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  Prevention Through Delay

Symptoms and Progression

Early Detection

Diagnosis

>Treatment

  Contrary to a general belief that AD treatment does not work, currently available mediations for Alzheimer's disease (AD) are beneficial and, in many cases, delay disease progression for 2 to 4.5 years. Combining these pharmacologic treatments with other types of treatments brings the maximum benefits to the patients. Other types of treatment include:
  • Over-the-counter medications and supplements
  • Cognitive, occupational and speech therapies
  • Life style modifications (e.g. mental and physical exercise, and healthier diet)
  • Caregiver education and social support

Today there are five FDA-approved medications for treatment of AD (e.g. Cognex (tacrine), Aricept (donepezil), Razzadyne (galantamine), Exelon (rivastigmine) and Namenda (memantine)) and all of them have shown positive treatment outcomes in long-term studies.

Cholinesterase Inhibitors
Cognex, Aricept, Razzadyne and Exelon 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 (the primary cause of AD), which delays AD progression.

Glutamate Receptor Modulators
Namenda 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.

 

 
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