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• W2049973352 abstract "Despite the fact that Alzheimer’s disease was identified more than 100 years ago, its cause remains elusive. Although the chance of developing Alzheimer’s disease increases with age, it is not a natural consequence of aging. This article proposes that dental X-rays can damage microglia telomeres – the structures at the end of chromosomes that determine how many times cells divide before they die – causing them to age prematurely. Degenerated microglia lose their neuroprotective properties, resulting in the formation of neurofibrillary tau tangles and consequently, the neuronal death that causes Alzheimer’s dementia. The hypothesis that Alzheimer’s is caused specifically by microglia telomere damage would explain the delay of one decade or longer between the presence of Alzheimer’s brain pathology and symptoms; telomere damage would not cause any change in microglial function, it would just reset the countdown clock so that senescence and apoptosis occurred earlier than they would have without the environmental insult. Once microglia telomere damage causes premature aging and death, the adjacent neurons are deprived of the physical support, maintenance and nourishment they require to survive. This sequence of events would explain why therapies and vaccines that eliminate amyloid plaques have been unsuccessful in stopping dementia. Regardless of whether clearing plaques is beneficial or harmful – which remains a subject of debate – it does not address the failing microglia population. If microglia telomere damage is causing Alzheimer’s disease, self-donated bone marrow or dental pulp stem cell transplants could give rise to new microglia populations that would maintain neuronal health while the original resident microglia population died." @default.
• W2049973352 created "2016-06-24" @default.
• W2049973352 creator A5021083386 @default.
• W2049973352 date "2011-07-01" @default.
• W2049973352 modified "2023-09-25" @default.
• W2049973352 title "Dental X-ray exposure and Alzheimer’s disease: A hypothetical etiological association" @default.
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• W2049973352 doi "https://doi.org/10.1016/j.mehy.2011.03.016" @default.
• W2049973352 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21458164" @default.
• W2049973352 hasPublicationYear "2011" @default.
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