Vascular Alzheimer's

The most common cause of dementia in the United States is Alzheimer's disease (AD). In 2000, there were 4.5 million people with Alzheimer's disease in the United States. Unless new discoveries facilitate prevention of Alzheimer's disease, there will be 13.2 million people with AD in 2050. About 3% of men and women aged 65-74 AD. Prevalence and incidence increases with age, and nearly half of those aged 85 years have AD. Cases of dementia, 70% are caused by AD and AD is often a contributing factor when other etiologies are discovered.

Most cases occur in people over 60 years AD. The exact cause of Alzheimer's disease late onset of this is not well known. Rarely, Alzheimer's disease develops in patients in their 30s, 40s, 50s or. A strong genetic component has been identified in many cases, and genetic transmission generally follows an autosomal dominant. On the other hand, the genetic aspects of late-onset AD is much less clear. It is known that the APOE * E4 allele is a risk factor for AD (as well as dementia with Lewy bodies and vascular). Beyond age and family history, other risk factors were female gender, low education, and a history of head trauma with loss of consciousness. Presence of atherosclerosis is a risk factor for AD and vascular dementia. histopathological markers of Alzheimer's disease include neuritic plaques (abnormal aggregations of amyloid protein), neurofibrillary tangles (tau protein hyperphosphorylation), and the death of brain cells. Neurofibillary tangles are preferentially distributed in the temporal lobe, hippocampus and amygdala, while senile plaques are widely distributed in the cerebral cortex.

Many neurotransmitters, including norepinephrine, serotonin, somatostatin and neuropeptide different show significant abnormalities in AD. Failure most exuberant neuro-chemical seems to be a deficiency in the enzyme choline acetyltransferase-O, resulting in a deficit of acetylcholine. The neuro-chemical changes may contribute to psychiatric symptoms associated with AD, such as depression, anxiety, agitation, and psychosis. Overall, the search for effective disease modifying therapies for Alzheimer bring us frustration and disappointment.

A strong concept etiopathogenic pathophysiological / is that the beta-amyloid peptide (Aa�) battles of the neuropathology of AD, and so anti-amyloid therapies are expected to slow the progression of AD effectively. The deposition of amyloid-a� (Aa�) in the brain is a neuropathological characteristics of AD and a potential cause of neuronal injury. The molecule was found to start the process is the Aa�42 peptide 42-amino acid, which is in soluble oligomeric forms and senile and diffuse plaques.

Tarenflurbil is a drug that lowers Aa�42 selective module?-Secretase activity and reduced the production of Aa�42 no effect on the production of Aa�40. Tarenflurbil was the first gamma-secretase modulator to be tested in a Phase 3 trial. Chemically, tarenflurbil is the single enantiomer of racemic NSAID flurbiprofen (proposed and tested at therapeutic doses, this drug has no antiinflammatory activity, not inhibiting COX-1 or or COX-1, since only S-enantiomers of arylpropionic acid NSAIDs molecules can potently inhibit COX, whereas on the contrary, the R-enantiomers have almost no COX activity).

Tarenflurbil has failed in its Phase 3 trial key. Patients who received a dose of 800 mg twice per day had almost the same decline in cognition and function as well as those who received placebo. Tarenflurbil was a phase 2 trial rather promising, noted last spring. In this study of 207 patients, those taking tarenflurbil experienced significant improvements in the overall operation and activities of daily living, and improvements in the short important in cognition. Unfortunately, however, such benefits do not happen in the ph.