Abstract

Among manifestations of neurodegenerative diseases, Alzheimer Disease (AD) contributes for 60-70% to elderly dementia. AD patients suffer from impaired cognitive function and from a compromised capacity to perform activities of daily living. Neurodegenerative diseases are characterized by neuronal loss, dystrophic neurites, and cerebrovascular amyloid. AD occurs more often in woman (2/3 of AD cases) compared with men. The presence of extracellular β-amyloid peptide and hyper phosphorylated tau protein are typical of the physiopathology of the AD brain. Developed under the age of 65 years, the PSEN1 gene is located on chromosome 14q24.3. In the elderly over 65 years, the late-onset of AD, the gene coding for PSEN2 is located on chromosome 1q31-q42. For the late onset AD, the apolipoprotein E was associated to the main risk factors of developing the disease (including molecules such as clusterin, complement receptor, phosphatidylinositol binding clathrin assembly protein and sortilin). Four genes have been identified on chromosome 11. The Amyloid P Protein precursor (APP) encoded by the gene (APP) is located on chromosome 21q. Altered APP processing and Aβ accumulation shed light on the AD pathogenesis. TNFα may act as a diagnostic marker with high sensitivity and specificity in patients with AD. Studies have identified altered oral health conditions (periodontitis, caries, gingival bleeding, probing depth >4 mm). Poor gingival health and oral hygiene increase with the severity of dementia. Dental professionals should use behaviour management techniques for developing preventive strategies in order to stabilize the lesions.

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