Treatment

Treatment of cognitive impairment should be based on the underlying medical conditions. Therefore, it is very important to obtain an accurate diagnosis.

In the case of Alzheimer’s disease (AD), contrary to general belief, currently available pharmacologic treatments are not only beneficial, but also in many cases, delay disease progression for 2 to 6 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
  • Cognitive Exercise
  • Physical Exercise
  • Social Activity
  • Caregiver Support
  • Proper structuring of the daily routine and good care management

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.