Elizabeth A. Reid, MD Alzheimer’s Disease Enters the Testing Age
NTIL RECENTLY, ALZ- heimer’s disease was a “rule-out” diagnosis, meaning that the memory loss and personality changes of de- mentia could only be diagnosed as Alzheimer’s disease after all other likely causes of memory loss and personality change were ruled out. Beyond this, diagnos- tic certainty could only be achieved after an individual’s death, when an autopsy of the brain could be performed. Newly developed tests, however, make earlier diagnosis a lot more cer- tain, and researchers hope these tests will lead to methods of halt- ing or slowing the current inevi- table loss of brain function in pa- tients with Alzheimer’s. But since no treatment is available yet that can change the course of Alz- heimer’s disease and since a di- agnosis of Alzheimer’s is a pain- ful label, a patient and his family might rightly be concerned about having the new tests. For them, and for everyone poised on the verge of old age, an explanation of these new tests is in order. Currently, routine brain scan- ning methods can show strokes, hemorrhages, tumors, and brain atrophy but not the microscopic pathology that defines Alz- heimer’s.
U More sophisticated
scans, such as PET—positron emission tomography—can show abnormal patterns of energy use in some patients with Alzheimer’s
10 PHOTO: GETTY
Researchers hope new tests will lead to methods of halting or slowing the current inevitable loss of brain function in patients with Alzheimer’s.
but are too variable for definitive
diagnosis.The new tests
that
have sparked media attention most recently are based on the identification of proteins clumped in characteristic “plaques and tangles” between and within dy- ing brain cells in the brains of patients with Alzheimer’s.
An Alzheimer’s Pattern Plaques and tangles are brain abnormalities and are the hall- marks of Alzheimer’s disease. Plaques are clumps of protein that form between the nerve cells in the brain, while tangles are twisted protein threads that form inside brain cells. Together these proteins have been the main tar- get of recent Alzheimer’s re- search and of attempts to de- velop new diagnostic tools. A new scanning method employs mate- rials that temporarily “tag” one of the proteins, making it visible dur- ing a scan, but a more promising
test uses the proteins as bio- markers and measures two of the proteins—beta-amyloid1-42 and tau—in a patient’s cere- brospinal fluid. Testing cerebrospinal fluid for Alzheimer’s disease–related pro- teins will raise a number of thorny issues, not the least of which is the labeling of patients with Alzheimer’s disease. Some medi- cal experts question the reliabil- ity of the test, and the fact re- mains that these proteins have not been proven to be the cause of the disease. In fact, no one knows what puts brain cell death in motion in Alzheimer’s disease, but this test’s promise lies in the fact
that reduced levels of the
beta-amyloid1-42 protein and in- creased levels of the tau protein have been found in much greater frequency in Alzheimer’s patients than in those patients not diag- nosed with the disease. This “Alzheimer’s pattern” has also
been found in the cerebrospinal fluid of some people with very mild memory problems who sub- sequently went on to have full- fledged Alzheimer’s disease.
What It Means for You How will the new protein tests change the diagnostic process for the patient seeking help for a declining memory? The most ob- vious change might be the addi- tion of a spinal tap to a compre- hensive dementia evaluation. To obtain cerebrospinal fluid, a doc- tor inserts a long needle between the bones of the lower back, into the central canal of
the spinal
column. A spinal tap is clearly a more invasive test than the rou- tine physical exam, blood tests, and scans a dementia work-up customarily entails, and this fac- tor will inhibit its use unless both patient and doctor see some value in adding information that makes an Alzheimer’s diagnosis more likely. Though dementia evaluations occasionally
indicate that a
patient’s normal mental function can be restored, most often they do not. The usual outcome is a diagnosis of mild cognitive im- pairment or dementia from vas- cular disease, alcohol abuse, Alzheimer’s disease, or a combi- nation of the three. The progno- sis for Alzheimer’s patients is grim, so cerebrospinal fluid that (Continued on page 76)
F E B R U A R Y 2 0 1 1
Page 1 |
Page 2 |
Page 3 |
Page 4 |
Page 5 |
Page 6 |
Page 7 |
Page 8 |
Page 9 |
Page 10 |
Page 11 |
Page 12 |
Page 13 |
Page 14 |
Page 15 |
Page 16 |
Page 17 |
Page 18 |
Page 19 |
Page 20 |
Page 21 |
Page 22 |
Page 23 |
Page 24 |
Page 25 |
Page 26 |
Page 27 |
Page 28 |
Page 29 |
Page 30 |
Page 31 |
Page 32 |
Page 33 |
Page 34 |
Page 35 |
Page 36 |
Page 37 |
Page 38 |
Page 39 |
Page 40 |
Page 41 |
Page 42 |
Page 43 |
Page 44 |
Page 45 |
Page 46 |
Page 47 |
Page 48 |
Page 49 |
Page 50 |
Page 51 |
Page 52 |
Page 53 |
Page 54 |
Page 55 |
Page 56 |
Page 57 |
Page 58 |
Page 59 |
Page 60 |
Page 61 |
Page 62 |
Page 63 |
Page 64 |
Page 65 |
Page 66 |
Page 67 |
Page 68 |
Page 69 |
Page 70 |
Page 71 |
Page 72 |
Page 73 |
Page 74 |
Page 75 |
Page 76 |
Page 77 |
Page 78 |
Page 79 |
Page 80