**Author details**

lipids. Alterations in the metabolism of the phospholipids phosphatidylcholine (PC) have been detected in the cerebrospinal fluid of AD patients [115]. Neural membrane glycero‐ phospholipids, particularly ethanolamine plasmalogens, are markedly decreased in au‐ topsy samples from AD brain compared to age-matched control brain [116]. This decrease in glycerophospholipids is accompanied by a marked elevation in phospholipid degradation metabolites such as glycerophosphocholine, phosphocholine, and phosphoe‐ thanolamine [117]. Furthermore, marked increases have been reported in levels of prosta‐ glandins and lipid peroxides in AD brain [118,119]. The marked changes observed in phospholipids and their catabolic products may be coupled to the elevated activities of lipolytic enzymes in AD brain [120]. Moreover, cortices of AD patients have decreased levels of PC and phosphatidylethanolamine, compared with age-matched controls [116]. PC synthesis is regulated by levels of its precursors [113,114]; therefore, stimulation of PC synthesis by increasing precursor levels prevents the disruption in normal phospholi‐ pid metabolism caused by AD. Furthermore, increasing cell membrane synthesis may have morphological consequences for the cell. For instance, dendritic atrophy and loss occur in mouse models of AD [121,122] and dystrophic neurites are observed in human

Data from a series of biochemical, genetic, epidemiological studies and others exhibited that cholesterol is a key factor in APP processing and Aβ production. For instance, high cholesterol levels are linked to increased Aβ generation and deposition. It appears that there are many different ways in which abnormalities in cholesterol metabolism can af‐ fect the development of AD. Some polymorphisms in genes involved in cholesterol ca‐ tabolism and transport have been associated with an increased level of Aβ and are therefore potential risk factors for the disease. The best known of these genes is apoE4, which is the major genetic risk factor known for late-onset AD. Other genes implicated include cholesterol 24-hydroxylase (Cyp46), the LDL receptor related protein, the choles‐ terol transporter ABCA1, acyl-CoA:cholesterol acetyl transferase, and the LDL receptor. Then, we may conclude that what is bad for the heart is bad for the brain. We must pay attention to risk factors associated with heart disease to prevent Alzheimer's disease also. Considerable interest has also arisen regarding the effects of lifestyle interventions such

We dedicate this paper to Dr. Pedro Garzón de la Mora; who was for some of us a guide,

and showed us to lose ourselves in the wonderful jungle of Biochemistry.

cases of AD [123]

162 Understanding Alzheimer's Disease

**8. Concluding remarks**

**Acknowledgements**

as exercise and dietary/nutriceutical manipulations.

Genaro G. Ortiz1\*, Fermín P. Pacheco-Moisés2 , Luis J. Flores-Alvarado3 , Miguel A. Macías-Islas4 , Irma E. Velázquez-Brizuela5 , Ana C. Ramírez-Anguiano2 , Erandis D. Tórres-Sánchez1 , Eddic W. Moráles-Sánchez1 , José A. Cruz-Ramos1 , Genaro E Ortiz-Velázquez1 and Fernando Cortés-Enríquez1

\*Address all correspondence to: genarogabriel@yahoo.com

1 Lab. Estrés Oxidativo-Mitocondria & Enfermedad, Centro de Investigación Biomédica de Occidente. Instituto Mexicano del Seguro Social (IMSS). Guadalajara, Jalisco, México

2 Dpto. de Química. CUCEI, Universidad de Guadalajara. Guadalajara, Jalisco, México

3 Dpto. de Bioquímica. CUCS, Universidad de Guadalajara. Guadalajara, Jalisco, México

4 Depto. de Neurología. UMAE,HE- IMSS. Guadalajara, Jalisco, México

5 OPD-IJC-SSA- Jalisco. Guadalajara, Jalisco, México
