Topiramate-responsive headache due to idiopathic intracranial hypertension in Behçet syndrome.

A 14-year-old adolescent was seen with an 8-month history of almost daily incapacitating headaches due to idiopathic intracranial hypertension in Behçet syndrome. All his clinical signs and symptoms, including headache, resolved 2 to 4 weeks after topiramate was initiated. An effect on carbonic anhydrase isoenzymes II and IV, reducing cerebrospinal fluid production, could potentially explain the beneficial effect of topiramate in intracranial hypertension.

Polymorphism at codon 469 of the intercellular adhesion molecule-1 gene is not associated with sporadic Alzheimer's disease.

Activation of microglia is a central part of the chronic inflammatory response in Alzheimer's disease (AD). Intercellular adhesion molecule-1 (ICAM-1) is a cell surface receptor that may act in AD to adhere microglia to beta amyloid fibrils within senile plaques. Preliminary evidence in an Italian population indicates that a polymorphism at codon 469 of the ICAM-1 gene is a predisposing factor for sporadic AD.

Age-dependent association between the Q7R polymorphism in the Saitohin gene and sporadic Alzheimer's disease.

A vigorous controversy exists over whether tau tangles or amyloid-beta plaques are the primary cause of neurodegeneration in Alzheimer's disease (AD), and it is not well established whether genetic variation in tau is associated with AD. A recently identified novel protein, named Saitohin (STH), shares tissue expression pattern with tau, and preliminary evidence in a North American population indicates that a polymorphism at codon 7 (Q7R) of the STH gene is a predisposing factor for sporadic AD. A case-control study utilizing a clinically well-defined group of 315 sporadic AD patients and 307 control subjects was performed to test this association.

Polymorphism at codon 174 of the prion-like protein gene is not associated with sporadic Alzheimer's disease.

Alzheimer's disease (AD) and prion diseases are associated with the occurrence of protein aggregates called amyloid fibrils, containing the amyloid-beta peptide in AD, and a modified form (PrP(Sc)) of the normal cellular prion protein (PrP(c)) in prion diseases. PrP(c) is encoded by the prion protein gene, and a common polymorphism at codon 129 of this gene is a determinant of susceptibility to acquired and sporadic prion diseases but not for sporadic AD. A recently identified novel protein, named Doppel, shares biochemical and structural homology with PrP(c).