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Antagonist activity in cerebellar hypermetria.

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with the presence or absence of neurofibrillary change (as
evidenced by tau-1 immunoreactivity). It is also evident from
the data in the Table that Af3 and apo E immunoreactivity
correlate, and both are an early change that precedes the
development of N l T s and the onset of dementia.
The percentage of apo E3/E4 individuals in the general
population is 15 to 20%. It is unclear why the apo E 4 frequency was so low in our DS population ( p = 0.0251, since
the frequency of apo E isotypes in another DS group was
reported to be like that of the general population [6]. I t is
possible that in our group of severely retarded, institutionalized DS patients, the apo E4 allele is selected against; although, larger numbers of DS patients will need to be studied
to clarify this point. Five of our 40 D S patients are apo
E3/E2 heterozygotes (12.59), which is close to the expected
12.0% found in the general population. However, these apo
E3/E2 DS individuals appear to have a similar amount of
4G8 and anti-apo E immunoreactivity, compared with their
apo E3 homozygote counterparts (see Table); hence, a protective effect on the neuropathology is not evident in this
particular DS population.
These findings suggest that the apo E4 isotype is not essential in itself for the production of A D pathology, and that
the importance of other factors must be stressed. A D is genetically heterogeneous with linkage to chromosomes 14, 17,
and 21, as well as at least one other site (review [l]). The
important risk factors for developing disease, such as the apo
E isotypes, will vary in each of these types of AD.
This research was supported by NIH grants KO8 AG00542,
AG08721, AGI 1481, and AG10953 (LEAD) and grant IIRG-91102 from the Alzheimer’s Disease and Related Disorders Association.
Antagonist Activity in
Cerebellar Hypermetria
Barbara Wild, M D
Recently Manto and colleagues 1) in a study of patients with
cerebellar lesions reported an increase of hypermetria in fast
wrist movements with increasing inertial load. They found
the following two changes of electromyographic activity
when compared with normals: (1) the previously reported
121 delay of antagonist activity and (2) a reduction of the
normal increase of antagonist activity with load. Their conclusion was that the cerebellum computes onset time and amplitude of antagonist muscular activity.
Although this proposal seems likely their data do not provide sufficient evidence, Marsden and co-workers [:i]showed
that the magnitude of antagonist activity in fast movements
increases with movement velocity. Unfortunately Manto and
colleagues C 11 did not give data on movement velocity. Peak
acceleration, however, which is well correlated with velocity,
was considerably lower under all conditions in their cerebellar patients (Table 3 in El]).
Therefore, it is possible that the reduction of antagonist
activity in cerebellar subjects compared with normals is due
to a reduction of movement speed and not to a genuine
cerebellar deficiency. A comparison of normal and cerebellar
antagonist activity in movements of the same peak velocity
or acceleration is needed.
Department of Neurology
University of Tiibingen
Tijbingen. Germany
Ref rences
Departmenls of Pathology, Neurology?and Pharmacology
New York Unii‘ersity Medical Center
Neui York. N Y 10016
Department of Pathologicaf Rieurobiology
Neuz York State Institute for Basic Research
in Dn~elopmentalDisabilities
Staten Island. N Y 10314
1. Manto M, Godaux E, Jacquy J. Cerebellar hypermetria is larger
when the inertial load is artificially increased. Ann Neurol 1994;
2. H o w J, Wild B, Diener HC. Cerebellar dysmetria at the elbow,
wrist, and fingers. J Neurophysiol 1991;65.563-57 1
3. Marsden CD, Obeso JA, Rothwell JC. The function of the antagonist muscle during fast limb movements in man. J Phvsiol 1983;
M. Manto, MD, E. Godaux, MD, and J. Jacquy, M D
I. Wisniewski T, Ghiso J, Frangione B. Alzheimer’s disease and
soluble AD. Neurobiol Aging 1994;15:143-152
2. Corder EH, Saunders AM, h s c h NJ, et al. Apolipoprotein E4
type 2 allele decreases the risk of late-onset Alzheimer’s disease.
Nature Genet 1994;7:180-183
3. Alzheimer’s Disease Collaborative Group. Apolipoprotein E genotype and Alzheimer’s disease. Lancet 1993;342:737-738
4. Van Broeckhoven C , Backhovens H, Cruts M, er al. Apo E genotype does not modulate age of onset in families with chromosome
14 encoded Alzheimer’s disease. Neurosci Lett 1994;169: 179180
5 . Hixson JE, Verner DT. Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with Hhal. J Lipid
Res 1990;31:545-548
6. Hardy J, Crook R, Perry R, et al. Apo E genotype and Down’s
syndrome. Lancet 1994;343:979-980
138 Annals of Neurology
Vol 37
N o 1 January 1975
W e have read with great interest the letter from D r Wild
concerning our work on cerebellar hypermetria. Dr Wild is
right that comparison between normal and cerebellar antagonist activity has to be carried out on movements with the
same peak velocity. In fact, we did so although we did not
mention it in our original work [I]. The values of the peak
velocities measured in each of the six experimental conditions ( 1 5 or 5 0 degrees, no overload o r 200 or 500 gm) and
for both the normal and patients groups are listed in the
Table. The repeated-measure analysis of variance performed
on these values showed that (1) the peak velocities decreased
when extra masses were added in both control and patients
groups (significance of F: p < 0.001 and p = 0.001 in the
normal group and in the patients group, respectively) but
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cerebellar, activity, antagonisms, hypermetria
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