Healthy living habits such as diet, improved sleep hygiene, participation in physical exercise, social connection, and stimulating brain activities can significantly impact quality of life, especially for those who have genetic or other predispositions to any type of dementia. It is important to note that it is never too late to implement lifestyle changes to modify disease progression. Self-Assessment Quiz Question #4 What is true about the plaques and tangles that present in the AD brain? a. Plaques and tangles will go away with proper hygiene. b. Plaques and tangles develop 15–20 years prior to an AD diagnosis. c. Plaques and tangles are in the spine. d. Plaques and tangles develop immediately after carbon dioxide exposure. Alzheimer’s disease is named after German psychiatrist Dr. Alois Alzheimer, who published the first case of the illness, initially called presenile dementia. He recognized that the disease stemmed from the cerebral cortex after studying the brain of a diseased patient who had struggled with memory loss and cognitive decline resulting in complete loss of According to the Alzheimer’s Association, up to 5% of all people with AD develop this type, and patients with Down syndrome have a higher risk. While these patients share the same symptoms as individuals with late-onset AD, they may also have accompanying muscle twitching and spasms, known as myoclonus. This type of AD is thought to be linked to defective DNA on chromosome 14. These patients also experience a greater loss of brain volume, as well as brain changes related to plaque development and expanded tangles (Rhagavan et al., 2018). Early-onset typically occurs when people are in their 40s or 50s. Gene mutations potentially correlated to early-onset AD are: • Amyloid precursor protein (APP) on chromosome 21 • Presenilin 1 (PSEN1) on chromosome 14 • Presenilin 2 (PSEN2) on chromosome 1 Late-Onset Alzheimer’s Disease Late-onset AD is most common in people older than age 65 (Mayo Clinic, 2022). People with this form are diagnosed by neurological testing, scans, and physical examination, but the confirmation of the disease can occur only postmortem. (Scans can show the presence of plaque and tangles.) There may not be a genetic component to late-onset AD but having the genetic variant of the apolipoprotein E (APOE) gene on chromosome 19 can be an indicator of risk. The APOE gene is involved in the composition of the protein that helps to deliver cholesterol and other fats throughout the bloodstream. Each person receives one APOE allele from each biological parent, for a total of two. • APOE e2 is the least common and very rare and may provide some protection against AD. • APOE e3 is the most common of these alleles and does not seem to impact the risk of AD. • APOE e4 is more common, and about 25% of people carry one copy of this allele that appears to increase the risk of AD; About 2%–3% of people carry two copies of APOE e4. Genetic research may offer insight into who may be predisposed to AD. For people who may carry any of the genes that can be correlated to AD, early lifestyle changes can be important to allay development of the disease. Table 1 discusses genes that are being researched as potential connectors to all forms of AD. Classification of Alzheimer’s disease Early-Onset Alzheimer’s Disease
independence. Dr. Alzheimer noted the presence of amyloid plaques and a diminished number of neurons in this brain. He shared his findings in an article read by his colleague Dr. Emil Kraeplin, considered the founder of modern psychiatry and psychiatric genetics. When Kraeplin wrote the eighth edition of his psychiatry handbook, he referred to this disease as Alzheimer’s disease. It was characterized by memory loss, as well as specific behavior and personality changes that rendered the person unable to perform activities of daily living (Breijyeh & Karaman, 2020). AD is traumatic for all involved, impacting the person as well as their loved ones. In 2022 it is estimated that over 6.2 million people in the U.S are afflicted (Young Shin & Habermann, 2022). The prevalence of AD and other dementias is expected to increase as society ages. As AD progression causes cognitive and physical health diminishment, the person will need care support. In 2020 U.S. dementia patients benefited from more than 11 million unpaid caregivers, for an estimated total of 15.3 billion hours, costing approximately $257 billion (Alzheimer’s Association, 2021). Understanding the cause of AD and other dementias is for the betterment of public health. While one day there may be a cure, today people need to manage and improve symptoms.
Table 1. Potential Gene Connectors Gene Description ABCA7
Linked to greater risk according to the delivery of cholesterol through the blood system Helps with the clearance of amyloid-beta from the brain The complement component receptor gene that has been identified as one of the top risks for developing AD
CLU
CR1
PICALM
Linked to communication between neurons
PLD3
Coding variant of this gene could be linked to an increase in AD Directly involved in the brain’s response to addressing inflammation AD patients carrying this mutated gene had increased risk of developing the disease seven years earlier than noncarriers
TREM2
SORL1
Note: Adapted from Raghavan et al., 2018 It is important for the appropriate people to participate in clinical research trials. Children of parents who have had early-onset AD may want to learn about clinical research trials, if available. Additionally, although genetic testing is not typically recommended for late-onset AD, testing for early-onset AD may open the door to therapeutic drug trials for people who meet the criteria. Some clinical research trials are exploring genetic correlations for AD and other dementias. Participation in these studies is also crucial to explore cures and treatments. Opportunities to participate in clinical trials can be found at Find Clinical Trials (alzheimers.gov).
Book Code: SWUS1525
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