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In 1906, German psychiatrist Alois Alzheimer first reported the histological features of unique plaques and neurofibrillary tangles in the post-mortem brain of a 50-year-old female patient, whom he had followed up for 5 years from admission until her death, for progressive sleep disturbance, memory dysfunction and behavioral changes such as paranoia, aggression, delusion, and confusion. The disease is now recognized as Alzheimer’s disease (AD), the most common form of senile dementia. The plaques are now known as Aβ plaques, and the neurofibrillary tangles are known as microtubule‐associated hyperphosphorylated protein τ in the paired helical filaments. More than 200 clinical research programs and clinical trials targeting Aβ amyloid and protein τ, either directly or indirectly, as a therapeutic strategy for AD have failed thus far. A growing database of the etiopathological, genetic, and biochemical features of AD indicate that it is a heterogeneous, polygenic, multifactorial, and complex disease. Hence, more rational therapeutic strategies for AD should be druggable target diversification, multi-targeting, or drug combinations. While current drug discovery programs for AD continue to focus on anti-Aβ and anti-τ strategies, a deeper understanding of the disease in recent years has opened drug discovery avenues involving neuroinflammation, metabolic derangements, stem cells, gene therapy and alternative therapies. CONTINUE READING…..
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