A doctor answers questions that he gets from patients and families regarding Alzheimer’s disease.
Come into my office for a moment, please, to peek into the life of a geriatric psychiatrist specializing in memory care. Among the many roles we play – assisting in diagnosis, treatment planning, coordination of care, prescribing medications, counseling, suggesting resources, and monitoring treatment progress – nothing is more important than answering the questions that patients and their care partners bring. I’d like to share with you five of the most frequently asked questions.
- What’s the Difference Between Alzheimer’s Disease (AD) and Dementia?
This question has a traditional answer and a new answer.
In the past, clinicians would typically say that AD is one variety of dementia, but by no means the only cause of cognitive decline. If each dementia were a unique type of animal, Alzheimer’s disease would be the blue whale, largest and most commanding of all, but only one member of the animal kingdom. Two-thirds of people with dementia have the Alzheimer’s type. The other most frequent dementias are vascular dementia and Lewy body dementia, which together account for the majority of non-AD dementias. There are more than a hundred distinct additional dementias, but most people with dementia suffer from one of these three most common conditions. The current term for dementia is “major neurocognitive disorder.”
There is an additional spin on this question, thanks to advances in biomarker science. Neuroimaging investigations (such as MRI or PET scans) and other studies have revealed that some people with AD do not have clinical dementia, so that AD can differ from dementia in this other way as well. Research has shown the presence of AD pathology, plaques and tangles, in the brains of people who show no clinical signs of major neurocognitive disorder. On testing, some of these individuals do show more limited cognitive changes, called mild neurocognitive disorder. Others seem to be without symptoms. Since all these people have plaques and tangles in their brains, a three-stage model of Alzheimer’s disease has recently been proposed.
During the first stage, AD pathology is developing, but noticeable symptoms are not present. As the second stage progresses, accumulation of plaques nears completion, and mild cognitive changes are measurable without loss of independence. During the third and final stage, the tau-associated tangles continue to intensify and spread. Alzheimer’s disease becomes Alzheimer’s dementia as cognitive impairment evolves and independence is lost.
- How is Alzheimer’s Disease Diagnosed?
The traditional answer to this question has been that AD is definitively diagnosed after death, at autopsy, by identifying a characteristic pattern of amyloid plaques and neurofibrillary tangles in the brain of someone who showed cognitive impairment sufficient for a diagnosis of mild or major neurocognitive disorder while alive.
During life, the characteristics suggesting typical AD dementia are gradual onset and disturbances of the following to such a degree that they disrupt independence:
- short-term memory;
- the ability to plan, organize, remember things, prioritize, or pay attention to tasks (executive functions);
- complex attention;
- the visual perception of spatial relationships among objects (visuospatial function);
- language; and
- social cognition.
During life we can diagnose “probable AD,” based on a careful process that includes taking a comprehensive history, doing a mental status examination that includes cognitive evaluation, obtaining a battery of specific blood tests and getting a neuroimaging study such as a CT scan or MRI. These steps all serve the purpose of finding other, potentially treatable, causes for cognitive impairment.
This question, too, has an evolving answer. Recent advances in neuroimaging and other biomarkers have provided tests that can increase the strength of our diagnostic certainty during a patient’s life and provide more reliable confirmatory information much earlier during the course of AD. FDG (fluorodeoxyglucose)-PET scans are already available to assess metabolic changes characteristic of AD. Newer PET scan tracers identify the presence and distribution of amyloid plaques, providing a more specific and predictive measure of AD’s probability. Tests of cerebrospinal fluid are available, too, to assist in diagnosis. Blood tests currently under investigation may prove even easier and more reliable, but they are not yet available for public use. It is likely that we will soon see AD diagnosed earlier and with greater certainty. Read more about diagnostic tests for Alzheimer’s disease.
- Is Dementia Treatable?
A small percentage of people with dementia can actually be cured through treatment of a specific disease that responds to medication or surgery. Medication toxicity, nutritional deficiency, infection, sleep apnea, and metabolic diseases, such as hypothyroidism, are among the reversible causes of cognitive impairment severe enough to rob a person of independence. For an excellent discussion of these and other treatable dementias, I refer you to an article by Drs. Tripathi and Vibha.1
One of my favorite teachers used to say that many of our patients are incurable, but none are untreatable. Patients with AD are among those who remain at present incurable yet likely to benefit from treatment. Primary prevention aims to reduce the likelihood of developing dementia. I’ll say more about that in the next question/answer.
