Migraine With Exclusive Olfactory Aura: Case Report and Literature Review.

Objectives: To report the case of a patient enduring migraine attacks preceded by hallucinatory olfactory symptoms, with characteristics which typically define migraine with aura (MWA).

Background: MWA accounts for about 30-40% of the total cases of migraine and is almost always preceded by visual disorders; and in rare cases migraine attacks are preceded by olfactory hallucinations which have not been so far recognized as a type of aura.

Results: We describe a 51-year-old male whose migraine attacks are preceded, unusually for migraine sufferers, only by olfactory hallucinations; in 10% of the attacks, the olfactory symptoms are not followed by any pain but always appear with the same characteristics.

Oxidative imbalance in patients with mild cognitive impairment and Alzheimer's disease.

Increasing evidence supports a role of oxidative imbalance, characterized by impaired antioxidant enzymatic activity and increased reactive oxygen species (ROS) production, in mild cognitive impairment (MCI) and Alzheimer's disease (AD) pathogenesis. Hyperhomocysteinemia, another risk factor for AD, also contributes to oxidative damage. Plasma total homocysteine (tHcy) and ROS levels, and total antioxidant capacity (TAC) were determined in 71 AD, 36 MCI and 28 vascular dementia (VaD) patients as well as in 44 age-matched controls.

Heparan sulfate proteoglycan induces the production of NO and TNF-alpha by murine microglia.

Background: A common feature of Alzheimer's disease (AD) pathology is the abundance of activated microglia in neuritic plaques containing amyloid-beta protein (Abeta) and associated molecules including heparan sulfate proteoglycan (HSPG). Besides the role as pathological chaperone favouring amyloidogenesis, little is known about whether or not HSPG can induce microglial activation. Cultures of primary murine microglia were used to assess the effect of HSPG on production of proinflammatory molecules that are known to be present in neuritic plaques of AD.

MCP-1 in Alzheimer's disease patients: A-2518G polymorphism and serum levels.

MCP-1 levels are increased in CSF of patients with Alzheimer's disease (AD) compared with controls, suggesting a role in the development of dementia. Recently, a biallelic A/G polymorphism in the MCP-1 promoter at position -2518 has been found, influencing the level of MCP-1 expression in response to an inflammatory stimulus. The distribution of the A-2518G SNP was determined in 269 AD patients and in 203 healthy age matched controls, showing no differences between the two groups.

Interleukin-1 beta and interferon-gamma induce proliferation and apoptosis in cultured Schwann cells.

This study reports that in Schwann cell tissue culture the administration of the two pro-inflammatory cytokines, interleukin-1 beta (IL-1 beta) and interferon-gamma (IFN-gamma), at different dosages, singly or in combination, can induce apoptosis and/or mitosis. Schwann cell apoptosis was maximal within 24 h of stimulation with 50 U/ml of IFN-gamma, while proliferation was at its peak within 24 h with 10 U/ml IL-1 beta, and both processes decreased progressively by 48 and 72 h. Moreover, the combination of the two cytokines did not show any synergistic effect.

Macrophage infiltration and death in the nerve during the early phases of experimental diabetic neuropathy: a process concomitant with endoneurial induction of IL-1beta and p75NTR.

This study describes the infiltration and death of monocyte/macrophages and concomitant endoneurial expression of the pro-inflammatory cytokine interleukin-1beta (IL-1beta) and neurotrophin receptor p75 (p75NTR) in the sciatic nerve at the early phases of experimental diabetic neuropathy induced in Lewis rats by streptozotocin (STZ) intraperitoneal injection. Immunocytochemistry and single nerve fiber immunostaining showed the presence of macrophages in diabetic nerves by weeks 2 and 3 after STZ administration, and the 15% of these cells were TUNEL positive. IL-1beta was evident in scattered macrophages, and along few isolated nerve fibers until week 5, when it became undetectable, in concomitance with complete endoneurial clearance of macrophages.