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. 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.
Checkbook doesn’t balance to the penny.
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.
Figure 2: Alzheimer’s Pathology at the Level of the Neuron
a. Beta-amyloid plaques block neuron-to-neuron transmission.
b. Neurofibrillary tangles impair the neuron’s microtubule transport system.
Note . Figure (a) from Alzheimer’s Association (2014). Alzheimer’s disease and dementia. Retrieved from http://www.alz.org. Jannis Productions. Rebekah Fredenburg, computer animation; Stacy Jannis, ullustration/art direction. Reprinted with permission. Figure (b) by William Rosenblum.
stay the clinical course of the disease. Researchers continue to try to correlate the neuropathological cascade of events with the clinical appearance of AD. This antecedent stage may be identifiable by biological markers (biomarkers) that portend the progression of the pathological process into the initial clinical stages of the disease. Biomarkers are identified through CSF and/or imaging studies (i.e., MRI, positron-emitting tomography [PET] scan) and currently, the National Institute on Aging (NIA) and the Alzheimer’s Association (AA) are refining the definition of “Alzheimer’s Disease” to refer to the presence of biomarkers as opposed to the presence of dementia in an effort to support a common language for Alzheimer’s research efforts (Jack et al., 2018). Whereas “Alzheimer’s disease” previously suggested the presence of dementia, the current language suggestion from NIA/AA is that the term “Alzheimer’s dementia” be used in place of Alzheimer’s disease when dementia is present and that the term Alzheimer’s disease be used when discussing pathology or the continuum of the disease (Alzheimer’s Association, 2018a). The intent is to allow researchers to have a common language for the preclinical stages of the disease; whereas in the clinical realm, this could be considered an issue of semantics only, thus, this course utilizes “AD” to indicate both Alzheimer’s disease and Alzheimer’s dementia.
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 20 years. This preclinical phase is important to researchers as an opportunity to determine therapeutic interventions that may
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