The Importance of Routine Psychometric Testing for Mild Cognitive Impairment in Geriatric Populations

The National Institute on Aging and Alzheimer’s Association (NIA-AA) defines Alzheimer’s Disease (AD) as a progressive disease with three stages, an asymptomatic pre-clinical stage, mild cognitive impairment (MCI), and Alzheimer’s dementia. In AD, there is an accumulation of β-amyloid protein at neuronal synapses, eventually leading to synaptic failure and neuronal death. Intracellularly, tau proteins accumulate which inhibit the transport of nutrients and other essential molecules, hastening the process the cell death. Initially the patient is able to compensate for the neuronal changes and shows no cognitive decline. Eventually, basic bodily functions such as swallowing are impaired. Patients will ultimately become bed-ridden, and will typically die from external factors such as pneumonia and infected pressure ulcers. The time of disease progression is highly variable among individuals.

MCI is an intermediate stage between the cognitive decline of normal aging and dementia. MCI will often, but not always, progress to dementia. Causes of MCI include neurodegenerative disease, medications, depression, vascular problems, and other disease processes. The cognitive deficit of MCI may not interfere with a patient’s ability to function independently. Patients will often attribute the subtle symptoms to aging or stress. The revised Mayo Clinic Criteria classifies MCI into two categories, amnestic MCI (a-MCI) and non-amnestic MCI (na-MCI). a-MCI primarily effects episodic memory, and na-MCI primarily effects language, decision-making, judgement, time-perception, or visuospatial abilities. Studies show up to 70% of those with a-MCI will develop Alzheimer’s, while other variants will develop dementia of other causes. The conversion rate from MCI to AD is estimated to be 15% per year. Those who revert back to a normal cognitive state, have an increased risk for entering MCI again, and for developing dementia. In a 2015 study of 1449 cognitively normal subjects, aged 70 to 89, in Olmsted County, Minnesota, 401 or 27.7% developed MCI. Although there are no medications currently approved for MCI, there is some evidence that cognitive training, aerobic exercise, dietary modifications, and nutritional supplementation may improve cognitive functioning.

In the research field, early MCI detection is crucial to study interventions that delay progression. In a clinical setting, early MCI detection is important because it allows physicians to rule out any non-AD causes, consider non-pharmacological intervention, and explore participation in clinical research trials with the patient. Patients and their families also benefit from identification of MCI as they can make future preparations while the patient is in a capable cognitive state.

Assessing the progression from MCI to Alzheimer’s dementia requires routine psychometric assessments. The use of formal psychometric testing by primary care practitioners for diagnosing dementia was estimated to be only 58%, with the main reported barrier being lack of time. Furthermore, commonly employed psychometric tools such as the Alzheimer’s Disease Assessment Scale (ADAS-cog) and Mini-Mental Status Exam (MMSE) are useful in monitoring AD progression, but lack sensitivity for MCI. The Clinical Dementia Rating Scale (CDR) was one of the first assessment tools that showed sensitivity for MCI, assessing daily functional activity, interviewing both patient and a caregiver. Unfortunately, the CDR is primarily subjective and has a long administration time.

The Montreal Cognitive Assessment (MoCA) is a psychometric tool developed by Dr. Z Nasreddine. The scale specifies parameters for normal controls, MCI, and AD, and estimates up to 90% specificity for MCI. Recent date indicates a statistically significant correlation with existing scales in terms of total score and individual parameters. The administration time for the MoCA is less that 10 minutes. It currently does not require any specific training or certification for administration, but does require an expert in the cognitive field to interpret the results. The ease of administration, accuracy, and sensitivity for both MCI and AD allows the MoCA to serve as a routine cognitive assessment by health care providers.

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Pharmaceutical companies have spent billions of dollars to find a treatment for Alzheimer’s Dementia. Unfortunately, all recent clinical studies have failed and the potential for the approval of an efficacious treatment in the foreseeable future remain slim.

A particular area of hope, is that researchers have identified a significant connection between diabetes and Alzheimer’s disease. Approximately 80% of people with Alzheimer’s disease also have some form of diabetes, insulin resistance, or disturbed glucose metabolism. The connection between Alzheimer’s disease and diabetes is so close, that researchers have now begun referring to Alzheimer’s as “type 3 diabetes”. This finding is significant because it suggests that the risk of developing Alzheimer’s dementia can be reduced through dietary and lifestyle modifications.

Dementia currently afflicts more than 35 million people worldwide. Almost half of people with dementia have Alzheimer’s disease, the most common form, characterized by progressive memory, cognitive and behavioral deficits. With aging demographics and current trends, the number of people affected by dementia is expected to reach 115 million by 2050. This trend is not only devastating for individuals burdened with the disease, but also families forced to care for their loved ones. Furthermore, the economic impact on society is immense, with the Alzheimer’s Organization predicting Alzheimer’s and other dementias could cost the United States of America almost $1.1 trillion by 2050.

Vita Columbia Clinical Research Inc. is taking the initiative to educate society on the new findings correlating Alzheimer’s disease with diabetes, and the possibility for prevention through lifestyle modifications, such as dietary changes.

