Alzheimer's disease (AD), a fatal neurodegenerative disorder, is the most common form of dementia today. It is estimated that more than 10% of people over the age of 65 are affected and, with this sector of the population increasing more rapidly than any other, So it is easy to see why developing pharmacologic treatments (medications) available for Alzheimer's disease that slows or stops the damage and destruction of neurons that cause Alzheimer's symptoms is the focus of much current research.
Several facts about Alzheimer's disease
• In 2016, approximately 476,000 people age 65 or older will develop Alzheimer's disease in the United States and, as the baby boom generation has begun to reach age 65 and beyond, the age range of greatest risk of Alzheimer's, this sector of the population will increase more rapidly than any other. When the first wave of baby boomers reaches age 85 (in 2031), it is projected that more than 3 million people age 85 and older will have Alzheimer's.
• According to data from the National Center for Health Statistics of the Centers for Disease Control and Prevention (CDC), 84,767 people died from Alzheimer's disease in 2013.
• In 2016 (in 2016 dollars), the total payments for people with Alzheimer's disease and other dementias are estimated at $236 billion.
• In the decade of 2002-2012, 244 drugs for Alzheimer's were tested in clinical trials registered with clinicaltrials.gov, a National Institutes of Health registry of publicly and privately funded clinical studies. Only one of the 244 drugs successfully completed clinical trials and went on to receive approval from the FDA.
Major causes of AD
Major causes of AD is undiscovered except for carrying the APOE-e4 gene. Microscopically, the most common findings found in the brains of AD patients are abnormal protein deposits, including senile neu-ritic plaques (SNP) and neurofibrillary tangles (NFT). Senile plaques are the result of the extracellularaccumulation of insoluble aggregates of β-amyloid protein (Aβ)while NFT occur intracellularly and are composed of paired heli-cal filaments of hyperphosphorylated tau protein (tau-P). The amyloid-β (Aβ) is generated by sequential proteolytic cleavage of the transmembrane amyloid precursor protein (APP) by two membrane-bound enzymes, β- and γ-secretase.
β-Secretase, a transmembrane aspartic protease known as BACE-1 or Asp-2, cleaves at the N-terminal end of the Aβ region, releasing the soluble sAPPβ, and this is followed by γ-secretase cleavage of the membranebound C-terminal fragment to release Aβ.
γ-Secretase activity is known to be closely associated with the presenilin (PS) proteins, and it has been demonstrated that at least three other proteins, nicastrin, aph-1 and pen-2, are required to form an active gsecretase complex.
The notion that tau dysregulation is a key mediator of neurodegeneration has stimulated the development of therapeutics for the treatment of AD and non-AD tauopathies. Given these treatments are currently being developed, a non-invasive method of determining the tau burden in the brain would allow a better understanding of the pathophysiology of AD, FTLD and other tau-related neurodegenerative conditions.
None of the pharmacologic treatments (medications) available today for Alzheimer's disease slows or stops the damage and destruction of neurons that cause Alzheimer's symptoms and make the disease fatal. The six drugs approved by the U.S. Food and Drug Administration (FDA) for the treatment of Alzheimer's temporarily improve symptoms by increasing the amount of chemicals called neurotransmitters in the brain. The medications include: Razadyne (galantamine), Exelon (rivastigmine), and Aricept (donepezil), Namenda (memantine), Namzaric (memantine extended-release and donepezil).
From clinicaltrial.gov (the clinical trials database of the National Institutes of Health.), there are 94 clinical trials of the AD drugs.
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