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Articles by S. A. Mousa
Total Records ( 2 ) for S. A. Mousa
  O. G Aderinwale , H. W Ernst and S. A. Mousa

Alzheimer’s disease (AD) is a devastating neurodegenerative disorder that currently affects millions of Americans. There is no cure at present and no real long-term hope for patients with AD. While partially effective in improving symptoms, currently available treatments approved by the US Food and Drug Administration (FDA) do not halt progression of AD, or address the underlying mechanism of the disease, in part because the etiology of AD is still an active area of investigation. Identification of risk factors and the pathogenic mechanism of AD hold the promise of bringing forth novel treatments and perhaps even a cure. In this review, we will summarize some of the risk factors for AD, AD diagnosis, and current treatments. Novel therapeutic strategies such as inhibition of β-amyloid peptide (Aβ), tau-mediated pathogenesis, and receptors for advanced glycation end products (RAGE), as well as neuroprotective and anti-inflammatory approaches and the impact of cholesterol-lowering, botanical, and nutritional agents are also reviewed.

  S. S Mousa , F. B Davis , P. J Davis and S. A. Mousa

The endogenous thyroid hormones L-thyroxine (T4) and 3,5,3'-triiodo-L-thyronine (T3) induce angiogenesis via an endothelial cell iodothyronine receptor on integrin Vβ3. This receptor also exists on platelets. Diiodothyropropionic acid (DITPA) and GC-1, a noniodinated thyroid hormone analog, also induce angiogenesis. Here we examined the effects of iodothyronines (L-T4 vs L-T3) and analogs DITPA and GC-1 on human platelet function. Subthreshold aggregation of platelets obtained from healthy human donors was induced with collagen. Platelet activation (proaggregation) and adenosine triphosphate (ATP) secretion (degranulation) induced by L-T 4, L-T4-agarose, L-T3, DITPA, or GC-1 were determined simultaneously. Platelet aggregation and ATP secretion induced by a subthreshold level of collagen were enhanced 3-fold by either L-T4 or L-T 4-agarose (0.01 µmol/L) as compared to control, whereas, L-T 3, DITPA, or GC-1 had no effect under the same conditions. The platelet proaggregatory and degranulation effects of L-T4 were blocked by the vβ3 antagonist XT199 (0.1 µmol/ L) and by tetraiodothyroacetic acid (tetrac; 0.1 µmol/L). Tetrac inhibits binding of thyroid hormone analogs to the receptor on vβ3 and lacks thyromimetic activity at this site; thus, the proaggregatory action of L-T4 likely involves the cell surface receptor on integrin vβ3. The thyroid hormone receptor (TR) on human platelets but not endothelial cells distinguishes among iodothyronines, reflecting quantitative differences in integrin sites on endothelial cells and platelets or qualitative differences in the phospholipids/protein microenvironment of endothelial and platelet membranes that can affect integrin function. Additional studies in different populations with larger sample sizes are warranted to determine the impact of the current findings on clinical interventions.

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