A simple method to reduce added sugar consumption, is by substituting table sugar and high fructose corn syrup with vitaSWEET in cooking, baking, and beverages. vitaSWEET tastes like sugar, but is 0 on the glycemic index, meaning that it has no effect on blood glucose levels.

vitaSWEET is formulated with two simple ingredients: monk fruit and erythritol. Monk fruit or luo han guo is native to southern China and northern Thailand, and has almost 300 times natural sweetness than that of sugar. It has been used for centuries in traditional Chinese medicine as a cold and digestive aid, and was first mentioned in the records of 14th century Chinese monks. Erythritol is a naturally occurring sugar alcohol derived from fruits and plants. Vita Columbia’s unique blend of both monk fruit and erythritol is as sweet as sugar and can be used as a 1-to-1 replacement in recipes.

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Type-3 Diabetes as Alzheimer’s Disease: Hyperinsulinemia as a mechanism in Alzheimer’s Pathology

The world is currently facing a diabetes epidemic, affecting over 400 million people worldwide. This figure is more likely to be double, as one in two people currently living with diabetes are undiagnosed. Type 2 diabetes is the most commonly known form of diabetes and without prompt diagnosis and management can lead to complications such as blindness, limb amputation, kidney disease, heart attack and stroke. In congruence with the rise of diabetes mellitus (DM) in the past century, humanity is facing another epidemic, dementia, which currently afflicts more than 35 million people worldwide. Almost half of people with dementia have Alzheimer’s disease (AD), the most common form, characterized by progressive memory, cognitive and behavioral deficits.

In a 2016 study published in the journal Diabetologia (the journal of the European Association for the Study of Diabetes), researchers uncovered that genes responsible for the production of toxic neuroproteins not only lead to Alzheimer’s symptoms, but also lead to diabetic complications. In response to the study results, lead researcher, Professor Bettina Platt stated, “Many people are unaware of the relationship between diabetes and Alzheimer’s disease, but the fact is that around 80% of people with Alzheimer’s disease also have some form of diabetes or disturbed glucose metabolism. This is hugely relevant as Alzheimer’s is in the vast majority of cases not inherited, and lifestyle factors and comorbidities must therefore be to blame.” The connection between Alzheimer’s disease and diabetes is so close, that researchers have now begun referring to Alzheimer’s as “type 3 diabetes”.

Scientists hypothesize that the pathological process leading to the development of AD encompasses two main features: amyloid plaques and neurofibrillary tangles. Amyloid plaques form as a result of the extracellular accumulation of beta-amyloid (Aβ), believed to trigger a cascade of events leading to neurodegeneration, and is the primary therapeutic target in AD pharmacotherapy. Neurofibrillary tangles (NFTs) on the other hand are intracellular inclusions, formed by the aggregation of tau proteins, which are microtubule-associated proteins that function to stabilize microtubules. Cognitive decline in AD is closely correlated with the progressive pathological accumulation of NFTs, believed to directly cause neuronal malfunction and cell death. Extensive clinical research has focused on Aβ or tau proteins as therapeutic targets, but clinical trials have had disappointing results thus far. The most promising therapeutic strategy, on the other hand, may be focusing on risk factors such as DM.

Science has only recently accepted the role of insulin in the brain, which include neuronal development, synapse formation, learning and memory, glucoregulatory function and feeding behavior. Researchers suspect that the high concentration of insulin found in the brain is the result of local production in the brain and active transported across the blood-brain-barrier via a specific transporter, affected by hyperglycemic states such as diabetes.

Several independent research groups have shown insulin resistance to have a significant effect on Aβ synthesis, aggregation, and clearance mechanisms. The studies demonstrated that diet-induced insulin resistance increases Aβ synthesis on a molecular level, and also correlated excessive sucrose intake with increased cerebral Aβ peptide levels and worsened learning impairment in Alzheimer’s transgenic mice. Furthermore, insulin-degrading enzyme (IDE) is an important enzyme involved in the proteolytic degradation of accumulated Aβ in the brain. In states of hyperinsulinemia, as in DM, excessive insulin levels directly compete with Aβ for IDE, reducing Aβ degradation and increasing Aβ levels.

Physiologically, tau proteins are involved in stabilizing neuronal microtubules. In pathological states, such as AD, tau proteins undergo phosphorylation leading to aggregation, the formation of neurofibrillary tangles and neuronal toxicity. Glycogen synthase kinase-3 (GSK-3) is an important regulator of tau phosphorylation. Studies have shown that diabetes and obesity-induced insulin resistance cause excessive activation of GSK-3β which induces tau hyper-phosphorylation, leading to the formation of neurofibrillary tangles responsible for the cognitive changes in AD. Activation of GSK-3 is another suspected mechanism in which diabetes triggers the development of or accelerates the progression of AD.

With aging demographics and current trends, the number of people affected by dementia is expected to reach 115 million by 2050. This trend is not only devastating for individuals burdened with the disease, but also families forced to care for their loved ones. Furthermore, the economic impact on society is immense, with the Alzheimer’s Organization predicting Alzheimer’s and other dementias could cost the United States of America almost $1.1 trillion by 2050.

A optimal method to reduce the personal, social, and economic impacts of the DM and AD epidemics is through prevention, which can be best achieved through dietary changes and physical exercise. One simple dietary change involves substituting sucrose or table sugar for low-glycemic alternatives such as vitaSWEET in cooking, baking, and beverages. vitaSWEET is all-natural and as sweet as sugar, but without the metabolic consequences.

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