information coming into the brain. The ventricular system is a communicated system of CSF with two lateral ventricles and the more centrally located third and fourth ventricles. The human brain is made up of billions of neurons. Each neuron has a cell body with a nucleus that controls the cell’s activities, an axon, and many dendrites. The axon extends out from the cell body and transmits electrical impulses or messages to other neurons. Dendrites branch out from the cell body to receive messages from other nerve cells. Each nerve cell is connected to thousands of other nerve cells through its axon and dendrites. Neurons communicate with one another The brain in Alzheimer’s disease Serious memory loss (that impacts function), confusion, and major changes to executive functioning are not components of normal aging. They may be signs that brain cells are failing. In an effort to facilitate early diagnosis, the Alzheimer’s Association has introduced the Know the 10 Signs campaign (Alzheimer’s Association, 2018b). Ongoing issues with any of the following 10 signs may be of concern: 1. Memory loss that disrupts daily life. 2. Challenges in planning or solving problems. 3. Difficulty completing familiar tasks at home, at work, or at leisure. 4. Confusion with time or place. 5. Trouble understanding visual images and spatial relationships. 6. New problems with words in speaking or writing.
through the transmission of electrical impulses and the release of neurotransmitters. Typical aging brings structural and functional changes to the brain. There is shrinkage in brain volume and increase in ventricle size. The volume changes in the normal aging brain appear to be less related to neuronal loss and more related to shrinkage of neurons, decrease in synapses, and decreased length of myelinated axons (Fjell & Walhovd, 2010). Cognitive changes with normal, healthy aging include decreased processing speed, slower retrieval, and benign forgetfulness. 7. Misplacing things and losing the ability to retrace steps. 8. Decreased or poor judgment. 9. Withdrawal from work or social activities. 10. Changes in mood or personality. Often older adults become overly concerned when they acknowledge that they are not as “sharp” or “fast” as they used to be, or if they notice themselves struggle a bit with word finding or multitasking. It is useful to encourage older individuals to compare themselves to their age-matched peers as opposed to their younger selves when they evaluate their own cognitive abilities. This can be reassuring to individuals experiencing typical aging effects. Table 2 represents the contrast between typical and atypical (pathological) cognitive and memory changes.
Table 2: Typical Versus Atypical Cognitive and Memory Issues with Aging TYPICAL : These things are frustrating (!) but consistent with typical aging.
ATYPICAL : These things are representative of pathological cognitive changes.
Checkbook doesn’t balance to the penny.
Can’t figure out steps to balancing checkbook despite having done it monthly for decades. Can’t figure out how to replace vacuum cleaner bag despite having done it regularly for years. Ongoing confusion, indifference, or lack of awareness related to day, date, or time. Consistently and uncharacteristically require reminders and prompting to meet obligations or otherwise will miss them. Get lost trying to find the way to the neighborhood restaurant at the end of the block.
Forget to replace vacuum cleaner bag before vacuuming.
Difficulty keeping track of the day or date (because when you’re retired, every day feels the same!) Miss an appointment because had the wrong date or time. Can’t come up with the name of the new owner of the restaurant at the end of the block. Demonstrate emotional responses that are slightly exaggerated or dampened.
Demonstrate personality changes.
Note . From Western Schools, 2020.
In individuals with AD, the brain undergoes the typical changes of aging, and it also demonstrates pathological changes that impair neuronal activity and eventually destroy brain tissue. The pattern of destruction is somewhat predictable. Initially, neurons in the hippocampus, a key area of the brain involved in memory, are affected. As stated previously, amyloid plaques and neurofibrillary tangles are the pathological hallmarks of AD. Beta-amyloid is an insoluble protein fragment that is also seen to a lesser degree in the normal aging brain. It is not entirely clear whether beta-amyloid is a cause or a by-product of AD. These abnormal clusters of protein fragments build up between cells and create plaques that block cell-to-cell transmission. Neurofibrillary tangles are twisted fibers of abnormal tau protein. Tau protein is present in a normal aging brain, but it is chemically altered and present in abundance in the AD brain. Neurofibrillary tangles are present within the neuron’s microtubule transport system and inhibit the cell’s ability to import and utilize essential nutrients. Figure 2 represents these typical pathological changes in AD.
The formation of beta-amyloid plaques and neurofibrillary tangles represents a major focus of research to better understand the cause and pathology of AD. It is widely known that beta-amyloid plaques and neurofibrillary tangles are prevalent on autopsy of AD brains. When amyloid precursor protein, a normal constituent of the brain, begins to break down and the by-products combine with cellular debris, beta-amyloid plaques are formed, but many questions remain about the specifics of formation and deposition of these plaques and their impact on neurons. Neurofibrillary tangles, or bundles of twisted filaments made up of abnormal tau protein, wreak havoc on the internal structural support and transport system of nerve cells, and the study of how the tau protein becomes chemically altered is another area of focus in efforts to determine the etiology of AD. Gradual destruction of neuronal communication and death of neurons leads to a fairly predictable pattern of loss of function. Early changes in the region of the hippocampus and medial temporal lobe expand gradually. The pathological changes of the AD brain precede clinical evidence of the disease by up to
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