**1. Introduction**

582 Lipoproteins – Role in Health and Diseases

1650.

536.

neurosci., 29: 3579-3589.

Science 336: 161-162.

neuroinflammation 3: 26-33.

leukoc. biol. 84: 893-899.

Mult. scler. 13: 610-615.

Study. Eur. j. neurol. 17: 332-334.

Acta neurol. scandinav. 66:497-504.

Disorders. Mol. Neurobiol. 26: 369-388.

*Drosophila*. Proc. natl. acad. sci. USA 105: 7088-7093.

Peripheral Tissues. Mol. psychiatry 13: 1118-1128.

Aging Central Nervous System. Cell stem cell 10: 96-103.

[106] Thomas EA, Sutcliffe JG (2002) The Neurobiology of Apoliporoteins in Psichiatric

[107] Muffat J, walker DW, Benzer S (2008) Human ApoD, an Up-Regulated in Neurodegenerative Diseases, Extends Lifespan and Increases Stress Resistance in

[108] Terrise L, Poirier J, Bertrand P et al (1998) Increased Levels of Apolipoprotein D in Cerebrospinal Fluid and Hippocampus of Alzheimer's Patients. J. neurochem. 71: 1643-

[109] Digney A, Keriakous D, Scarr E et al (2005) Differential Changes in Apolipoprotein E

[110] Huang JT-J, Wang L, Prabakaran S et al (2008) Independent Protein-Profiling Studies Show a Decrease in Apolipoprotein AI Levels in Schizophrenia CSF, Brain and

[111] Zatorre RJ, Fields RD, Johansen-Berg H et al (2012) Plasticity in Gray and White: Neuroimaging Changes in Brain Structure During Learning. Nat. rev. neurosci. 15: 528-

[112] Karasinska JM, Rinninger F, Lütjohann et al (2009) Specific Loss of Brain ABCA1 Increases Brain Cholesterol Uptake and Influences Neuronal Structure and Function, J.

[113] Ruckh JM, Zhao J-W, Shadrach JL et al (2012) Rejuvenation of Regeneration in the

[114] Redmond SA, Chan JR (2012) Revitalizing Remyelination–the Answer Is Circulating.

[115] Cunnigham TJ, Yao L, Oetinger M et al (2006) Secreted Phospholipase A2 Activity in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis. J.

[116] Hesse D, Krakauer M, Lund H et al (2011) Disease Protection and Interleukin-10 Induction by Endogenous Interferon-β in Multiple Sclerosis? Eur. j. neurol. 18: 266-272. [117] Matarese G, Procaccini C, De Rosa V, (2008) The Intricate Interface Between Imuune and Metabolic Regulation: a Role for Leptin in the Pathogenesis of Multiple Sclerosis? J.

[118] Hietaharju A, Kuusisto H, Nieminen R et al (2010) Elevated Cerebrospinal Fluid Adiponectin and Adipsin Levels in Patients with Multiple Sclerosis: a Finnish Co-Twin

[119] Sena A, Couderc R, Vasconcelos JC et al (2012) Oral Contraceptive Use and Clinical

[120] Neu IS, Prosiegel M, Pfaffenrath V (1982) Platelet Aggregation and Multiple Sclerosis.

[121] Hawkes CH, (2007) Smoking is a Risk Factor for Multiple Sclerosis: a metanalysis.

Outcomes in Patients with Multiple Sclerosis. J. neurol. sci. 317(1-2): 47-51.

in Schizophrenia and Bipolar I Disorder. Biol. Psychiatry 57: 711-715.

Stroke is the leading cause of neurological disability and among the leading causes of death worldwide. It is a focal neurological deficit that results from events that decrease or stop cerebral blood flow. As the consequence neurons cease functioning and irreversible neuronal ischemia and injury occur.

Broadly, strokes are classified into two main types-ischemic and hemorrhagic. Ischemic stroke (IS) is characterized by blockage in blood flow to a focal area of the brain, until hemorrhagic stroke is caused by bleeding into the brain. Acute IS is more common than hemorrhagic stroke. Although according the previous literature data about 80% of strokes were ischemic, the retrospective review from a stroke center found that about 60% were ischemic 1. Except their causes and pathophysiology ischemic and hemorrhagic types differ in their treatments and outcomes 2.

Based on the system of categorizing stroke developed in multicenter Trial of Org 10172 in Acute Stroke Treatment (TOAST), IS may be divided into the following major subtypes: large artery infarction, small-vessel (lacunar) infarction, and cardioembolic infarction. This classification on the basis of inferred origin of cerebrovascular occlusion 3 is the most frequently used. Other studies used systems based on clinical presentation or location and size of the lesion within the brain (such as the Oxfordshire Community Stroke Project system) 4. It classifies patients in five infarct types: cerebral infarction, lacunar infarct, total anterior circulation infarct, partial anterior circulation infarct, and posterior circulation infarcts. Many other classifications have been proposed, such as those from the Lausanne Stroke Registry and the Étude du profil Génétique de l'Infarctus Cérébral (GÉNIC) study 5,6. The first one included atherosclerosis with stenosis, atherosclerosis without stenosis,

© 2012 Stankovic et al., licensee InTech. This is an open access chapter distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2012 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

emboligenic heart disease, hypertensive arteriopathy, cerebrall hemorrhage, mixed causes and undetermined causes. The former included atherothrombotic stroke, cardioembolic stroke, lacunar stroke, arterial dissection, unknown causes stroke. Although stroke is often considered a disease of elderly persons, one third of strokes occur in persons younger than 65 years.

Risk factors for IS includes modifiable and non-modifiable etiologies. Non-modifiable risk factors include: age, sex, race, ethnicity, heredity, etc. Modifiable risk factors include the followings: hypertension, diabetes mellitus, hypercholesterolemia, atrial fibrillation, lifestyle factors, etc. Unfortunately, modifiable risk factors accounts for only approximately 60% of the population-attributable risk for stroke 7.
