In the beginning of this year, a research paper was published in The Journal of the American

Alzheimer disease (AD) is the most common cause of dementia in the elderly, accounting for 65–70% of all cases (Jellinger, Janetzky, Attems, & Kienzl, 2008). The other dementias are of the Parkinson 's group, the fronto-temporal group and the vascular group. The total worldwide yearly costs for the treatment and care of patients suffering from dementia are estimated to be around 250 billion US dollars. The lifetime risk for AD between the ages of 65 and 100 is 33% for men and 45% for women with an annual increase of 1–2% in the seventh decade to almost 60% in the 10th decade with doubling every 5 years (Jellinger et al., 2008). AD is incurable, and thus represents a major public health problem. AD represents a challenge to humanity due to its relatively recent discovery, progressive nature of the illness, and complex diagnosis.

Alzheimer’s Disease has been one of the top leading causes of death in our country. It is understood that this disease is identified as an excess of the protein amyloid-ß within an increase of plaque (Seneff, Wainwright, and Mascitelli, 2010). Additionally, as the brain ages, it gets used to the inflammation and oxidative stress, so it is important to take the right amount of antioxidant micronutrients like vitamin C and vitamin E as well as anti-inflammatory macronutrients such as omega-3 polyunsaturated fatty acids to protect the brain from ageing (Whalley et. al, 2004). This is a devastating disease that affects most people over the age of fifty. Recently, there have been many studies done to figure out what causes this disease, if there is anything that can cure it, and how to prevent the disease. Seneff, Wainwright, and Mascitelli, believe Alzheimer’s develops with consuming too many carbohydrates, especially fructose and having a deficiency in cholesterol and dietary fats as well (2010). Whalley, Starr, and Deary have seen that poor diet, poverty, and failing health are links to developing Alzheimer’s Disease (2004). Furthermore, seeing increase in plasma homocysteine concentration increases risk of Dementia, which can result from an inadequate intake of vitamin B12/folate (Walley et. al, 2004). Additionally, Gray supports Walley’s findings and even believes having an adequate intake of vitamin B12/folate will have a positive effect on the overall health

The FDA recently has allowed two treatments to be used for Alzheimer patients. One of the treatments is a Partial Glutamate Antagonist, which is an important transmitter to the brain. It is said that Glutamate helps patients more than sugar pills do, however; it is said that too much

Some other researchers are trying to determine the possible roles of cholesterol metabolism, oxidative stress (chemical reactions that can damage proteins, DNA, and lipids inside cells), estrogen, vitamin E, and microglia in the development of AD. Scientists also are investigating the role of aging – related proteins (Florida Health Care Association 2005).

Curcumin has been proven to help recover from neurodegenerative diseases, even aiding in their prevention, and inhibiting inflammatory molecules in the brain (Petraglia, et al., 2011, p.4). Foods high in curcumin include Indian curries, yellow rice flavored with turmeric, and mustard (Curinga 1). Caffeine, although showing mixed results in some studies, shows reductions in neurological deficits (Petraglia, et al., 2011, p.8). One of the best high caffeine options is green tea at a recommended three cups per day (Maroon, et al., 2011, p.6). As seen in some research on green tea, the result of its high consumption in Asian countries leads to the “Asian paradox,” or the significant prevention of neurological problems in Asia (ibid). Vitamin E in nuts, seeds, vegetable oils, and cereals has been tested to show improved cognitive performance, improved spatial memory, and less neuropathology (Petraglia, et al., 2011, p.9). Vitamin E intake is improved in conjunction with Vitamin C (ibid). Foods high in Vitamin C include citrus fruits, tomato juice, and potatoes (“Office of Dietary Supplements – Vitamin C,” 2016, p.2). Finally, Omega 3 has been consistently shown to help in recovery from PCS and inflammation (Maroon, 2011, p.1). They are the most effective natural anti-inflammatory food and has been tested to be neurotherapeutic for PCS (Maroon et al., 2010,

Alzheimer’s disease (AD) is a progressive and fatal form of dementia, frequently seen in the elderly altering their cognition, thought process and behavior. AD is reported in about half of patients that have a dementia diagnosis; one study states that about 10.3% of the population over 65 years is affected by dementia with an increase to almost 50% over the age of 8 (Beattie, 2002). Alzheimer’s disease is not a normal part of the aging process in humans, but rather found in a group of diseases that affect the brain leading to a decline in mental and physical control. AD when diagnosed has a very slow and gradual course, initially affecting the individual’s short term memory (Beattie, 2002). Alzheimer’s disease is the 6th leading cause of death, affecting more than five million people in the United States and is also one of the most common forms of dementia. Dementia can be defined as a disorder of progressive cognitive impairment severe enough to affect daily functions of an individual’s life (Fillit, et al., 2002).

