Alzheimer’s disease (AD) is the most common form of dementia, and worldwide affects 20–30 million individuals over 60 years of age. In 1907 Alois Alzheimer first described AD following an autopsy on the brain of a 55-year-old women who had died following progressive mental deterioration, increasing confusion, and memory loss.

Researchers from the Epidemiology and Prevention of Dementia group (EURODEM) have estimated that the prevalence increases from ~2% in the 65–69-year-old population to ~22% of those 85–89 years of age.¹ Independent of the etiological agents, on a histopathological level AD is characterized by extracellular deposition of amyloid β (Aβ) protein in senile plaques and intraneuronal accumulation of paired helical filaments (PHFs) in neurofibrillary tangles, dystrophic neurites, and neuropil threads. There is growing evidence that altered metabolism of the Aβ precursor protein (APP) with progressive deposition of its Aβ fragment is a crucial event in the pathogenesis of AD.² The fibrillar Aβ can bind the complement factor C1 and activate the classic complement pathway. The activated complement products play a key role in the recruitment and activation of microglia at the sites of fibrillar Aβ deposits.³ In turn, this activated microglia produces multiple pro-inflammatory cytokines, chemokines, and reactive oxygen species that can ultimately influence plaque and tangle formation and can lead to neuronal damage.⁴ Additionally, Aβ itself can stimulate microglia, astrocytes, and oligodendrocytes to secrete proinflammatory cytokines, chemokines, and reactive oxygen species (ROS), which can lead to neuronal damage.⁵

To read full article please click here