Memory and aging – The Washington Post

Surveys show that half of middle-aged adults worry about getting dementia. People who feel isolated, get less sleep or have taken care of someone with memory loss tend to be particularly concerned. Fear of cognitive maladies is widespread; scientists have found that people are more scared of dementia than of other top causes of death, such as heart disease and strokes.

Decades of research has made clear that cognitive change with advancing age is perfectly normal. Most adults become worse at recognizing faces and remembering new information beginning in their 30s, and then continue to decline over the rest of their lives. This means that the typical retiree can recall fewer items from a long grocery list than her 20-year-old grandchild, even if both are cognitively normal. Memory for well-learned facts last longer, but these skills eventually wane, too. So the question of whether something is amiss in the brain is not “Have I declined?” but rather “Have I declined too much?”

Inaccurate cognition assessments

We are notoriously inaccurate in assessing our own cognition. Studies illustrate that we have particularly poor insight when quantifying our processing speed and dexterity. When Alzheimer’s disease or other afflictions are present, our ability to self-judge our cognitive aptitude becomes even less reliable, starting in the earliest stages of disease. Loss of self-awareness is so common in these conditions that it is sometimes included in the diagnostic criteria for the maladies.

So how should someone figure out whether they are experiencing normal aging-related memory process, or something more significant?

Rather than trying to assess yourself, enlist a close friend or family member to detect whether you are having a problem. Studies show that a spouse’s description is more reliable than a person’s own opinion of their memory and thinking skills. The most useful questionnaires for measuring cognitive impairment are not filled out by patients, but rather by someone who knows them well. In my own memory clinic, we compensate for imperfect self-awareness by asking patients to come to the visit with a friend or family member whom we can talk to separately.

As cognitive specialists, we evaluate brain health along two planes.

First, we consider the macroscopic: How well does a person function in the real world? We ask whether a patient forgets to pay bills, gets lost on familiar driving routes, or leaves ingredients out of recipes. We discuss word-finding difficulties and changes in behavior.

Second, we try to predict what is happening at a microscopic scale inside the head: Do we suspect that the patient’s brain has accumulated damaging molecules? Our brains are made of more than a septillion molecules, each formed by connected atoms, akin to Lego blocks clicked together. Most of these molecules help us thrive, but some can turn on us, wreaking havoc on the organ they were meant to serve. We don’t always know the exact molecules that cause Alzheimer’s disease and similar conditions, but in many cases we know which abnormal molecules tend to be associated with the afflictions.

Tests of thinking

To assess whether a dangerous molecule may be accumulating in a patient’s brain, we use tests of thinking, similar to brain games, that can quantify memory, multitasking ability, language skills and spatial judgment.

We look at pictures of a patient’s brain, usually an MRI, searching for areas that are small or damaged. Sometimes, we incorporate added results from blood or spinal fluid. Compiling the information together, we hypothesize what abnormal molecules, if any, may be collecting in the person’s brain. “If I were to look at a piece of your brain under a microscope,” I can tell my patients, “I suspect I would find this.”

Alzheimer’s disease, Lewy body disease, frontotemporal dementia and other types of dementia are each associated with particular molecular changes, so linking a person’s symptoms to their microscopic roots allows us to predict what will happen to a patient in the future. Three people who start to repeat themselves in conversation may confront completely different fates. One, whose symptoms are caused by Alzheimer’s disease, will go on to experience progressive amnesia. Another, whose repeating stems from frontotemporal dementia, may become strikingly disinhibited. Still another, with no problematic molecules accumulating in the brain at all, might eventually stop the repetitious behavior and revert to normal after tackling mood symptoms or sleep problems.

Predicting what molecule is associated with a patient’s disease is important for not only prognosis but also drug discovery. The idea of a single cure for dementia — a magical pill or a universal vaccine — has long fallen out of fashion. A drug that treats Alzheimer’s disease is unlikely to help patients with frontotemporal dementia, because the diseases are thought to be caused by different molecular disasters. The same is true of a treatment for Lewy body dementia or Huntington’s disease. So scientists are simultaneously searching for multiple drugs, each of which would work on a particular, nefarious molecule.

Tailored medications

The cure for dementia will ultimately be an arsenal of medications that doctors can tailor to each patient based on the unique molecular signatures in the individual’s brain.

As the search for cures continues, the most valuable action you can take if you are concerned about your memory is to talk to a friend or family member. “Can you keep an eye on my memory and thinking,” you might ask. “And tell me honestly if I seem worse than other people my age.” If that person has concerns, bring them up with your doctor.

If everything seems normal for your age group, put your unease aside and ask again in six months; statistically speaking, rest assured that your family and friends probably know better than you do.

Meanwhile, stop worrying about forgetting the names of acquaintances and leaving your keys on the kitchen counter. In most cases, these are simply signs of normal cognitive aging.

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