Jornal de Neurologia Clínica e Neurocirurgia

Alzheimer's disease (AD) a progressive neurodegenerative disease that destroys memory and other important mental functions. More than 5 million Americans are living with AD. This number is expected to drastically increase as the baby boomer population transitions into the late-adulthood age group. Currently, the treatment for AD includes FDA drugs that focus on treating the symptoms. These types of drugs lose their efficacy as the disease progresses. Therefore, preventive measures are very critical in decreasing the incidence rate of AD. Many epidemiological studies have been conducted on the treatment of Alzheimer's that suggest enhanced coffee/caffeine intake during aging reduces the risk of AD. As one of most popular beverages in the World, many experimental studies have been done to test the effects of coffee consumption on AD. This paper will aim to review the important discoveries that have been made recently and present the possible mechanisms behind the neuroprotective effects.

The purpose of the present study was to determine the ability of nerve cryopreservation approaches, slow freezing, to preserve electric properties of sciatic nerves and histological structure. In the present manuscript, the electric resistivity (R) at different temperatures (T) was studied in frog sciatic nerve in two approaches i) nerve freezing between 300 K to 200 K and ii) nerve warming from 200 K to 300 K. Firstly, when the electrical contacts were leaned into frog sciatic nerve we note a semi-conductor behavior and a striking decrease of nerve resistivity at 252 K showing a super conductor-like behavior. Secondly, when electrical contacts were embedded to the nerve we note a metallic behavior and a fall of resistivity was shown at 252 K indicating a superconductor-like behavior. In addition, findings illustrate the importance of electric and histological studies to examine cryo-sensitivity of nerve.

PRKN and PINK1 genes mutations represent the most common cause of autosomal recessive early onset Parkinson’s disease (EOPD). We describe coexistence of both genes mutations and apparently dominant Parkinsonism in a family. Two sisters, presenting parental consanguinity and EOPD, carried a homozygous PINK1 deletion and a heterozygous missense PRKN mutation. Their father had late onset PD and resulted compound heterozygous for both mutations. The mother presented action tremor and harbored only one PINK1 deletion. Late onset Parkinsonism in the father could be related to the combination of heterozygous variants in both genes that might lower the threshold of the disease.