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Alzheimer’s disease is a progressive degenerative disease of the brain that causes the most common form of dementia, and is strongly associated with advanced age. However, Alzheimer’s disease should NOT be considered a part of the normal aging process.

Scientific studies of people with Down’s syndrome find the risk of developing an Alzheimer’s-like dementia doubles with each 5-year interval after age 30, and range from 10-25% when aged 40-49 years, 20-50% when aged 50-59 years, 60-75% when older than 60, and close to 100% in people with Down’s syndrome who are older than 70. Therefore, the average age of onset of Alzheimer’s-like dementia is considerably younger in the Down’s syndrome population, and it appears to be independent of living arrangement, degree of mental retardation and gender. However, there is a subset of Down’s syndrome individuals who do NOT appear to develop Alzheimer’s-like dementia, even in old age.

People with Down’s Syndrome Are More Susceptible to Common Health Problems

It has been known for many years that people with Down’s syndrome are more susceptible to common health problems such as obesity, cataracts, and congenital heart conditions. In addition, with aging, people with Down’s syndrome are more susceptible to thyroid and cardiovascular dysfunction, skeletal problems such as osteoporosis, arthritis and muscular disorders, and depression (this process of early aging is referred to as “precocious aging”).

Life Expectancy and Down’s Syndrome

For the majority of human history, people with Down’s syndrome died at an early age, and in the 1920s, life expectancy for people with Down’s syndrome was just 9 years. This increased to 12 years by 1949 and 35 years of age by 1985. Now, people with Down’s syndrome, live an average of 55 years or more; so, their increased life span has increased their susceptibility to conditions that are associated with aging, including Alzheimer’s disease.

People with Down’s syndrome Have Increased Levels of B-amyloid in the Brain

Interestingly, people with Down’s syndrome have increased levels of B-amyloid in the brain, with deposits of B-amyloid in the cerebral cortex beginning as early as age 8, and these B-amyloid deposits increase with age. It is thought that this B-amyloid forms senile plaques that cause Alzheimer’s disease.

Anatomical and Chemical Differences in the Brains of People with Down’s Syndrome

People with Down’s syndrome have anatomical and chemical differences in their brains compared to persons without Down’s syndrome. For example, people with Down’s syndrome already have a reduced brain volume, especially in the hippocampus, and people with Down’s syndrome have other developmental abnormalities, such as reduced dendritic arborizations, and abnormalities of pyramidal neurons. Therefore, it is not difficult to see that the dementia associated with Down’s syndrome is NOT an exact biological replica of Alzheimer’s disease, and Down’s syndrome dementia is often considered by many researchers as a different entity.

Mental Retardation and Alzheimer’s-like Dementia

Individuals with mental retardation from causes other than Down’s syndrome do NOT have Alzheimer’s-like dementia more commonly than individuals without mental retardation. Also, mental retardation is universally seen in Down’s syndrome, but the development of Alzheimer’s-like dementia in people with Down’s syndrome appears to be unrelated to the degree of mental retardation.

Amyloid Precursor Protein Gene is on Chromosome 21

All recognized mutations for Alzheimer’s disease are associated with increased deposition of B-amyloid, a peptide fragment from 39-43 amino acids long, which are products of the catabolism of the amyloid precursor protein (APP) molecule. The discovery that the amyloid precursor protein gene is on the 21st chromosome led to the hypothesis that the early and universal development of Alzheimer’s disease-like pathology in people with Down’s syndrome is due to a third copy of the amyloid precursor protein gene (one on each of the three copies of chromosome 21).

Superoxide Dismutase Gene is on Chromosome 21

There are several other genes that might play a role in the development of Alzheimer’s disease-like pathology that are found on chromosome 21. Among them are superoxide dismutase genes important in the production of hydrogen peroxide (H ₂ O ₂ ), a potentially toxic metabolite that causes cell death. The excess activity of superoxide dismutase is not limited to the brain and has also been observed in erythrocytes, B and T lymphocytes, and fibroblasts of people with Down’s syndrome. Therefore, an alternative hypothesis suggests that increased oxidative stress leads to structural damage to the membranes and DNA of brain cells.

