because beta-amyloid is an inflammatory protein (Hull 1996; McGeer et al. 1999).
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