Learn about the key differences between the early and late onset forms of Alzheimer’s disease.
Early- and Late-Onset Alzheimer's: How do they Differ?
Early-onset Alzheimer’s disease (EOAD), which is thought to affect between 220,000 and 640,000 Americans, begins between age 45 and 64. It looks different than late-onset AD, and it has different consequences because it arrives during the prime years of adulthood. That may be why the delay between symptom onset and diagnosis is greater for EOAD than for AD that manifests in older individuals. However, early recognition is especially important in cases of EOAD.
Here are some key differences between EOAD and typical, late-onset AD.
- The majority of EOAD does not run in families. However, some cases of EOAD have a stronger pattern of genetic inheritance than late-onset AD. There is likely to be a parent who developed AD at an age less than 65 in as many as 13 percent of EOAD cases. In these families, there may be a gene mutation that is passed along as an autosomal dominant trait, which means that it affects half of the offspring of the person with this form of AD.
- Memory loss may develop later in the course of the disease and be less prominent in people with EOAD than in those with typical later-onset AD.
Dr. Mario F. Mendez (see Further Reading below) describes how EOAD can present atypically, and he groups these together as “Type 2 AD”:
- Some people with EOAD show difficulty finding words, which could look like a condition called aphasia (the loss of ability to understand or express speech) or variant of frontotemporal dementia;
- Posterior cortical atrophy, which is sometimes another variant of EOAD, is recognized by the occurrence of difficulty reading (alexia) and other visual complaints despite apparently normal functioning of the eyes. The problem is in the brain, specifically in the areas that process and make sense of the sensory information that the eyes deliver to the brain;
- Another EOAD syndrome, called progressive ideomotor apraxia, can cause a person to have trouble demonstrating learned movements of the limbs, both when asked to do so and when asked to imitate the physician's limb movements;
- Frontal variant AD (behavioral-dysexecutive AD) can confuse clinicians because it presents with apathy (a lack of concern, interest, enthusiasm, emotion, or concern) that would suggest depression but the response to antidepressant treatment might be very limited.
MRI brain images of people with EOAD can look a little different than the images for typical AD. For example, shrinkage of the hippocampi and temporal lobes is less, and shrinkage of the parietal lobes is more prominent, with EOAD. Also, changes in white matter (the nerve fibers that connect parts of the brain and spinal cord) may be more significant in MRI brain images in people with EOAD.
As with later-onset AD, no specific medication will cure or even reverse the disease, but medications such as Aricept® (donepezil) and Namenda® (memantine) can nonetheless reduce symptoms in some people. Amyloid PET scanning may help with the differential diagnosis in some situations if that is available. Genetic tests will identify the small number of individuals with the form of the disease than can be passed along to their children, and that is important for assisting with genetic counseling.
Interventions, which should take place once the diagnosis is well-established, can include support groups for the patient and help for family members. With an adult in his or her 50s, discussion often includes counseling regarding how to modify or exit from employment. Patients and families can be guided toward available resources, support groups, and services for EOAD patients and their caregivers. Given the early-onset and projected survival time, some patients will choose to participate in a clinical trial. That may offer the patient and care system some hope while contributing to general knowledge that will help many others as well.
- Mendez MF. Early-Onset Alzheimer Disease. Neurol Clin 2017;35:263-81.
- Geschwind MD, Belkoura CR. Non-Alzheimer’s and Atypical Dementia. 2016, John Wiley & Sons Ltd., Chichester, West Sussex, UK.
This content was last updated on: Wednesday, October 11, 2017
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