What methods are biologists using to try and solve the problem of Alzheimer's disease? Specifically, can you talk about some of the new treatment modalities, such as the drug called bapineuzumab? [ 05/18/11 ]
We are fortunate that this is an era of important advances in the understanding the causes of Alzheimer's disease (AD). Furthermore, progress is likely to be accelerated as a result of recommendations from a recent task force that redefines clinical Alzheimer's disease as the final stage of a disorder that begins with a long pres-symptomatic phase (demonstrable through the use of cerebrospinal fluid and PET scan measurements, among other biomarkers), followed by a symptomatic pre-dementia phase (mild cognitive impairment), during which individuals may be more amenable to therapeutic interventions. Studies of individuals in these earlier disease phases are likely to increase our understanding of the risk factors for development of AD, the mechanisms by which it develops, and the therapeutic approaches most helpful in delaying or preventing AD's damaging effects.
Currently, much interest in the treatment of AD focuses on reducing the amount of beta amyloid that is produced and accumulated in the brain. Researchers have been enthusiastic about “immunotherapeutic” approaches that attempt to lower beta amyloid levels through immunologic mechanisms. Initial testing of a vaccine (which is an “active immunotherapy” because it induces the formation of amyloid-reducing antibodies in the vaccine recipient) was aborted due to unacceptable adverse effects, ushering in an era of testing “passive immunotherapies.” These medications are called “passive” because they provide pre-made antibodies rather than inducing production of antibodies in the patient. These antibodies attach to the damaging beta amyloid molecules and help the body remove them. Bapineuzumab is one of several “passive immunotherapy” interventions currently in testing and has been in the news, in part, because a large phase III clinical trial is nearing completion, the results of which are eagerly awaited.
Is there a connection between gum disease and Alzheimer’s disease? [ 04/28/11 ]
At first glance, it might be difficult to imagine how inflamed gums might be associated with Alzheimer's disease (AD), but the possible links are many, and the interactions between periodontitis and AD have been the subject of a significant amount of research. Periodontal disease is known to be associated with systemic inflammatory diseases such as rheumatoid arthritis and atherosclerosis. AD, too, has an important inflammatory component. A link between periodontal disease and AD could conceivably represent the consequence of increased systemic inflammation associated with higher levels of circulating pro-inflammatory cytokines that may contribute to the ongoing inflammatory neurodegenerative component of AD. Other hypotheses include the possibility that periodontal bacteria influence the neurodegenerative process, that anaerobic oral flora interact with dental amalgam to produce neurotoxic mercuric compounds that in turn affect the brain, or that severe tooth disease with tooth loss and dentures that are removed at night might result in a compromised airway and obstructive sleep apnea with nocturnal hypoxemia (low levels of oxygen in the blood).
These proposed relationships suggest ways in which the occurrence of periodontal disease might increase the risk for AD, but the link may be more complex: some authorities have suggested that a genetic predisposition to produce increased proinflammatory factors might underlie a concurrent greater risk for periodontal disease and AD. In that case, there would be relationship of association rather than causality. A further possibility is that dementia is associated with reduced self-care and oral hygiene neglect. The possibility that the stress of living with AD, as either patient or caregiver, might also help us understand the observation of increased gingivitis observed in caregivers of AD patients. In any case, it seems clear that oral hygiene's importance reaches far beyond the mouth.
My mother has Alzheimer's disease, and has been taking Aricept and Namenda for years. Recently, her primary care physician stopped the Aricept symptoms because of severe side effects (very loose bowels and stomach pain). I am concerned that her symptoms will become worse more quickly now. Could you give me your opinion? [ 04/13/11 ]
It is true that studies have demonstrated a rapid loss of the cholinesterase inhibitor benefits following cessation of treatment. Your mother, if she has benefited from the donepezil, may show an increase in symptoms. On the other hand, it would be a shame to expose her to a medication that has probably created gastrointestinal discomfort. A transdermal delivery system, such as the patches used to administer rivastigmine, may provide your mother with the therapeutic benefits of a cholinesterase inhibitor while avoiding the gastrointestinal side effects so common with these medications.
Is there any increase in likelihood of developing Alzheimer's disease if you have had electroconvulsive therapy (ECT) to treat depression? [ 04/12/11 ]
ECT is not generally thought to increase the likelihood for developing Alzheimer's disease or other causes of dementia. In fact, ECT has been used to treat depression or agitation, common “noncognitive behavioral symptoms,” seen in dementia patients. The limited evidence available does not find ECT producing lasting cognitive impairment in patients with dementia.
Are there any scholarly articles addressing rehabilitation outcomes of Alzheimer's patients following hip replacement surgery? [ 04/11/11 ]
A strong correlation was found by Hirose and colleagues between dementia rating, walking ability and mortality a year after hip surgery (Arch Phys Med Rehabil 2010;91(1):67-72.) A similar association had been reported earlier by Cree and Nade, who found that dementia was a predictor of poorer prognosis following hip fracture (Scand J Caring Sci. 2005;19:119-27.) Delirium, a common complication of dementia, has also been found to be a predictor of poor rehabilitation outcome in elderly patients treated for femoral neck fractures (Olofsson et al. Aust N Z J Surg 1999;69:723-5.) Several studies have assessed the value of consultation and proactive efforts in reducing postoperative delirium, an intervention particularly relevant to the high-risk dementia patients.
I have frontotemporal dementia? Should I do all the things that are supposed to help people with Alzheimer’s disease? The front and side areas of my brain have decreased in size, and I have many problems, such as loss of memory for people and places. [ 04/09/11 ]
Frontotemporal dementia (FTD) comprises a group of disorders that are separated from Alzheimer's disease by their different microscopic pathologic findings in brain tissue, and by their different course of symptoms. No specific medications are FDA-indicated for the treatment of FTD, though many patients are put on cholinesterase inhibitors or memantine in an effort to see if they provide some benefit. The cholinesterase inhibitors such as donepezil, rivastigmine, or galantamine have not been consistently helpful to patients with FTD, however.
Does fluoride cause Alzheimer's disease? [ 04/08/11 ]
The safety of fluoride, added to drinking water as a preventive treatment for tooth decay, has been questioned by various groups concerned about its possible toxicity. With Alzheimer's disease, however, no firm evidence supports a harmful effect of fluoride. To the contrary, there is speculation that fluoride may have a beneficial effect by competing with aluminum for absorption, which is suspected to be neurotoxic; however, this has not been proven.
What are common problems associated with diagnosing Alzheimer's disease? [ 03/22/11 ]
Diagnostic problems generally fall into the categories of "false positives" (people incorrectly diagnosed with the disease who do not have it), or "false negatives" (people who have the disease and are incorrectly diagnosed as NOT having it).
Sometimes the false positives can result from other disorders that affect cognition, such as depression, delirium, medications, substance use, or a wide range of medical disorders. The false negatives can arise when a person's cognitive level prior to becoming ill was so high that functional reserve covers any growing deficit. In addition, since the diagnosis of Alzheimer's disease is based on a clinical syndrome rather than a definitive diagnostic test using blood, cerebrospinal fluid or brain imaging at this juncture, an atypical presentation can confuse clinicians. Some patients present with a disturbance of visuospatial or language functions that are more clearly apparent than the disturbance of cognition, which again confusing matters. When cerebrovascular disease is also present, the diagnosis may be "mixed," or the cerebrovascular disease may distract attention from the Alzheimer's disease. These are some of the common variations and problems in the diagnosis of this neurological disorder.