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Biomedical subjects

J F Foncin

Publications and source records attributed to J F Foncin.

At least 109 records · Page 6Linked to original sources
PubMedDate not supplied

Beta AP deposition and head trauma.

Head trauma is considered to be a risk factor for Alzheimer's disease, because a high prevalence of beta AP deposits has repeatedly been reported in patients who died within a few days following head injury. To evaluate this statement, we undertook two studies using immunohistochemistry for beta AP and found a surprisingly low prevalence of beta AP diffuse deposits. We first selected 23 patients aged 17-63 years, who died 0-76 days after head trauma. Using beta AP antibody at the usual dilution (1:100), we did not find any deposits. With a high concentration of antibody (dilution 1:2) we found beta AP diffuse deposits in one 46-year-old case. In a second study, 17 patients aged 60-79 years old, who died 1-35 days after head injury, were compared to a control group. We did not find any significant difference in the density of beta AP diffuse deposits between cases and controls using usual dilutions of beta AP antibody. The density of beta AP diffuse deposits was linked only to aging and the presence of senile plaques.

Adolescent↗
PubMedDate not supplied

[Classical and ultrastructural neuropathology of aging processes in the human: a critical review (author's transl)].

Although the primary interest in the course of studies on aging is focused on problems of function, morphology has an important role to play as a marker and as a control. Processes concomitant with brain aging are multiple and diverse. They ought to be correlated individually with functional changes. Statistical problems in population sampling for reference morphological studies are difficult. Bias is often a consequence of unstated underlying theories (Brain aging: a physiological process v. one of many pathological processes). Morphological criteria do not allow close application of animal models to aging problems in the human. The review considers the following lesions: 1. Brain shrinkage; 2. Neuronal loss; 3. Alterations in the outline of neurons; 4. Lipofuscin accumulation; 5. Corpora amylacea; 6. Senile plaques and amyloid deposits; 7. "Neurofibrillar degeneration"; 8. "Granulovacuolar degeneration"; 9. Hirano bodies. Vascular changes and their consequences are not considered. Lesions in the first group (1 to 5) are interpreted as non-specific and non-specifically correlated with aging; their correlation with functional loss is low. Lesion in the second group (6 to 9), on the contrary, are strongly correlated with each other and with dementia; they are interpreted as characteristic, not of aging itself, but of a widespread pathological condition: Alzheimer's disease sensu lato. A current line of research involves the hypothesis of a viral origin of this condition.

Aging↗
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[Critical follow-up study of subjects with senile plaques: neuropathological, clinical, and electroencephalographic data (author's transl)].

Frontal isocortex biopsy or operative specimens exhibited senile plaques in 25 patients aged 40 to 73 years, association with Alzheimer's "neurofibrillary degeneration" in 20 of them. These patients were followed up for up to 14 years. 3 patients died 1 to 3 months after operation. 16 patients evolved into confirmed dementia, 12 of them most probably of the Alzheimer type. 6 patients recovered fully, and their subsequent evolution appears incompatible with a diagnosis of Alzheimer's dementia (follow-up period of 3 to 14 years). Retrospective evaluation of EEG data showed a good predictive value of previously described EEG changes, as indicative of later confirmation of alzheimer's dementia.

Adult↗
PubMedDate not supplied

The genetic defect in familial Alzheimer's disease is not tightly linked to the amyloid beta-protein gene.

Amyloid beta-protein (AP) is a peptide of relative molecular mass (Mr) 42,000 found in the senile plaques, cerebrovascular amyloid deposits, and neurofibrillary tangles of patients with Alzheimer's disease and Down's syndrome (trisomy 21). Recent molecular genetic evidence has indicated that AP is encoded as part of a larger protein by a gene on chromosome 21 (refs 5-7). The defect in the inherited autosomal dominant form of Alzheimer's disease, familial Alzheimer's disease (FAD), has been mapped to the same approximate region of chromosome 21 by genetic linkage to anonymous DNA markers, raising the possibility that this gene product, which could be important in the pathogenesis of Alzheimer's disease, is also the site of the inherited defect in FAD (ref. 5). We have determined the pattern of segregation of the AP gene in FAD pedigrees using restriction fragment length polymorphisms. The detection of several recombination events with FAD suggests that the AP gene is not the site of the inherited defect underlying this disorder.

Alzheimer Disease↗
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Alzheimer's disease: a model from the quantitative study of a large kindred.

