What Type of Doctor Should I See About Short Term Memory Loss?


What doctor should I see if I feel that my short term memory is decreasing?


You should start your line of inquiry with your primary care physician to assess whether your symptoms are due to normal aging or not. Everyone forgets things from time to time, and your physician can provide a more thorough assessment of what is considered normal aging.

You should certainly consider a doctor who is familiar with Alzheimer’s disease (AD) in particular. He or she can help with your concerns, and if needed, direct you toward a specialist. You can also find resources through the Alzheimer’s Association website.

It’s a good idea for you to look into this issue, because if you do have concerns, it helps to address them earlier, rather than later.

Why is early diagnosis important?
Early diagnosis is beneficial for several reasons. Having an early diagnosis and starting treatment in the early stages of AD can help preserve function for months to years, even though the underlying AD process cannot be changed.

Having an early diagnosis also helps patients and their families:

  • plan for the future
  • make living arrangements
  • take care of financial and legal matters
  • develop support networks

Finally, an early diagnosis can provide greater opportunity for people with AD to get involved in clinical trials. Clinical trials are research studies in which scientists test the safety, side effects, or effectiveness of a medication or other intervention.

Normal Cognitive Aging, Cognitive Decline, and AD: What’s the Difference?
Improvements in public health, medical care, nutrition, and living standards have resulted in our now living longer than ever before. Many older adults enjoy active, productive lives, but they also face the risk of memory and other cognitive problems. This challenge has provided a major impetus for research into healthy cognitive aging. Scientists—and the public—want to know how and why some people remain cognitively healthy all their lives while others do not. Answers to these questions also can help researchers understand what goes wrong in AD or other neurodegenerative diseases and can point the way to interventions that might maintain successful brain and cognitive aging.

As knowledge about the spectrum of stages from healthy cognitive aging to AD grows, it has become increasingly evident that no clear distinctions separate a healthy brain and a diseased brain. Most people develop some plaques and tangles in their brains as they get older, but not everyone develops cognitive problems, MCI, or AD. At what point does an age-related process become a disease-causing process? Several studies published in 2008 and 2009 explored this question.

  • Researchers at the University of Pittsburgh School of Medicine conducted PiB PET scans to image amyloid deposits in the brains of 43 adults, 65 to 88 years old, who did not have clinical AD or MCI (Aizenstein et al., 2008). The 9 participants with beta-amyloid deposits in at least one brain region performed as well on cognitive tests as the 29 participants who had no amyloid deposits and the 5 participants with “intermediate” evidence of amyloid deposits. The finding that an older person with “significant amyloid burden” can be cognitively normal suggests either that some people may have a high level of cognitive reserve or that beta-amyloid deposition alone does not explain cognitive impairment. Another possibility is that some of these individuals will go on to develop AD, even though they are cognitively normal to start. In that case, PiB PET may be useful in identifying AD before clinical symptoms appear. These findings mirror those previously found in post-mortem studies, where the brains of some people with normal cognition were found to have significant amyloid deposits.
  • A team of scientists at the Banner Alzheimer’s Institute in Phoenix, Arizona, conducted PiB PET scans in 28 cognitively normal older people, correlating the results with the presence of the APOE ε4 gene (Reiman et al., 2009). The researchers found higher levels of beta-amyloid deposits in people with one and two copies of the APOE ε4 gene than in those without this version of the gene. These results echo earlier findings showing that APOE ε4 carriers have higher levels of amyloid in their brains at death than do people without this risk factor. Findings from these two studies suggest the possible usefulness of PiB PET scans to detect AD before clinical signs and symptoms appear. This will be crucial for testing promising prevention therapies.
    Longitudinal studies also are being conducted to determine the long-term consequences of beta-amyloid deposits in brain and whether they invariably lead to AD.
  • University of California Berkeley scientists looked at the relationship between extent of brain amyloid deposits (measured using PiB PET scans), hippocampal volume (measured using MRI), and episodic memory (for example, memory of times or places) in three groups: cognitively healthy participants in the Berkeley Aging Cohort, cognitively healthy participants in the AD Neuroimaging Initiative (ADNI), and ADNI participants with MCI (Mormino et al., 2009). In the Berkeley Aging Cohort participants and ADNI participants with MCI, brain amyloid deposits were associated with smaller hippocampal volumes and worse episodic memory. In the healthy ADNI participants, brain amyloid deposits were associated with smaller hippocampal volumes but normal episodic memory. The researchers conducted analyses suggesting that beta-amyloid deposition, hippocampal atrophy, and declines in episodic memory occur sequentially in elderly subjects, with beta-amyloid deposition being the triggering event. In other words, declining episodic memory in older individuals may be caused by hippocampal atrophy induced by beta-amyloid.

Source: National Institute on Aging, 2010