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MAJOR CATEGORIES OF NEUROLOGIC DISEASE
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Table 39-1 Genetic defects associated with Alzheimer disease
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NOTATION CHROMOSOME GENE GENETICS AGE CLINICAL FEATURES
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APP PS1 PS2 ApoE Trisomy 21
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21 14 1 19 21
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Amyloid precursor protein Presenilin 1 Presenilin 2 Apolipoprotein E Amyloid precursor protein
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Rare but clinically simulates sporadic Alzheimer disease
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As above As above These variants modify susceptibility to typical Alzheimer disease Middle age Alzheimer change is almost universal in Down syndrome
autosomal dominant
(presenilin 1, Sherrington et al), accounting in some series for up to 50 percent of familial cases, and on chromosome 1 (presenilin 2), which may account for many of the remaining ones (LevyLahad et al) These are summarized in Table 39-1 The age of onset of the disease in these familial forms, as in the Down cases, is earlier than that in sporadic forms Notable is the common occurrence of asynchronous myoclonus, epilepsy, aphasia, and paratonia in the familial cases It has been clear for some time that an excess amyloid alone is an incomplete explanation for the disease Apolipoprotein E (ApoE), a regulator of lipid metabolism that has an af nity for the -amyloid protein in Alzheimer plaques, has been found to be another genetic marker that greatly modi es the risk of acquiring Alzheimer disease Of the several isoforms of ApoE, the presence of E4 (and its corresponding gene allele e4 on chromosome 19) is associated with a tripling of the risk of developing sporadic Alzheimer disease (Roses, Strittmatter et al, and Polvikoski et al) This is the same allele that contributes to an elevated low-density lipoprotein fraction in the serum Possession of two e4 alleles virtually assures the development of disease in those who survive to their eighties The e4 allele also modi es the age of onset of some of the familial forms of the disease In contrast, the e2 allele is underrepresented among Alzheimer patients For these reasons it has been proposed that ApoE, by interacting with APP or tau protein in some way, modi es the formation of plaques Indeed, possession of the e4 allele correlates with increased deposition of A in the brain (McNamara) Furthermore, as pointed out by Hardy, ApoE appears to act after the various genetic mutations have in uenced the cell dysfunction that causes Alzheimer disease These ndings have led to interest in using the e4 genotype as a marker for the risk of Alzheimer disease, but it must be pointed out that these are statistical relationships that do not invariably connect the allele to the disease in a particular individual In other words, the e4 allele does not act as a mendelian trait but as a susceptibility (risk) factor It follows that many individuals without the allele also develop Alzheimer disease Moreover, many individuals with the e4 allele live into their seventies and eighties without developing Alzheimer disease Therefore the results of such testing must be interpreted with caution All that can be stated with certainty is that, on average, the presence of the e4 allele accelerates the appearance of Alzheimer disease by about 5 years Studies of the molecular genetics of Alzheimer disease are yielding new information at such an astonishing rate that much of the foregoing text will soon be outdated Useful basic reviews of this subject are those of Martin and of Selkoe, listed in the References
Diagnostic Studies The most useful, but not de nitive, ancillary tests in use are CT scanning and MRI (Fig 39-3) In patients with advanced Alzheimer disease, the lateral and third ventricles are enlarged to about twice normal size and the cerebral sulci are widened As stated previously, ne-section coronal MRI of the medial temporal lobes reveals a disproportionate atrophy of the hippocampi and a corresponding enlargement of the temporal horns of the lateral ventricles Early in the disease, however, the changes do not exceed those found in many mentally intact old persons For this reason, one cannot rely on imaging procedures alone for diagnosis CT and MRI scans are most valuable in excluding brain tumor, subdural hematoma, cerebral infarction, and hydrocephalus The EEG undergoes a diffuse slowing, but only late in the course of the illness The CSF is also normal, though occasionally the total protein is slightly elevated Using the constellation of clinical data, CT scanning, and MRI along with the age of the patient and time course of the disease the diagnosis of senile dementia of Alzheimer type is being made correctly in 85 to 90 percent of cases Of some value in our experience have been studies of cerebral blood ow (single-photon emission tomography, or SPECT) and metabolism (positron emission tomography, or PET), which show diminished activity in the medial temporal lobes, sometimes early in the disease Nevertheless, in most cases, when such changes were evident, the diagnosis was already obvious on clinical grounds alone Our recent experience has been that the pattern of Alzheimer change on these blood ow and metabolic studies is too often applied indiscriminately Neuropsychologic tests show deterioration in memory and verbal access skills Testing is particularly useful when there is a serial decline in ability The use of these examinations is described in Chap 21 Certain aspects of attention and executive function in Alzheimer disease have recently been reviewed by Perry and Hodges There is no rm biologic marker of Alzheimer disease with the exception of an imprecise association with the disease-modifying e4 apolipoprotein allele, as mentioned earlier The ratio of A to tau in the cerebrospinal uid (curiously low in Alzheimer disease) has been proposed as a useful test, but is not yet well enough validated for routine use (Maddalena et al) Differential Diagnosis (See also Table 21-3, page 374) Formerly, when virtually all forms of presenile and senile dementia were untreatable, there was little advantage to either the patient or the family in ascertaining the cause of the cerebral disease Such patients were customarily left at home or committed to an institu-
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