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Cerebrospinal fluid taurine in alzheimer's disease.

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4. Voiculescu V, Alexianu M, Popescu-Tismana G, et al. Polyneuropathy with lipid deposits in Schwann cells and axonal degeneranon in cerebrotendinous xanthomatosis. J Neurol Sci 1987;82:
89-99
5. Salen G, Shefer S, Berginer VM. Familial diseases with storage
of sterols other than cholesterol: cerebrotendinous xanthomatosis
and sitosterolemia with xanrhomatosis. In: Stanbury JB, Wyngaarden JB, Fredrickson DS, et al, eds. The
basis of inherited disease, ed 5. New York: McGraw Hill, 1983:713-738
*Department of Nezlrology
Hospital 2Elx
Cerebrospinal Fluid
Taurine GI Alzheimer’s
Disease
Un&wPty of Alacant
J. Alom,* J. N. Mahy,? N. Brandi,? and E. Tolosat
The article by Kowall and Beal [l}describes how glutamate-,
glutaminase-, and taurine-immunoreactive neurons develop
neurofibrillary tangles in Alzheimer’s Disease (AD). Although glutamate 123,among other neurotransmitters E31,
has been involved in the neurochemical degenerative process
in AD, less is known about taurine. Their interesting report
suggests that taurine-containing neurons could also be involved in this pathological process. We would like to communicate our results about recent measurements of cerebrospinal fluid (CSF) taurine, among other amino acids, in the same
group of A D patients in which we previously found CSF
neuropeptide Y decrements [4].
Twenty consecutive patients (7 men and 13 women with
a mean age of 64.4 yr, range 52-75 yr) were entered in
the study. All met the diagnostic criteria for probable AD
according to the NINCDS-ADRDA Work Group. Symptomatic causes of dementia were excluded by laboratory examination, electroencephalography, and computed tomography. All patiencs included in the study had a Hachinski
ischemic score of <4. Cognitive evaluation was carried out
with the Mini Mental State Examination. The patients were
also evaluated with the Blessed Dementia Scale. The controls
were 19 hospitalized subjects (8 men and 11 women, mean
age 67.7 yr, range 50-80 yr) with no known central nervous
system disorder. The samples were collected between 9:OO
AM and 11:OO AM, after the patient had spent 8 hours in a
recumbent position. The samples were frozen and stored at
-20°C until assayed. The amino acids were measured by
high pressure liquid chromatography. Comparison between
subject groups was performed using Student’s t test and
Pearson’s correlation coefficient.
CSF taurine levels were lower in patients with AD (4.8 ?
1.4 FM) than in controls (6.4 1.7 kM) (p = 0.005). The
other CSF amino acid levels did not show any statistical difference between patients and controls: aspartic acid (5.9 k
1.3 vs 5.8 t 1.4 pM, p = 0.76); serine (14.2 k 4.8 vs 15.1
5.9 p M , p = 0.16); glutamine (398.2 f 87.1 vs 432.1
111.3,p = 0.30); alanine (19.4 5.5 vs 24.6 ? 1 2 . 1 , ~=
0.13); and homocysteic acid (2.5 2 1.1 vs 2.4 t 0.8, p =
0.13). We found a correlation between the disease duration
(yr) and the levels of serine (r = 0.64, p = 0.002) and
glutamine (r = 0.46, p = 0.02). We also found a negative
correlation between the levels of alanine and the Blessed
scores (r = 0.50,p = 0.01).
*
*
*
Mainly, we are describing CSF taurine decrements in A D
patients. As far as we know, there are no previous studies in
the literature about CSF taurine levels in AD, and we consider that our findings agree with the report of Kowall and
We do not know if these CSF taurine decrements are
a reflection of changes in an astrocytic versus a neuronal
taurine pool. It would be desirable in future to investigate
the role of taurine-containing neurons in the neurochemical
pathology of AD.
*
f Department of Biochemistry
University of Bari-elona
$Department of Neurology
Hospital Clinic i Provincial
University of Barcelona
Barcelona, Spain
References
1. Kowall NW, Beal MF. Glutamate-, glutaminase-, and taurineimmunoreactive neurons develop neurofibrillary tangles in Alzheimer’s disease. Ann Neurol 1991;29:162-167
2. Hyman BT, Van Hoesen GW, Damasio AR. Alzheimer’s disease:
glutamate depletion in the hippocampal perforant pathway zone.
Ann Neurol 1987;22:37-40
3. Beal MF, Martin JB. Neuropeptides in neurological disease. Ann
Neurol 1986;20:547-565
4. Alom J, Galard R, Catalan R, er al. Cerebrospinal fluid neuropepride Y in Alzheimer’s disease. Eur Neurol 1990;30:207-210
Continuous Muscle Fiber
Activity Associated with
Thymoma
V. Homberg, MD,* and H.-J. Freund, MDI‘
We read with interest the article by Garcia-Merino and colleagues (February 1991 issue of Annab), concerning an association of Continuous Muscle Fiber Activity, Peripheral Neuropathy, and Thymoma [l). The authors claim that this
association has not previously been recognized. We published two similar cases 4 years ago and discussed possible
autoimmune mechanisms underlying this condition t2). Associations of malignancy and neuromyotonia have been described previously [ 3 , 41. In the French literature, cases labeled “choree fibrillaire de Morvan” closely resemble this
type of neuromuscular hyperactivity [ 5 ] . This condition had
also been reported to be associated with thymoma 161 in a
case which took a fatal course. Both of our patients showed a
proliferative thymoma with high serum titers of acetylcholine
receptor (AchR) antibodies without signs of myasthenia gravis. Unfortunately, Garcia-Merino and colleagues did not
look at AchR antibodies. We discussed the possibility in our
cases that AchR antibodies may facilitate rather than inhibit
neuromuscular cholinergic transmission. Electrophysiological
studies showed multiple discharges on needle EMG recordings and some minor neurographic abnormalities, including
F-wave failures, which resemble the mild signs of peripheral
Annals of Neurology
Vol 30 N o 5 November 1991 735
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