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DIAGNOSTIC WORKUP: A few blood tests are necessary after physical and neurological exams have been conducted. To make a proper diagnosis, a complete blood chemistry is required to check liver and kidney function, as well as a blood count to see if the patient is anemic. Additionally, bloodwork is needed to determine the patient’s thyroid levels, vitamin B12, and VDRL for serology. Brain imaging studies such as CT scan and MRI may show atrophy and/or small vessel ischemic changes, seen in over 90% of patients.

It should be noted that current biomarkers, APOE, Volumetric MRI, PET scan for amyloid, and FDG PET scan are presently research tools.

A simple psychological test called MMSE (Mini-Mental Status Exam) was introduced in New York City in 1975 at the University of Cornell. Since then, it has been standardized in thousands of patients and translated into many languages. It is used by the government, drug companies, and neurologists who treat patients with Alzheimer’s disease to determine the stage of illness. This test is not diagnostic of Alzheimer’s disease, but gives us a very good idea about the degree of cognitive deterioration (mild, moderate, or advanced). This testing consists of 30 questions; 10 of them are related to orientation, 6 for recall, and 9 questions are about language. Each is worth 5 points, and the patient must choose between spelling and calculation. The maximum score the patient can get is 30. Mild cognitive impairment pertains to scores between 29-26, mild dementia 26-20, moderate dementia 19-10, and advanced dementia 9-0.

A very simple screening tool that requires no special training is Mini-Cog. This test can be done in the office of a primary care physician. It consists of a 3-word recall and the draw-a-clock test.

TREATMENT: Alzheimer’s disease therapies are divided into two groups.

Symptomatic therapy may partially slow the progression of the symptomatology without impacting the underlying disease process. This type of therapy includes drugs which affect neurotransmission by increasing acetylcholine in the postsynaptic receptor, such as donepezil, rivastigmine, and galantamine. The drug memantine impacts neurotransmission by blocking excessive glutamate.

Neuroprotective therapies are thought to have a direct impact on the pathology of the disease. The pathology of Alzheimer’s disease was initially described back in 1906 by Dr. Alois Alzhimer. It is characterized by intraneural abnormalities (tangles-tau) and extraneural abnormalities (plaques-amyloid). In the middle of these plaques is a protein called amyloid. It is thought that there is an accumulation of this protein over 15 years before the patient has any kind of symptomatology. When it reaches a critical point, the amyloid begin to destroy synapses and neurons, and is the reason for the progressive deterioration in cognition. Most studies regarding neuroprotection are oriented in one way or another to try to decrease or stop the production of amyloid and, as a result, prevent the death of brain cells and synapses. Immunotherapy carries the best future regarding neuroprotection in Alzheimer’s disease, of which there is an active and passive type. Passive immunotherapy appears to be leading the pack. We may be able to stop and possibly even clear the deposit of amyloid in the brain, thereby delaying the presentation of Alzheimer’s disease or modifying it.


Interested in learning more about Alzheimer’s research? Please call 561-296-3824. The Premiere Research Institute in West Palm Beach regularly conducts clinical research studies in the field of Alzheimer’s Disease. To find out more about these studies click here or sign up for their newsletter to keep informed about the newest treatments, articles, and research that are being conducted in the field of Alzheimer’s.