Many parts of your body change as you age. Your bones become more brittle as the production of bone-building osteoclasts slows.
Vision becomes diminished as your eyes weaken. Your skin loses its elasticity and wrinkles more easily.
Over time, your brain changes as well. Nerve cells, unlike other cells of our body, have limited capacities to regenerate. Those that exist may shrink in size. Synapses that allow for proper communication between cells may disappear, and certain neurotransmitters become blocked. The brain shrinks in size. All these changes may diminish your ability to learn new tasks, as your short-term memory becomes less capable of storing infor¬mation. You may have a harder time paying attention. In addition, you may notice that you are less coordinated, less balanced, and more clumsy.
Though you may be horrified by your inability to recall details or to learn new skills, none of these diminished abilities are life-threatening. In fact, all these changes are normal. What occurs in Alzheimer’s disease however, is not a normal part of the aging process.
The Brain With Alzheimer’s
In people who have Alzheimer’s, the neurons become disabled. For starters, Alzheimer’s interferes with the neuron’s ability to produce the energy they need to do their work, a process known as metabolism. Neurons derive energy from oxygen and glucose— a sugar found in your blood—which is made available through the bloodstream. Without this energy, neurons can no longer com¬municate with one another and carry impulses to other neurons. They also lose the ability to repair themselves, which ultimately causes them to die.
Exactly what interferes with the functioning of the neurons is unclear, and the rate at which the disease progresses also varies a great deal. But the brains of all people with Alzheimer’s do share some common characteristics. Whether these changes in the brainare the cause of Alzheimer’s or the result of the disease remains a mystery, but these are two common traits:
Beta Amyloid Plaques
Tucked in the spaces between neurons are thick, sticky deposits of plaque, made up primarily of a substance called beta amyloid. The plaque also contains other proteins, neuron remnants, and immune cells known as microglia, which surround and digest damaged cells or foreign substances that cause inflammation.
Beta amyloid is a protein fragment that has been snipped from a larger protein called aymloid precursor protein (APP), a substance believed to play a role in the growth and survival of neurons. APP rests partly inside a cell and partly outside of it. The part on the out¬side of the cell is then clipped by any of three different enzymes, substances that speed up or cause a chemical reaction. Most of the resulting segments are soluble, or dissolvable, but some, namely the beta amyloid protein fragments are less soluble and stickier.
As their numbers increase, these fragments cluster together into larger fragments called oligomers. When the oligomers come together, they become even less soluble and form insoluble fibrillar beta-amyloid aggregates. Over time, the fibrillar amyloid congeals into the insoluble plaques that characterize the Alzheimer’s brain.
Another defining characteristic of the Alzheimer’s brain is the neurofibrillary tangle. Inside the neurons are proteins known simply as tau, which help give neurons their structure by binding to microtubules in the cell. Like support beams in a building, tau holds up these microtubules, which allows them to perform the essential tasks of guiding nutrients and molecules through the cell.
In a person with Alzheimer’s, tau undergoes a chemical change. It breaks down, causing the microtubules to disintegrate and the cell structure to collapse. Rather than bind to microtubules, tau binds to other threads of tau, creating neurofibrillary tangles. At first, it’s believed, these tangles may cause poor communication among nerve cells. Later on, they cause the cells to die.