|
|
 |
|
Viewing report
|
|
|
|
Advances in Alzheimer’s Disease Drug Discovery
Business Insights, May 2011, Pages: 273
This report details existing and emerging hypotheses to explain the cause of late-onset AD. The progress of multiple potential under investigation is reviewed. In addition the potential application of neurogenic stimulation using intrinsic (or extrinsic) stem cells and related neurotrophic factors has been considered.
Features and benefits
- Gain an overview of disease-modifying approaches in discovery and early clinical development for the treatment of Alzheimer's disease.
- Identify the major hypotheses proposed to explain the cause of AD and evaluate potential clinical development candidates testing each hypothesis.
- Assess the competitor landscape and progress of specific compounds for disease modification in AD.
- Analyze the potential of active and passive immunization strategies with particular reference to previous trials that failed on safety grounds.
- Gain insight into newer therapeutic strategies, including neurogenic stimulation and the use of stem cells.
Highlights
In 2010 an estimated 35.6 million people worldwide had dementia. This number will double every 20 years, reaching 65.7 million in 2030 and 115.4 million in 2050. Over 50% of these individuals will be in developing countries. The total estimated worldwide costs of dementia, including direct and indirect costs of care, were $604bn in 2010.
Inhibition of BACE1( ß-secretase) is a preclinically validated disease-modifying target in AD. Inhibitors of BACE1 have been reported by several groups, but clinical progress has been slow owing to difficulties in identifying compounds that are selective, non-peptide mimics, orally active, and CNS penetrant.
Passive and active immunization strategies against Aß are being pursued by many companies and are in late Phase ll and Phase lll trials. To avoid a Th1 response most vaccines and monoclonal antibodies now in development are targeted towards the N-terminal amino acids.
Your key questions answered
- What therapeutic targets are being explored as disease-modifying agents in Alzheimer's disease and which are likely to demonstrate efficacy?
- Are there alternative approaches to the “amyloid cascade hypothesis” and what progress has been made?
- Do the novel cognitive enhancers under investigation have properties that may make them especially useful in disease modification?
- Do the novel cognitive enhancers under investigation have properties that may make them especially useful in disease modification?
- Which drugs currently in the clinic are best placed to achieve the badly needed breakthrough in the treatment of Alzheimer's disease?
|
|
|
|
