| Abstract: | The present article describes polymorphism in senile dementia of the Alzheimer type (SDAT) from a view point of senile plaque formation. Senile dementia of the Alzheimer type is a disorder in which cerebral β amyloid deposition progresses with age and, finally, causes dementia. Aging, apolipoprotein E (apoE) ε4 gene and head trauma are risk factors for senile plaque formation. Senile plaques begin to appear in some subjects in their 40s, whereas other subjects over the age of 100 years do not have any senile plaques. The apoE gene and other unknown factors may cause this difference in the age onset of plaque formation. Plaque density reaches a plateau before clinical dementia appears. As a result, some non-demented subjects have considerable amounts of senile plaques and it may take 20–30 years from the beginning of senile plaque formation for the clinical manifestations of dementia to appear. In this subclinical period, areas of plaque formation spread throughout the cortex from association areas to the primary cortex. The pattern of this progression is consistent in SDAT subjects and, therefore, the pattern of plaque distribution is an important factor for the pathological diagnosis of SDAT. The predominant plaque type is also different among subjects: whereas diffuse plaques are predominant in some SDAT subjects, typical plaques and amyloid angiopathy are predominant in others. This polymorphism cannot be explained by the apoE genotype. Further studies are required to understand the relationship between plaque formation and both known and yet unidentified risk factors in order to explain the polymorphism of SDAT. |
