Abstract
The cholinergic hypothesis has been reported first being the cause of memory dysfunction in the Alzheimer’s disease. Researchers around the globe have focused their attention on understanding the mechanisms of how this complicated system contributes to processes such as learning, memory, disorientation, linguistic problems, and behavioral issues in the indicated chronic neurodegenerative disease. The present review reports recent updates in hybrid molecule design as a strategy for selectively addressing multiple target proteins involved in Alzheimer’s disease (AD) and the study of their therapeutic relevance. The rationale and the design of the bifunctional compounds will be discussed in order to understand their potential as tools to investigate the role of the cholinergic system in AD.
Highlights
Alzheimer’s disease (AD) is the most common form of dementia among geriatric people since the beginning of the 21st century
A particular beneficial therapeutic meaning may be associated with allosteric agonist compounds which differ from pure allosteric modulators
The muscarinic receptors are involved in diverse functions throughout the body with particular focus on the bladder, gastrointestinal tract, eye, heart, brain, and salivary glands [71]
Summary
Alzheimer’s disease (AD) is the most common form of dementia among geriatric people since the beginning of the 21st century. Presynaptic cholinergic dysfunctions, loss of the cholinergic neural network, and overactivation of acetylcholinesterase (AChE), which leads to weakened neurotransmission, support the cholinergic hypothesis of the disease. These compounds can improve cognitive the nervous tissue the ((1–3), brain ((1–3), 1) These compounds can the improve the deficits of the disease onlydisease for a couple of months before losing activity. Figure 1) being a glutamatergic in time, another drug was introduced treatment of AD, i.e. 1) being a antagonist which protects nerve tissue against glutamate-mediated excitotoxicity. AChR locations are illustrated (modified from Auld et al [24])
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