Attenuation of AD-like neuropathology by harnessing peripheral immune cells: local elevation of IL-10 and MMP-9.

Immunization with an altered myelin-derived peptide (MOG45D) improves recovery from acute CNS insults, partially via recruitment of monocyte-derived macrophages that locally display a regulatory activity. Here, we investigated the local alterations in the cellular and molecular immunological milieu associated with attenuation of Alzheimer's disease-like pathology following immunotherapy. We found that immunization of amyloid precursor protein/presenilin 1 double-transgenic mice with MOG45D peptide, loaded on dendritic cells, led to a substantial reduction of parenchymal and perivascular amyloid beta (Abeta)-plaque burden and soluble Abeta((1-42)) peptide levels as well as reduced astrogliosis and levels of a key glial scar protein (chondroitin sulphate proteoglycan).

Spontaneous spinal cerebrospinal fluid leaks as the cause of subdural hematomas in elderly patients on anticoagulation.

Subdural hematoma is a relatively common complication of long-term anticoagulation, particularly in the elderly. The combination of anticoagulation and cerebral cortical atrophy is believed to be sufficient to explain the subdural bleeding. The authors report a series of elderly patients who were on a regimen of anticoagulation and developed chronic subdural hematomas (SDHs) due to a spontaneous spinal CSF leak.

Spontaneous spinal cerebrospinal fluid leak as a cause of coma after craniotomy for clipping of an unruptured intracranial aneurysm.

Spontaneous spinal CSF leaks are best known as a cause of orthostatic headache, but may also be the cause of coma. The authors encountered a unique case of a spontaneous spinal CSF leak causing coma 2 days after craniotomy for clipping of an unruptured aneurysm. This 44-year-old woman with autosomal dominant polycystic kidney disease underwent an uneventful craniotomy for an incidental anterior choroidal artery aneurysm.

Absence of TGFBR2 mutations in patients with spontaneous spinal CSF leaks and intracranial hypotension.

A heritable connective-tissue-disorder often is suspected in patients with spontaneous spinal CSF leaks and intracranial hypotension, but the nature of the disorder remains unknown in most patients. The aim of this study was to assess the gene encoding TGF-beta receptor-2 (TGFBR2) as a candidate gene for spinal CSF leaks. We searched the TGFBR2 gene for mutations in eight patients with spontaneous spinal CSF leaks who also had other features associated with TGFBR2 mutations, i.

Frequency of spontaneous intracranial hypotension in the emergency department.

Spontaneous intracranial hypotension is considered a rare disorder. We conducted a study on the frequency of spontaneous intracranial hypotension in the emergency department (ED). We identified patients with spontaneous intracranial hypotension evaluated in the ED of a large urban hospital between 1 January 2003 and 31 December 2006.

Upright MRI in spontaneous spinal cerebrospinal fluid leaks and intracranial hypotension.

Orthostatic headaches are the hallmark of spontaneous intracranial hypotension, but MRIs are traditionally obtained in the supine position. We investigated the utility of upright MRI of the brain in 6 patients with spontaneous intracranial hypotension. No discernable differences were noted between the supine and upright images.

Cerebrovascular Involvement in Ehlers-Danlos Syndrome.

Ehlers-Danlos syndrome type IV is one of the most prominent heritable disorders of connective tissues associated with neurovascular disease. It is an uncommon disorder characterized by thin translucent skin, distinctive facial features, excessive bruising, and rupture of blood vessels or viscera. The typical neurovascular complications of this syndrome are carotid cavernous fistulas, intracranial aneurysms, and cervical artery dissections.

A herpes simplex virus type 1 mutant deleted for gamma34.5 and LAT kills glioma cells in vitro and is inhibited for in vivo reactivation.

To create an oncolytic herpes simplex virus type 1 (HSV-1) that is inhibited for reactivation, we constructed a novel herpes recombinant virus with deletions in the gamma34.5 and LAT genes. The LAT gene was replaced by the gene for green fluorescent protein, thereby allowing viral infection to be followed.