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Biomedical subjects

F Coria

Publications and source records attributed to F Coria.

63 records · Page 4Linked to original sources
PubMed1985

Demyelination-induced plasticity in the axon membrane: an ultrastructural cytochemical study of lead neuropathy in the rat.

We examined the distribution of ferric ion-ferrocyanide stain (a marker for excitable regions of myelinated fibers) in the lead-induced demyelinating neuropathy of the rat. By electron microscopy, we found that paranodal degeneration resulted in spreading of the reaction product from nodal to internodal axolemma. During repair, nodal-like stained areas formed at the contact zones between preremyelinating Schwann cells. These data suggest that the location and extent of excitable axonal regions are influenced by axoglial relationships. Additionally, some fibers displayed staining at paranodal axolemma adjacent to demyelinated segments, suggesting it might be an alternative site for impulse generation in demyelinated fibers.

Animals↗
PubMed1984

Axon membrane remodeling in the lead-induced demyelinating neuropathy of the rat.

Single-teased fibers stained with the ferric ion-ferrocyanide method allowed us to study axonal remodeling in the lead-induced demyelinating neuropathy of the rat. Our findings, in agreement with recent physiological data, pointed to a transitory reorganization of the demyelinated axons to maintain impulse conduction until remyelination and formation of new cytochemically normal nodes had restored a secure saltatory conduction.

Animals↗
PubMed1983

Occipital dysplasia and Chiari type I deformity in a family. Clinical and radiological study of three generations.

Three generations of a family affected by a craniocervical malformation (CCM) were subjected to clinical and radiological studies. Occipital dysplasia (OD) and Chiari type I deformity (CD.I) were the main features, inheritance being autosomal-dominant. The malformation was variably expressed; it ranged from OD with basilar impression (BI) to OD without BI and from CD.I with OD to CD.I without obvious osseous malformation. Its pathogenesis, and that of other related familial disorders (Klippel-Feil syndrome and syringomyelia), is discussed, the conclusion being drawn that all were elements of one genetic disorder which finds expression in a very variable sequence. The value of high-resolution CT in the detection of asymptomatic carriers is emphasized.

Adult↗
PubMed1982

Occipitoatlantal instability and vertebrobasilar ischemia: case report.

A 37-year-old woman had occipitoatlantal instability due to hypoplasia of the occipital condyles. Neck pain and transient ischemic attacks in the vertebrobasilar territory occurred with extension of the neck, which also caused convergence spasm. Angiography demonstrated that these manifestations were due to compression of the vertebral arteries during neck extension. Immobilization of the neck in a Minerva cast resulted in complete relief of symptoms.

Adult↗
PubMedDate not supplied

Alzheimer's disease, beta-amyloidosis, and aging.

Alzheimer's disease (AD) is rapidly moving from the obscure category of degenerative diseases to the more precise one of metabolic disorders. Recent discoveries have substantiated the hypothesis that AD results from the deposition of beta-amyloid, which is formed by polymers of a proteolytic fragment of the amyloid protein precursor (APP), and may induce intraneuronal aggregation of the microtubule-associated protein tau into paired helical filaments and neuronal death. There is also evidence that AD is a heterogeneous age-related disorder of multifactorial origin, which may arise as a consequence of point mutations of genes encoding APP or other proteins involved in its metabolism (familial AD), or a combination of genetic and non-genetic factors (sporadic AD). Familial AD displays genetic and phenotypic heterogeneity, meaning that mutations of different genes may cause the AD phenotype, and that different mutations of the same gene may cause phenotypically distinct disorders, including Alzheimer-type dementia and cerebral amyloid angiopathy with cerebral hemorrhages and stroke. On the other hand, aging, gender, head trauma, and variants of the apolipoprotein E gene have been shown to increase the risk of developing the more prevalent sporadic form of AD. The mechanisms by which these factors influence amyloidogenesis are beginning to be understood, and this will provide a rational basis for future therapy. Knowledge of the molecular basis of AD would eventually allow accurate risk prediction before the disease becomes clinically apparent, and better chances for early treatment and prevention.

Aging↗