Alzheimer’s disease is the most common form of dementia, causing approximately two-thirds of all cases of dementia. Other major forms of dementia are vascular dementia (effecting up to 20% of patients with dementia), dementia with Lewy bodies (approximately 15% of all dementia cases), frontotemporal dementia (less than 5% of dementia cases).36 The boundaries between different forms of dementia are indistinct and mixed forms, as well as dementia as a comorbidity with other diseases, may co-exist.29 Additionally, less common forms of dementia include: Parkinson’s Disease Dementia, Huntington’s Disease, Creutzfeldt-Jakob Disease and Other Prion Diseases, Dementia in HIV/AIDS, Traumatic Brain Injury, and Wernicke-Korsakoff Syndrome (includes dementia from alcohol abuse).37
Risk factors for dementia are multifactorial and vary throughout life. Educational attainment early in life, e.g., number of years spent in education, is protective against dementia and a higher level of education may delay the onset of dementia later in life.38 Additionally, hypertension, type 2 diabetes mellitus, hyperlipidemia, cognitive activity, social activity, exercise, alcohol use, diet, and smoking have also been associated with dementia development.38,39 Late-onset Alzheimer’s, the most common form of dementia, is thought to be a multifactorial disease wherein development of the disease likely includes a combination of genetic, lifestyle and environmental factors. Genetically, a polymorphism of the apolipoprotein E (APOE) gene, specifically APOE ε4 on chromosome 19, increases individual’s risk for developing late onset Alzheimer’s Disease.40 This gene and other genes are implicated in the risk of development of Alzheimer’s Disease, including increasing the production of presenilin and β-amyloid precursor protein (BAPP), have been shown to enhance deposition of β-amyloid protein in brain tissue.41 In addition to these genetic risk factors, epigenetic alterations of the genome (modification of the genome to turn genes off) may be a role for environmental and lifestyle factors to influence gene expression and ameliorate or potentiate underlying genetic risk factors.42 Finally, recent studies have identified breakdown of the blood-brain barrier, including increased permeability, microbleeds, impaired nutrient transport, and impaired clearning of neurotoxins, as a mechanism for introduction of neurotoxic substances, potentially including bacteria and bacterial byproducts, into the brain in neurodegenerative diseases.43
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