Potential Therapies
Caring for and treating patients with Alzheimer’s disease costs over $100 billion annually in the United States alone. The introduction of FDA-approved cholinesterase inhibitors for treatment, and their potential utility in treating memory loss due to the aging process, has given rise to new hope that we are on the way to meaningful therapies for this terrible illness. There are suggestions that vitamin E, ginkgo biloba, estrogens, and anti-inflammatory agents may slow the progression of Alzheimer’s disease, but some of these agents may be even more useful in preventing memory loss due to the aging process. I will discuss these therapies in the next major section in this book.
Other Dementias
Vascular Dementia
After Alzheimer’s disease, the second most common form of dementia is vascular dementia, which is a direct result of multiple strokes destroying large portions of brain tissue (discussed in chapter 12).
Lewy Body Dementia
Diffuse Lewy body disease is a diagnosis that has gained in popularity in the 1990s. Lewy bodies are microscopic structures present in the brains of patients with Parkinson’s disease. At least one-third of Alzheimer’s patients also have clinical features of Parkinson’s disease: tremor, slow movements, rigidity of muscles, and difficulty in walking. Some of these patients have Lewy bodies in addition to the typical Alzheimer’s autopsy findings of neurofibrillary tangles and amyloid plaques. A British group headed by Ian McKeith has led the charge in calling for a separate diagnostic category called diffuse Lewy body disease, which has the clinical features of dementia, Parkinsonian signs, fluctuating memory loss and confusion, hallucinations, and extreme sensitivity to antipsychotic medications. Many cases previously called Alzheimer’s are now called Lewy body disease; this topic remains controversial.
Frontotemporal Dementia
Frontal or frontotemporal dementia is a less common subtype. Earlier, all such cases were thought to have Pick’s bodies, a specific type of microscopic abnormality, but many cases of frontotemporal dementia do not show this lesion. The clinical features overlap with those of Alzheimer’s disease, but ‘‘frontal lobe disinhibition” signs are more prominent: overeating, sleeping excessively, hypersexuality, motor agitation, and impulsive and unpredictable behavior. Following damage to the temporal and frontal lobes, impulsive behaviors are unleashed from lower parts of the brain, as in the case of Phineas Gage, the railroad foreman whose frontal lobes were crushed by a tamping iron over a hundred years ago. For example, I remember a patient of mine with frontal lobe dementia who gained eighty pounds in one year and lost a hundred pounds in the next. These changes happened without any conscious effort on her part to either diet or put on weight. It was as if the appetite center in the hypothalamus (in a deep part of the brain) was receiving different inputs from the damaged frontal lobes in different calendar years. Some patients with frontal lobe dementia develop complete apathy and lethargy, a near vegetative existence. This can happen even when memory loss is only mild to moderate in severity.
Currently, there is no specific, approved treatment for either Lewy body disease or frontotemporal dementia.
Taken From: The Memory Program How to Prevent Memory Loss
and Enhance Memory Power
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