ABOUT MEMORY LOSS

Memory and The Brain

Causes of Memory Loss

MCI and Dementia

Alzheimer's Overview

Progression of Alzheimer's

Diagnosis of Alzheimer's

>Treatment of Alzheimer's

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Contrary to the notion that current AD treatments are ineffective, timely intervention with appropriate mediations can have substantial benefits and, in some cases, can delay disease progression for several years. Combining pharmacologic treatments with a balanced diet, regular physical exercise, routine social stimulation, and a well-informed caregiver is widely documented as the most beneficial approach.

Today there are five FDA-approved medications for treatment of AD (e.g. Cognex® (tacrine), Aricept® (donepezil), Razzadyne® (galantamine), Exelon® (rivastigmine) and Namenda (memantine) all of which have shown positive treatment outcomes in long-term studies. While the overall efficacy of these medications on a treated population is statistically unimpressive, a percentage of individual patients respond well to treatment, especially when intervention begins early in the disease process and the therapeutic regimen is carefully sustained.

CHOLINESTERASE INHIBITORS
Cognex® (Tacrine), Aricept® (donepezil), Razzadyne® (galantamine) and Exelon® (rivastigmine) belong to a class of medications called cholinesterase Inhibitors. Cholinesterase inhibitors increase the availability of acetylcholine, an important transmitter that helps control mood, behavior, memory and other cognitive abilities. Acetylcholine is markedly reduced in AD, Parkinson's disease, Lewy body disease and many other dementing disorders.

Cholinesterase inhibitors also appear to slow the production of beta amyloid. Published five-year data on Exelon®, four-year published data on Razadyne® and three-year published data on Aricept® all show that AD progression can be delayed by 50% or more.

GLUTAMATE RECEPTOR MODULATORS
Namenda® (memantine) belongs to a class of medication called glutamate receptor modulators. Glutamate is the transmitter for 75% of all neurons in the gray matter on the surface of the brain (cerebral cortex). Excessive amounts of glutamate are released in a wide variety of brain disorders, including stroke, Parkinson's disease, multiple sclerosis, traumatic brain injury, and probably AD. The excessive release of glutamate triggers certain suicide genes in neurons to cause their self-destruction. Namenda® blocks this self destruction plus allows normally released amounts of glutamate to exert their proper function in brain communication. Namenda® may also block neurofibrillary tangle formation (a hallmark of AD pathology) to delay AD progression.

NEW TREATMENTS IN PIPELINE
There are many AD treatments in clinical trials. Flurizan® (Myriad, Inc.) is likely to be FDA-approved in 2009. Flurizan belongs to a class of selective amyloid lowering agents (SALA). By reducing beta-amyloid production (another hallmark of AD pathology), SALA not only promises to improve various cognitive and functional abilities, but also appears to markedly delay AD progression.