Although Alzheimer’s Disease (AD) is the most widely known cause of dementia in the elderly population, there are many other explanations and clinical diagnoses that

Factors that are not preventable include family history, heredity, and age. Risks for eFAD include head trauma, and head to head connections. To help cope with the deteriorating disease, it is important for a nutritious diet as well as physical activity, social engagement, and mentally stimulating activities. Healthy diet helps ensure a healthy brain and heart which helps protect the body. Regular exercise is also important, this increases oxygen and blood flow which benefits cardiovascular system. Treatment for eFAD includes helping to maintain mental function and manage behavioral system. Medications that are used to comfort systems include Donepezil, Rivastigmine, and Galantamine used to treat mild to moderate Alzheimer’s. Targets for future drugs include Beta Amyloid (main components for plaque), and Tau proteins (main component in tangles.) Other hopes for drugs and therapies include the targeting of the overall inflammatory response as well as therapies to target specific areas of genetic, molecular, and cellular

AD is a progressive age-related neurodegenerative disorder that poses increasing challenges to the global healthcare system and economic development. AD is characterized by extracellular neurotic plaques composed of Aβ deposits and intracellular neurofibrillary tangles composed of hyperphosphorylated tau with progressive loss of synapses in the brain [1]. Evidence demonstrates a potential link between oxidative stress, mitochondrial dysfunction and AD development [2]. Oxidative damage has been known to occur at a very early stage of AD even prior to Aβ plaque formation and the onset of symptoms [3, 4, 5]. Several cellular changes by oxidative stresses have been related with Aβ plaques formation and pathophysiological events of AD [6].

You are the nurse doing home visits in a retirement community. Your patient is an 85-year-old male who has been diagnosed with AD. His adult children are with him for the visit. They want to know about the disease and what treatment options exist. They ask the following questions:

As previously discussed, the cause of AD is not well understood, which makes the diagnosis of AD more difficult as there is not one biological marker (Atchison & Dirette, 2012). AD is diagnosed by eliminating other conditions that display similar symptoms, such as Parkinson’s disease or cardiovascular disease (Atchison & Dirette, 2012). Once other conditions are ruled out, diagnostic tools such as magnetic resonance volumetry, magnetic resonance spectroscopy, diffusion-tensor imaging, cerebrospinal fluid assays, positron emission tomography, and electroencephalography can be used to detect some of the brain abnormalities that are characteristic of AD (Atchison & Dirette, 2012). These diagnostic tools are not always the most accurate, and there is not a demand for better diagnostic tools due to the lack of effective treatment options following an AD diagnosis (Atchison & Dirette, 2012).

New studies have been released that had an adequate control group that demonstrated multivitamins are crucial to maintaining short-term memory. This can help delay the onset of Alzheimer's disease. Those who value recognizing the faces of friends and family members will undoubtedly find benefit in taking a multivitamin.

Prior to advances in imaging, the primary means of diagnosing AD is from the patient history and cognitive impairment testing (Long, Chen, Jiang, & Zhang, 2017). Interviews with the family members and caregivers are part of the assessment (Long et al., 2017). The diagnosis based on neuropsychological scale is subjective and less repeatable and a rich clinical experience of physicians is required (Long et al., 2017). The presence of neurofibrillary tangle, plaque buildup and tissue loss in the brain parenchyma indicates the progressive degenerative nature of AD (Long et al., 2017). Early detection of the disease is crucial in the patient management (Long et al., 2017). Short-term memory loss and paranoia are the earliest symptoms

In the next stages of AD, more genitive damage is evident as well as problems with expression, emotion, language, and reasoning. In the middle stages of AD patients have trouble identifying people they know, they are unable to learn new things, and they are very uninhibited. The final stages are significantly different form the beginning and middle stages. In the final stage a person’s body begins to

We are the first team in the world to study the hypo-NMDA theory of Alzheimer's disease in clinical studies. We found that sodium benzoate, the NMDA enhancer (a D-amino acid oxidase [DAO] inhibitor) can significantly improve the cognitive abilities of the early patients with Alzheimer's disease (Lin and Lane et al, Biol Psychiatry 2014), which indicates that hypo-NMDA or hyper-DAO may play an important role in early treatment of Alzheimer's