Symptoms of People with Down’s Syndrome and Dementia

The symptoms of people with Down’s syndrome and dementia include: memory and weight loss, apathy, personality changes, loss of conversation skills, poor mobility and increasing dependency on others in activities of daily living. People with Down’s syndrome and dementia show a higher prevalence of mood changes, overactivity, auditory hallucinations, disturbed sleep, and less aggression than people who have dementia alone. 84% of people with Down’s syndrome develop epilepsy (seizures) in the later stages of their Alzheimer’s-like dementia.

Research shows that people with more education have more rapid memory loss after diagnosis of dementia. It appears that with each additional year of formal education, the memory decline associated with dementia was delayed by approximately two and one half months. However, once that accelerated decline started, the people with more education saw their rate of cognitive decline accelerate 4% faster for each additional year of education.

The greatest risk factor for Alzheimer’s disease is advancing age, but Alzheimer’s is not a normal part of aging.

A small percentage of Alzheimer’s disease cases, probably less than 1 percent, are caused by rare genetic variations found in a small number of families worldwide. These variations involve chromosome 21 on the gene for the amyloid precursor protein, chromosome 14 on the gene for the presenilin 1 protein and chromosome 1 on the gene for presenilin 2. In these inherited forms of Alzheimer’s, the disease tends to develop before age 65, sometimes in individuals as young as 30.

A genetic factor in late-onset Alzheimer’s disease (Alzheimer’s disease developing at age 65 or older) is apolipoprotein E-e4 (ApoE-e4). ApoE-e4 is one of three common forms of the ApoE gene, which provides the blueprint for a protein that carries cholesterol in the bloodstream. Everyone inherits one form of the ApoE gene from each of his or her parents. Those who inherit one ApoE-e4 gene have increased risk of developing Alzheimer’s disease. Those who inherit two ApoE-e4 genes have an even higher risk. However, inheriting one or two copies of the gene does not guarantee that the individual will develop Alzheimer’s.

People taking both types of medications experienced functional decline 50% faster than those people who were only receiving medications for dementia.

The study suggests that physicians should carefully consider the implications when prescribing anticholinergic medications to older adults.

This randomized, placebo-controlled clinical trial was carried out at 5 academic medical centers in the United States to see whether treatment with G biloba in a dose of 120 mg 2 times/day could prevent incident dementia or Alzheimer’s disease vs. placebo. A total of 2587 subjects older than 75 years with normal cognition at baseline, and 482 subjects with mild cognitive impairment were included. Patients were assessed every 6 months for dementia.

After a median follow-up of 6.1 years, 523 subjects were diagnosed with dementia, 246 (16.1%) in the group taking placebo, and 277 (17.9%) in those taking G biloba. Of the total dementia cases, 92% were classified as possible or probable Alzheimer’s disease or Alzheimer’s disease with evidence of cerebrovascular disease.

The authors feel that it is unethical to recommend a treatment in the absence of evidence of its efficacy
simply because it could possibly help and initially appears harmless. Ginkgo biloba, even if it were free, is NOT recommended for the treatment or prevention of dementia.

The highest standard of evaluation of new treatments is the randomized, placebo-controlled, double-blind trial; so, a multicenter, randomized, double-blind, placebo-controlled trial investigating prednisone, rofecoxib, and naproxen, for treatment of Alzheimer’s disease was completed by researchers who found there were no differences in the rates of cognitive decline among patients with Alzheimer’s disease in the groups that received the active medication relative to the groups that received only placebo.

The 30 people treated with Razadyne plus memantine had significantly improved cognition at week 12 relative to the people treated with Razadyne alone.

In a separate double blind study (were neither the treating physicians nor the people in the study knew which pills were Namenda or placebo) people with mild to moderate Alzheimer’s dementia were randomly assigned to receive the combination therapy of Namenda and the cholinesterase inhibitor Aricept or Aricept and placebo.

The study lasted for  24 weeks (6 month) and the group of people receiving Namenda and the cholinesterase inhibitor Aricept improved considerably in cognitive performance, behavioral presentation (including decreased agitation, aggression, and irritability) improved appetite, and decreased incident of diarrhia compared with the use of Aricept alone.

All five medications that have FDA approval for Alzheimer’s dementia were successful in randomized, placebo-controlled, double-blind trials. Clearly, there is not only significant improvement with a single agent, but that improvement is magnified when Namenda and any cholinesterase inhibitor are used in combination. Remember this fact when some one representing socialized medicine argues against using either or both of these agents.