In an Italian kindred (family N), early onset Alzheimer's disease has been transmitted in a Mendelian autosomal fashion since the early 18th century. The age at death of affected members of the family varies widely, and was taken as an index of the age of expression, a measure of phenotypic variability. Either a gamma or a log-normal algorithm provides the best fit for the age at death distribution. Subsets of family N widely different as to time and place have the same age at death of patients: Environment appears to play a negligible role in the expression of disease. Pairwise correlation between an affected parent and child is zero: The disease is monogenic (no major expression gene). The same stochastic distribution of age of expression, but with late onset, and after correction for death from other causes, is compatible with the epidemiology of Alzheimer's disease in general. Mendelian genetics is a possible model for Alzheimer's disease etiology.

Adult↗
PubMedDate not supplied

Involvement of cochlear nerve in acoustic tumours.

With conventional light and transmission electronmicroscopy we studied 10 cases of acoustic nerve tumour, 3 of which proved to be instances of von Recklinghausen neurofibroma and 7 of schwannoma. Schwannomas were not found to infiltrate the cochlear nerve. Hearing loss, if present in cases of schwannoma, could be related to non-specific lesions of the uninfiltrated cochlear nerve in the vicinity of the vestibular nerve tumour. Only neurofibromas were found to infiltrate the cochlear nerve. Distinction between tumour infiltration and non-specific lesion could be made by electron microscopy.

Adolescent↗
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[Infectious endocarditis in a neurosurgical unit].

Clinico-pathological study of 15 cases of cerebral complications of bacterial endocarditis referred to a neurosurgical unit for suspected cerebral abcess. In all cases but one, cerebral symptoms appeared with the cardiac condition undiagnosed, and complete diagnosis was made only at autopsy. Cerebral lesions consisted mainly in focal softening due to embolisms, generally multiple, with in about half the cases histological manifestations of bacterial seeding, without any abcess such as could be amenable to neurosurgical treatment. Surgical treatment of mycotic aneurysms was unsuccessful, due mainly to their multiplicity.

Adolescent↗
PubMedDate not supplied

[Association of Alzheimer's disease and Creutzfeldt-Jakob's disease (author's transl)].

Serial EEG studies and full neuropathological investigations (optic and electronic microscopy of biopsy and necropsy material) were carried out on two patients: 1. A 68-year-old man: development in two and a half months of Creutzfeldt-Jakob's disease signalled by early clinical and EEG changes and confirmed by associated spongiosis of the triad characteristic of Alzheimer's disease, which was unexpected in this case. 2. A 43-year-old man: first phase of four years of progressive deterioration, followed by an encephalopathic syndrome with myoclonus developing in twelve months. The serial EEG studies showed discontinuous periodic paroxystic activity from the start of the second phase of the disease, although the first biopsy still showed nothing but the signs of Alzheimer's disease. A fortnight later, a second biopsy revealed ultrastructural microspongiosis. Examination of necropsy material confirmed the extensive association of the characteristic images of the two processes. On the basis of these two case studies and some similar cases published in the literature, the authors discuss the possible etiological links between these two diseases and stress the importance of the EEG and cerebral biopsy for the purposes of differential diagnosis. (Acta neurol. belg., 1977, 77, 202-212).

Adult↗
PubMedDate not supplied

The origin of acoustic neuromas.

Small acoustic neuromas, operated on through transpetrosal approaches were studied by light and transmission electron microscopy. All schwannomas were found to interpenetrate the vestibular ganglion without a space or a capsule. In the abnormal ganglion areas, free tumour Schwann cells were observed. These results suggest that acoustic neuromas originate from the vestibular ganglion. The fact that the sheath of vestibular ganglion bipolar cells in man are devoid of myelin may account for the elective origin of acoustic neuromas in the Scarpa ganglion in the human.

Humans↗
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[The sheath of Scarpa ganglion cells in the baboon Papio papio].

The sheath of the bipolar perikarya of the vestibular ganglion (Scarpa) in Papio papio is made up of several Schwann cells which concur to form loose myelin, and at most five layers of compact myelin. Most of the Schwann cytoplasmic layers stop at the emergence of both neurites, forming at the point an incomplete Ranvier half-node. The constitution of the vestibular perikaryal sheath in Papio is intermediate between those previously described in the Rat and in the Human.

Animals↗
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[The origin of acoustic neurionoma. An ultrastructural study of operated neurinoma incipiens (author's transl)].

The origin of eighth nerve neurinoma has been studied by several authors with the light microscope, particularly on serial sections of decalcified temporal bone. The microsurgical approach of small neurinomas has led the present authors to an ultrastructural study of this problem. In the cases in which the origin could be seen, the tumor appeared to arise from the ganglion vestibulare (Scarpae). This fact is correlated with the neural crest origin of the ganglion, and with its ultrastructural characteristics in the normal human.

Humans↗