Morphology and neurochemistry of canine corneal innervation.

PURPOSE: To determine the architectural pattern and neuropeptide content of canine corneal innervation. METHODS: Corneal nerve fibers in normal dog eyes were labeled immunohistochemically with antibodies against protein gene product (PGP)-9.5, calcitonin gene-related peptide (CGRP), substance P (SP), vasoactive intestinal polypeptide (VIP), and tyrosine hydroxylase (TH). Relative innervation densities and distribution patterns for each fiber population were assessed qualitatively by serial line-drawing reconstructions and quantitatively by computer-assisted analyses. RESULTS: More than 99% of all corneal PGP-9.5-immunoreactive (IR) nerves contained both CGRP and SP, approximately 30% contained TH, and none contained VIP. Distribution patterns of corneal PGP-9.5-, CGRP-, SP-, and TH-IR nerves were indistinguishable, except that TH-IR fibers were absent from the corneal epithelium. Morphologically, canine corneal innervation consisted of a rich anterior stromal plexus, divided on the basis of morphologic criteria into anterior and posterior levels, and a rich epithelial innervation, characterized by large numbers of horizontally oriented, basal epithelial "leash" formations. Leash axons in all quadrants of the corneal epithelium oriented preferentially toward a common locus in the perilimbal cornea. CONCLUSIONS: The results of this study demonstrate for the first time the detailed architectural features, distinctive basal epithelial leash orientations, and peptidergic content of canine corneal innervation. The normal innervation pattern described in this study will provide other investigators with essential baseline data for assessing corneal nerve alterations in canine patients with spontaneous chronic corneal epithelial defects (SCCED) and other ocular diseases or injuries.

A Polish pedigree with Alzheimer's disease determined by a novel mutation in exon 12 of the presenilin 1 gene: clinical and molecular characterization.

The presenilin 1 (PS-1) gene, recently identified on chromosome 14q24.3, is a major gene involved into the autosomal dominant forms of early onset Alzheimer's disease (EOAD). Mutations of the PS-1 gene are responsible for the majority of familial EOAD. We found a novel mutation in a Polish family with EOAD from the Poznan region. The mutation at codon 424 in exon 12 of the PS-1 gene leads to an amino acid substitution Leu-Arg in a transmembrane domain VIII of the presenilin 1 molecule. The change is predicted to have a drastic effect on the protein function because it is associated with a very early age of onset (a range of 30-35 years) and a quick progression (about a 4-5 years duration) of the disease.

Apolipoprotein E genotypes in sporadic early and late-onset Alzheimer's disease.

Recent data have demonstrated that presence of apolipoprotein E (APOE) epsilon *4 allele is a major risk factor of Alzheimer's disease (AD). We determined the APOE genotypes in 64 patients with sporadic probable AD and 43 non-demented aged controls selected from Poznan region and the western part of Poland using the polymerase chain reaction (PCR) followed by the restriction fragment length polymorphism (RFLP) analysis. We confirmed a strong correlation of the APOE epsilon *4 allele with sporadic late-onset AD. In contrast to many previous reports we did not found an association between the APOE epsilon *4 allele and sporadic early-onset AD.

Screening for presenilin-1 gene mutations by PCR-SSCP analysis in patients with early-onset Alzheimer's disease.

The majority of early-onset familial Alzheimer's disease (EOAD) has been associated with mutations in a novel gene on chromosome 14 which has been termed presenilin-1 gene. We screened for mutations within the presenilin-1 gene in twenty patients with EOAD using a PCR-SSCP analysis. We found three aberrant (mutant?) band patterns for exons 4 and 7 in three unrelated patients.

Association between the PI*M3 allele of alpha 1-antitrypsin and Alzheimer's disease? A preliminary report.

The deposition of beta A4-amyloid in senile plaques in the brain and small cerebral vessels is one of the pathological hallmarks of Alzheimer's disease (AD). Serine protease inhibitors (serpins) such as alpha 1-antitrypsin and alpha 1-antichymotrypsin have been found to be associated with beta-amyloid deposits; interest in their role in the pathogenesis of AD has therefore recently increased. We have analyzed alpha 1-antitrypsin phenotypes in a sample of 29 Polish patients with probable Alzheimer's disease. We have found an increased frequency of the PI*M3 allele (0.1897) in patients in comparison with the general population control (0.0563).

[Comparative analysis of the epidemiology of amyotrophic lateral sclerosis in the province of Poznan]. / Porównawcza analiza epidemiologiczna stwardnienia bocznego zanikowego w województwie poznanskim.

In the Province of Poznan on the point day Dec 31 1986 the prevalence of lateral amyotrophic sclerosis was found to be 1.9 per 100 thousand and the incidence in 1986 was 1.1 per 100 thousand. In relation to a similar study in 1965 these results are insufficient for accepting a change in the prevalence of amyotrophic lateral sclerosis in the last twenty years.

[Epidemiology of Parkinson disease in the Pozna'n province]. / Epidemiologia choroby Parkinsona w województwie poznanskim.

The authors analyzed the prevalence and incidence of parkinsonism in the Poznan region. The research led to the following conclusions: 1. Incidence of parkinsonism in the Poznan region amounts to 12.6 per 100,000 of population, which is the middle value of scatter in the investigation on a world-scale. The prevalence of the disease--65.9 per 100,000--is the lower range of values found in many countries of the world. This seems to point to a shorter survival time of patients with parkinsonism in our country. 2. Among various age groups, the highest incidence and prevalence of parkinsonism is found in the age groups of 70-79 and 80-89, with slightly higher prevalence rates among males. 3. The authors found in the Poznan region irregular prevalence of parkinsonism, that is the existence of small focuses of the disease, which seems to depend on unfavourable genetic factors existing in those places.