Recent years have brought major advances in understanding the fundamental changes in the brain that lead to Alzheimer's disease. The human brain is made up of billions of nerve cells called neurons, which share information with one another through a complex array of connections. Each neuron has a cell body and multiple branches that interconnect at structures called synapses. The brain can tolerate some loss because of its inherent redundancy and natural repair mechanisms, but beyond a certain point dysfunction begins to set in. In Alzheimer's disease, communication between nerve cells involved in higher cognitive functioning breaks down.
Neurons become dysfunctional, lose connections with other nerve cells and degenerate.
Ironically, the nerve cells in brain circuits that serve learning and memory and higher cognitive functions are the most vulnerable to Alzheimer's disease. Many believe that those cells that are the most sensitive and sophisticated for encoding change also are the most vulnerable. The final pathological signatures in the Alzheimer's-diseased brain are synaptic loss, neuronal death, and the formation of neuronal tangles and senile plaques. Over the last several years, much new and exciting research has led to a better understanding of the reasons that these changes occur. The signature of tangles and plaques in the Alzheimer's disease brain was first observed by Alois Alzheimer in 1907.