**Risk Factors for Alzheimer's Disease**

Dongming Cai and Farida El Gaamouch

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/64270

#### **Abstract**

[167] Orta‐Salazar E, Aguilar‐Vázquez A, Martínez‐Coria H, Luquín‐De Anda S, Rivera‐ Cervantes S, Beas‐Zarate C, Feria‐Velasco A, Diaz Cintra S. REST/NRSF‐induced changes of ChAT protein expression in the neocortex and hippocampus of the 3xTg‐ AD mouse model for Alzheimer's disease. Life Sci. 2014;116:83–89. DOI: 10.1016 / j.lfs.

[168] Boissie F, Faucheux B, Agid Y, Hirsch EC. Choline acetyltransferase mRNA expression in the striatal neurons of patients with Alzheimer 's disease. Neurosci Lett.

[169] Orta‐Salazar E, Feria‐Velasco A, Medina‐Aguirre G, Morphological analysis of the hippocampal region associated with an innate behaviour task in the transgenic mouse model (3xTg‐AD) for Alzheimer disease. Neurologia. 2013;28:497–502. DOI: 10.1016/

[170] Ruehl WW, Bruyette DS, DePaoli A, Cotman CW, Head E, Milgram NW, Cummings BJ. Canine cognitive dysfunction as a model for human age‐related cognitive decline, dementia and Alzheimer's disease: clinical presentation, cognitive testing, pathology

[171] Ardiles AO, Tapia‐Rojas CC, Mandal M, Alexandre F, Kirkwood A, Inestrosa NC, Palacios AG. Postsynaptic dysfunction is associated with spatial and object recognition memory loss in a natural model of Alzheimer's disease. Proc Natl Acad Sci USA.

[172] Sparks DL, Schreurs BG. Trace amounts of copper in water induce beta‐amyloid plaques and learning deficits in a rabbit model of Alzheimers's disease. Proc Natl Acad

[173] Miklossy J, McGeer PL. Common mechanisms involved in Alzheimer's disease and type 2 diabetes: a key role of chronic bacterial infection and inflammation. Aging

[174] Duff, F. Suleman F. Transgenic mouse models of Alzheimer's disease: how useful have they been for therapeutic development? Brief Funct Genomic Proteomic. 2004;3: 47–59.

and response to 1‐deprenyl therapy. Prog Brain Res. 1995;106:217–225.

2012;109:13835–13840. DOI:10.1073/pnas.1201209109.

(Albany NY) 2016; 8:575-88. DOI: 10.18632/aging.100921..

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Re‐ trieve&db=PubMed&dopt=Citation&list\_uids=15163359.

Sci USA. 2003;100:11065‐11069.

2014.09.013

224 Update on Dementia

1997;225:169–172.

j.nrl.2013.01.014.

Alzheimer's disease (AD) is the most common form of dementia in the elderly. Currently there is no effective treatment available. Senile plaques and neurofibrillary tangles are hallmarks of AD pathology, and patients demonstrate cognitive com‐ plaints with deficits in various neuropsychological domains. Familial AD (FAD) accounts for 0.5% of all AD cases and usually presents before the age of 65 years. Approximately 50% of the FAD patients carry mutations in one of the following genes: APP, PSEN1, and PSEN2. Inheriting any of these genetic mutations increases Aβ<sup>42</sup> production, which has been linked to AD pathogenesis. Late-onset AD represents the majority of AD cases, with evidence suggesting impaired Aβ clearance. However, the etiology of late-onset AD is more complex. Several findings suggest that multiple risk genes and factors may contribute to the pathogenesis of LOAD. In this chapter, we elaborate some of these factors and their involvements in the development of AD.

**Keywords:** Alzheimer's disease, risk genes, risk factors
