**Part 1**

**Role of Immune System in Acute and Chronic Inflammatory Diseases** 

**1** 

*Rajasthan* 

**Dementia – A Complete Literature** 

Sidharth Mehan\*, Rimpi Arora, Vandana Sehgal,

 Deepak Sharma and Garuav Sharma *Research & Development, SHPL, Jodhpur,* 

**Review on Various Mechanisms Involves in** 

 **Pathogenesis and an Intracerebroventricular** 

**Streptozotocin Induced Alzheimer's Disease** 

Dementia is a brain disorder characterized by a decline in several higher mental functions (e.g. memory, intellect, personality) that causes significant impairments in daily functioning (Kuljis, 2007)*.* The prevalence of dementia rises with age, doubling every 5 years between the ages of 60 and 90 (Corrada et al., 2008). Based on the epidemiological data, dementia is widely recognized as a major medical, social and economic problem in developed countries where the age over 65 accounts for an increasingly high percentage of the dementic population (Breitner et al., 2009). Unfortunately, dementia is now becoming a major problem in developing countries where it did not exist 50 years ago (Zilkens et al., 2009). More than 50 million people worldwide have dementia and the most common and irreversible cause of this dementia is Alzheimer's disease (AD) (Adlard et al., 2009). AD is a neurodegenerative disorder divided into two forms namely familial (FAD) and sporadic (SAD) cases characterized by cognitive deficits and extensive neuronal loss in the central nervous system (CNS) (Michon et al., 2009; Reed et al., 2009) and at the molecular level by the presence of specific cytoskeletal abnormalities, including intracellular neurofibrillary tangles (NFT) formed by hyperphosphorylated tau protein and the presence of high levels of the 40- and 42-amino acid long amyloid beta (A) (Woodhouse et al., 2009). The early onset form (i.e. FAD) has a strong genetic correlation that exists between characteristic features of AD pathogenesis and mutations in amyloid precursor protein (APP), (Bernardi et al., 2009), presenilin (PS-1) and PS-2 (Huang et al., 2009). Of particular interest, the other form of AD, SAD is a multifactorial disease to which both genetic and epigenetic factors contribute (Zawia et al., 2009). The well confirmed genetic factors for SAD are apolipoprotein E (APOE) epsilon 4 allele (Wharton et al., 2009) and PS-2 promoter polymorphism (Liu et al., 2008). Accumulating data indicates that disturbances of several aspects of cellular metabolism appear pathologically important in SAD. Among these, increased brain insulin resistance (Salkovic-Petrisic, 2008), decreased glucose utilization and energy metabolism are observed in the early stages of the disease (De la Torre, 2008),

**1. Introduction** 

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Corresponding Author