Secondary prevention, which is more often what families and patients seek from clinicians, has the goal of harm reduction through reducing the progression or impact of dementia.
Much of our treatment approach focuses on identifying and managing potentially aggravating conditions. Medical diseases such as delirium, psychiatric conditions such as depression, improper medications, adverse living circumstances, and lifestyle factors are chief among these.
Clinicians offer support, education, and information about resources to patient and care partners. Care management might include discussion of driving safety and home safety, decisions about where to live and what level of supervision is needed, advance planning, and consideration of legal and financial needs.
Symptomatic medications can help some with cognitive and behavioral manifestations of dementia and improve quality of life for patients and their care partners even though no curative medication is yet available. Clinical trials offer patients an opportunity for treatment with newer medications, but to date, none of these has been disease-modifying.
- How Can I Prevent Dementia?
Start now! Even in the absence of a curative medication, the best available evidence suggests that a “brain-healthy lifestyle” can still delay or prevent the development of dementia in a significant number of people.2 A brain-healthy lifestyle generally includes managing hypertension and other medical disorders which affect cognition, eating a healthy diet such as the Mediterranean Diet (low in saturated fats and high in good fats and fiber), remaining socially engaged, and exercising both your physical and mental “muscles” through activity and cognitive stimulation.3
There is much controversy about which of these lifestyle factors, if any, is most effective and whether more can be gained by a multidimensional lifestyle makeover than by emphasizing a single factor. There is less controversy when timing is discussed. Authorities seem to agree that it is preferable for preventive lifestyle changes to begin long before cognitive changes develop. Some of these lifestyle factors, however, may still be important even after cognitive impairment has settled in. A physical exercise program, for example, was recently shown to improve physical fitness in a group of older adults with dementia even though it did not have significant cognitive benefits.4
- Is Dementia Inheritable?
The short answer to this question is that “it depends.” Some dementias are inherited, and others are not.
Huntington’s disease (HD) is an example of a dementia that is passed down in a genetically predictable manner. If you have one parent with HD, you have about a 50 percent chance of developing HD yourself. Some other dementias, uncommon ones like HD, can also be passed down in this fashion. The most common dementia, AD, is inherited in this way in only a very small number of people that have early-onset AD.
Much more commonly, the clinical symptoms and signs of AD become apparent after age 60, and this is called late-onset AD. In this form of the disease, the combined effect of a number of genes have been identified that can increase risk. The most important of these is the E4 version of the apolipoprotein gene, referred to as ApoE4.
Read more about the genetics of Alzheimer’s.
- Alzheimer’s Disease Toolkit (Helpful Information to Understand and Manage Alzheimer's Disease)
- Expert Information on Alzheimer's Disease (Articles)
- Amyloid Plaques and Neurofibrillary Tangles (Medical Illustration)
- Treatments for Alzheimer’s Disease (Fact Sheet)
- Medical Conditions that can Mimic Dementia (Article)
- “Is It Something I'm Taking?” Medications That Can Mimic Dementia (Article)
- Diagnostic Tests for Alzheimer's Disease (Article)
- Treatments for Alzheimer’s Disease (Fact Sheet)
- Decreasing Your Risk of Alzheimer’s (Article)
- Early-Onset Alzheimer's Disease (Article)
- What Is Your Risk?—Heredity and Late-Onset Alzheimer's Disease (Article)
- Is Alzheimer’s a Genetic Disease (Article)
- Tripathi M, Vibha D. Reversible dementias. Indian J Psychiatry 2009 Jan; 51(Suppl1): S52–S55. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3038529/
- Livingston G, Sommerlad A, Orgeto V, et al. Dementia prevention, intervention, and care. Lancet. 2017 Dec 16;390(10113):2673-2734.
- Fernandez A, Goldberg E, Michelon P. The SharpBrains Guide to Brain Fitness: How to Optimize Brain Health and Performance at Any Age 2nd Edition. Sharp Brains Inc. 2013.
- Lamb SE, Sheehan B, Atherton N, et al. Dementia And Physical Activity (DAPA) trial of moderate to high intensity exercise training for people with dementia: randomised controlled trial. BMJ 2018;361:k1675.
This content was last updated on: October 2, 2018
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