ABSTRACT
During the past decade it has become evident that immunological, infl ammatory and vascular processes play an important role in the etiology and pathogenesis of various neuro-degenerative diseases. Alzheimer’s disease (AD) is a complex and genetically heterogeneous disease that is the most common form of dementia and aff ects up to 15 million individuals worldwide. Th e presenting pathology of AD includes extacellular neuritic plaques composed of beta-amyloid peptide (Aβ) and intracellular neurofi brillary tangles composed of hyperphosphorylated tau, with neuronal loss in specifi c brain regions. A large body of evidence suggests that some form(s) of the polymorphic Aβ are neurotoxic and induce neuronal death, tau hyperphosphorylation and neuronal death. However, the mechanisms underlying these pathological changes are still largely unknown. Th e early stages of symptomatic AD are characterized by memory impairment and subtle behavioral changes that are associated with changes in synaptic function. Th e loss of synapses strongly correlates with cognitive decline in AD and is now thought to result from the interactions of toxic forms of Aβ peptide with molecules that are essential for neuronal integrity and synaptic connections. A combination of cell culture and animal studies has recently shown that adhesion molecules play important roles in synapse initiation, maturation, and function. Functional studies of individual adhesion molecules have begun to provide information on their role in synapse assembly and synaptic plasticity. In this chapter, we review the roles of diff erent
families of adhesion molecules, including the immunoglobulins, integrins, cadherins and selectins, in normal brain and in dementia, particularly Alzheimer’s disease.
