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Alzheimer’s disease (AD) is a chronic neurodegenerative disorder that primarily disturbs cognitive and memory functions of elderly people. Amyloid beta (Aβ) protein deposits and neurofibrillary tangles in brain parenchyma with additional brain atrophy as a consequence of massive loss of neurons are key pathological features of this disease. Chronic neuroinflammation also plays a very important role in progression of AD. Microgliosis, astrogliosis, overexpression of cytokines and chemokines are notable features of ongoing neuroinflammatory processes. Innate and cellular arms of immune system play a very decisive role in shaping the progression of AD neuropathology. Such innate or cellular immune responses can either be detrimental or beneficial. Nuclear factor kappa B (NFκB) family transcription factors regulate both immune as well as neuroinflammatory functions in many pathophysiological conditions. Taming detrimental neuroinflammation while harnessing benefits of own immune activation is a promising avenue for current therapeutic strategies. Immunomodulation by genetic and pharmacological agents is a good experimental tool to understand the role of neuroinflammation in AD pathogenesis. Our present thesis is a combination of two experimental studies that were designed to study the role of neuroinflammation in AD pathogenesis. In both studies we employed APPswe/PS1dE9 transgenic mice as an animal model of AD. In our first study, we used a clinically well-known anti-inflammatory and immunomodulator known as human polyclonal intravenous immunoglobulin (hIVIG). We treated young and aged APP/PS1mice with …