Described herein are methods of the treatment and diagnosis of bone mineral density related disorders. More particularly, described herein are methods of diagnosing or predicting a bone mineral density related disease, or a risk of a bone mineral density related disease, in a subject, which method comprises detecting a mutation in the TBXAS1 gene, wherein the presence of such a mutation is indicative of a bone mineral density related disease or of a risk of a bone mineral density related disease. Also described are compounds such as a thromboxane synthase (TXAS) encoding polynucleotide, a TXAS, thromboxane A2 or an analog thereof for treating or preventing a disease associated with an increased bone mineral density (e.g., Ghosal hematodiaphyseal dysplasia syndrome). Additional aspects describe an inhibitor of TBXAS1 gene expression or a thromboxane inhibitor for treating or preventing a disease associated with a decreased bone mineral density (e.g., osteoporosis).

Described herein are methods of the treatment and diagnosis of bone mineral density related disorders. More particularly, described herein are methods of diagnosing or predicting a bone mineral density related disease, or a risk of a bone mineral density related disease, in a subject, which method comprises detecting a mutation in the TBXAS1 gene, wherein the presence of such a mutation is indicative of a bone mineral density related disease or of a risk of a bone mineral density related disease. Also described are compounds such as a thromboxane synthase (TXAS) encoding polynucleotide, a TXAS, thromboxane A2 or an analog thereof for treating or preventing a disease associated with an increased bone mineral density (e.g., Ghosal hematodiaphyseal dysplasia syndrome). Additional aspects describe an inhibitor of TBXAS1 gene expression or a thromboxane inhibitor for treating or preventing a disease associated with a decreased bone mineral density (e.g., osteoporosis).

The present invention relates to a method for inducing production of vascular endothelial growth factor (VEGF). The method includes administering, to an individual, a composition including adeno-associated virus (AAV) carrying a hPGIS gene coding for human prostacyclin synthase (hPGIS) which synthesizes prostaglandin I.sub.2 (PGI.sub.2).

The present invention relates to a method for inducing production of vascular endothelial growth factor (VEGF). The method includes administering, to an individual, a composition including adeno-associated virus (AAV) carrying a hPGIS gene coding for human prostacyclin synthase (hPGIS) which synthesizes prostaglandin I.sub.2 (PGI.sub.2).

The present invention relates to a method for inducing production of vascular endothelial growth factor (VEGF). The method includes administering, to an individual, a composition including adeno-associated virus (AAV) carrying a hPGIS gene coding for human prostacyclin synthase (hPGIS) which synthesizes prostaglandin I.sub.2 (PGI.sub.2).

The present invention provides a novel method of treatment for treating brain disorders that manifest oxidative stress by providing targeted populations of neurons with the ability to catabolize the acetylated amino acid derivative, N-acetylaspatic acid (NAA) and further supply extraphysiological levels of ATP to neurons via the targeted expression of the NAA catabolic enzyme aspartoacylase (ASPA) in neurons and astrocytes.

The present invention provides a novel method of treatment for treating brain disorders that manifest oxidative stress by providing targeted populations of neurons with the ability to catabolize the acetylated amino acid derivative, N-acetylaspatic acid (NAA) and further supply extraphysiological levels of ATP to neurons via the targeted expression of the NAA catabolic enzyme aspartoacylase (ASPA) in neurons and astrocytes.

Synthetic polynucleotides encoding human methylmalonyl-CoA mutase (synMUT) and exhibiting augmented expression in cell culture and/or in a subject are described herein. An adeno-associated viral (AAV) gene therapy vector encoding synMUT under the control of a liver-specific promoter (AAV2/8-HCR-hAAT-synMUT-RBG) successfully rescued the neonatal lethal phenotype displayed by methylmalonyl-CoA mutase-deficient mice, lowered circulating methylmalonic acid levels in the treated animals, and resulted in prolonged hepatic expression of the product of synMUT transgene in vivo, human methylmalonyl-CoA mutase (MUT).

There is provided a method for treating or reducing the effects of fructose intolerance and health problems associated with excessive fructose intake by administration of glucose isomerase. Other embodiments are also disclosed.

There is provided a method for treating or reducing the effects of fructose intolerance and health problems associated with excessive fructose intake by administration of glucose isomerase. Other embodiments are also disclosed.