Alzheimer’s disease (AD) is a neurodegenerative disease associated with the development of dementia. It has
been established that the pathological hallmarks of neurofibrillary tau protein tangles and senile β-amyloid protein plaques
lead to degeneration of neurons via inflammatory pathways. The progressive death of neurons, primarily cholinergic,
results in a gradual and fatal decline of cognitive abilities and memory. By targeting these pathological hallmarks and
their associated pathways, AD drug therapy can potentially attenuate the disease state. In this review article, we focus on
newly proposed and experimental AD drug treatment. We discuss three characteristic areas of AD treatment: prevention
of neurotoxic β-amyloid protein plaque formation, stability of neuronal tau proteins, and increase in neuronal growth and
function. The primary drug therapy methods and patents discussed include the use of neurotrophic factors and targeting of
the amyloid precursor protein cleavage pathway as prevention of β-amyloid formation and tau aggregation.
Keywords: Alzheimer's disease, β-amyloid, neurotrophic factors, colivelin.
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