By Suzanne De La Monte
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Extra info for Alzheimer’s Disease Pathogenesis-Core Concepts, Shifting Paradigms and Therapeutic Targets
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Glenner GG & Wong CW (1984) Alzheimer’s disease and Down’s syndrome: Sharing of a unique cerebrovascular amyloid fibril protein. Biochemical and Biophysical Research Communications. 12:1131-1135. Guillozet AL, Weintraub S, Mash DC & Mesulam MM (2003) Neurofibrillary tangles, amyloid and memory in aging and mild cognitive impairment. Arch Neurol. 60:729-736. Haass C & Selkoe DJ (2007) Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer’s amyloid beta-peptide. Nat. Mol. Cell Biol.
5, no. 3, p. 409-414. 2 Pathophysiology of Late Onset Alzheimer Disease Ahmet Turan Isik1 and M. Refik Mas2 1Bezmialem Vakif University, Faculty of Medicine, Department of Geriatric Medicine, Istanbul, 29 Eylul University, Faculty of Medicine, Department of Internal Medicine, Izmir Turkey 1. Introduction As the world population has aged, the number of people affected by Alzheimer Disease is rapidly increasing in the world. It is important for clinicians to recognize early signs and symptoms of dementia and to note potentially modifiable risk factors and early disease markers.
Some researchers have paid attention to low levels of vitamin B complex and the plasma elevation of homocysteine, as being responsible for age-related cognitive deficits and unleashing the AD pathology (Cuello, 2007). , 2010). While early onset AD is almost genetically based, there are no specific gene mutations that are associated with inheritance of the disease in late onset AD (LOAD). The expression of the apolipoprotein E (ApoE) 4 allele is one of the risk factors identified for LOAD. In the central nervous system, ApoE is synthesized by astrocytes, microglia, and, to a lesser extent, by neurons.