Although Alzheimer’s disease (AD) is most commonly diagnosed after age 65, changes in the brain may begin 10 – 20 years before symptoms appear. The pathological changes in the Alzheimer’s brain include a reduction of the neurotransmitters acetylcholine, dopamine, norepinephrine, glutamate and serotonin. There is an abnormal accumulation of proteins forming amyloid plaque on the neurons, which in turn leads to inflammation, cell death, and brain atrophy. While the plaque is causing cellular death outside the cell, the subsequent development of neurofibrillary tangles of Tau protein is occurring inside the cell body of the neuron. The combination of these events is what causes the loss of the ability of the neurons to communicate with each other and which compromises the functioning of whatever neurons that individual may have left.
When Alzheimer’s disease is diagnosed in an individual before age 65 it is called Early Onset Alzheimer’s disease. Early Onset AD is generally diagnosed when individuals are in their 40s and 50s. It is thought more often to be genetic as opposed the more common age-related AD, and its progression can be more rapid.
The risk of Alzheimer’s disease doubles every five years beyond age 65. The course of the disease varies from person to person. The entire disease course typically lasts from three to 12 years, although it can be as short as one or as long as 20 years. The stages vary too, with Stage I (Early Stage) typically lasting three to five years, Stage II (Middle Stage) two to three years, and Stage III (Late Stage) one to two years. Alzheimer’s disease is a terminal illness.
The way an individual develops from infancy to adulthood, first sucking and then eating from a spoon, to walking, toileting, dressing, and developing a social personality is reversed in someone with Alzheimer’s disease. This unraveling of competency and function is commonly referred to as “retrogenesis.”