Science and Research Questions

Your question is an important one that concerns individuals with a family history of dementia, clinicians who wish to advise their patients accurately, and researchers seeking to understand the course of dementia’s development in order to improve our understanding of its various causes. Although early signs of dementia can be variable, one frequently used summary of dementia’s stages was published by Dr. Reisberg and colleagues in 1982 and is still commonly used. You may want to seek out the article, which is in the American Journal of Psychiatry (1982;139:1136-9). They described the earliest manifestations of dementia, particularly Alzheimer’s, as including memory lapses with names or words and misplacing of objects, but recognized that these behaviors also can occur in normal cognitive aging. Don’t let yourself get alarmed if these are your experiences, since they are not strong predictors of dementia. At the next stage, early signs of dementia may be apparent as “mild cognitive decline” consisting of memory or concentration problems that can be objectively demonstrated on neuropsychological testing. It becomes more difficult to remember the names of newly introduced people. Performance in work or social settings may show some signs of decreased function and declining organization or planning ability. At this stage, friends or family may have noticed changes in an individual’s memory or behavior. If you are experiencing symptoms such as these, there are still many possible explanations other than dementia that should be explored. It would be sensible to seek evaluation with a clinician experienced in assessing the presence of cognitive impairment such as a behavioral neurologist, neuropsychologist, or geriatric psychiatrist.

Many investigators and clinicians suspect that diet may have a connection to Alzheimer’s disease, though it is unlikely that diet is a primary cause. A recent National Institutes of Health conference on “Preventing Alzheimer’s Disease and Cognitive Decline” reviewed current data on this issue and concluded that there is preliminary evidence to support the idea that the Mediterranean diet, which is high in vegetables, fish, fiber, and healthy oils, may be associated with a decreased risk for cognitive decline or Alzheimer’s disease. By contrast, there was a suggestion that high intake of saturated fats and trans-fats might increase this risk. Some investigators have explored the idea that a “ketogenic diet” might benefit Alzheimer’s disease by providing the brain with an energy source other than the usual glucose (which is handled less effectively by the brain in Alzheimer’s disease). A prescribed “medical food” that induces ketosis is available but further studies are needed to fully assess its safety and effectiveness. In general, there is no rigorously documented prevention strategy for Alzheimer’s disease in humans; however, some preliminary data from animal studies show exiting promise. Much further research is necessary to confirm these findings.

Dementia is a term that describes a condition of decline from previous cognitive functioning, not explainable by adverse medication effects or other simple reversible medical causes. In addition, it is characterized by memory problems and problems in one or more other areas such as recognition, ability to do learned tasks, use language, or to problem-solve. Alzheimer's disease is the most common of dementias in the elderly, accounting for about 2 out of 3 cases, but there also are other conditions that can cause dementia. "Stage 4 Dementia" refers to moderately impaired cognitive and social functioning as described in Dr. Barry Reisberg's "Global Deterioration Scale." At stage 4, we'd expect to see decreased knowledge of recent events, impaired problem-solving ability, trouble with tasks such as bill paying, reduced memory, and a tendency to withdraw from challenging situations. Orientation, recognition of familiar people, and ability to travel to familiar places are typically preserved at this stage. This staging system is usually used to describe the progression of Alzheimer's disease, since symptom progression can be somewhat different in some other dementias.

Zinc, like many trace elements required by the human body, is a necessary ingredient in some physiologic processes but potentially dangerous at toxic levels. At appropriate levels zinc facilitates learning through a process called "long-term potentiation," but zinc is also an important component of the amyloid plaques found in Alzheimer's disease. An experimental medication that lowers zinc levels, clioquinol, has been claimed to show some promise in treating Alzheimer's disease, but this is based on very limited and preliminary results. If you like oysters, you should know that a half-dozen contain about twice the zinc present in your wife's pill. In any case, the effects of zinc on memory are thought by some researchers to depend on internal regulatory processes rather than exposure through food or supplements; however, this remains an area of controversy awaiting resolution.

Double vision is a rare occurrence in mild Alzheimer's disease, and the onset of double vision should prompt a visit to the ophthalmologist to rule out other causes of this disorienting and distressing symptom. The list of causes for double vision (diplopia) is very long and includes many conditions that affect the cornea, lens, muscles that move the eye, tissue around the eye, or brain. In addition, double vision might suggest the need to consider some other dementias that are not Alzheimer's disease, such as supranuclear palsy or Lewy body disease.

Acetylcholine is an important neurotransmitter in the brain and its availability is decreased early in Alzheimer's disease. This observation, noted several decades ago, led to widespread experiments aimed at increasing acetylcholine at the synapse (the structure where chemical information is passed from one nerve cell to another) by providing the ingredients from which the brain could produce this neurotransmitter. Other experiments sought medications that would slow down the destruction of acetylcholine present in the diseased brain. This slowing down of destruction of acetylcholine, by inhibiting the enzyme that breaks it down (called cholinesterase) is the mechanism of action of widely used medications for Alzheimer's disease: donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne). But the limitations on the effects of these medications, along with newer findings, has led researchers to believe that other basic brain changes result in the acetylcholine scarcity. The lack of acetylcholine is thought to be an important step in the disease process but not a "cause" of Alzheimer's disease.

Alzheimer's disease can certainly affect the ability to speak in a patient. Speech problems typically arise in Stage 2 of the disease, wherein patients may forget words for things or speak nonsensically. Complete loss of speech can also occur depending on what part of the brain is affected by the disease.

Alzheimer's disease medications in general help to slow the progression of the disease, and therefore may aid in slowing the decline in communicative ability. You should consult with your mother’s prescribing physician for more information. However, since your mother may be in a later stage of the Alzheimer’s disease, the medications may not be as effective as in earlier stages.

Alzheimer's disease and type-2 diabetes mellitus (T2DM) do share some pathological and biochemical similarities. For example, both diseases are known as amyloidoses in that both are characterized by an abnormal deposition of amyloidogenic proteins—amylin deposition in pancreatic islets in T2DM, and amyloid-beta protein deposition in the form of plaques in Alzheimer's disease brains. Also, when deposited in and around cells, both types of proteins are toxic and cause cell death—pancreatic beta-cells in T2DM and neuronal brain cells in Alzheimer's disease. The similarities between the two diseases and their associated amyloidogenic proteins have lead researchers to question whether there are other shared cellular or molecular mechanisms underlying their pathologies, and how such findings might influence the development of effective therapies for each of these diseases.

In addition, epidemiological studies suggest that metabolic syndrome (characterized by the “deadly quartet” of factors including high blood pressure, dyslipidemia, central obesity and insulin resistance), which is predictive of T2DM, may also be predictive of and/or increase the risk of vascular dementia, stroke, and even Alzheimer's disease. Taken together with the above evidence, it is understandable how some people actually consider Alzheimer's disease to be a form of “diabetes of the brain.”