Neurotransmitters in Prevention and Treatment of Alzheimer’s Disease

Abstract

Alzheimer’s disease (AD) is the most frequent cause of cognitive impairment in middle-aged and older populations. There is a lack of drugs that demonstrate significant efficacy in AD, so the study of the pathogenesis of AD is of great importance. More efficacious interventions are needed, as reflected by our population’s fast aging. Synaptic plasticity is the capacity of neurons to adjust their connections, and it is strongly tied to learning and memory, cognitive function, and brain injury recovery. Changes in synaptic strength, such as long-term potentiation (LTP) or inhibition (LTD), are thought to represent the biological foundation of the early stages of learning and memory. The results of numerous studies confirm that neurotransmitters and their receptors play an important role in the regulation of synaptic plasticity. However, so far, there is no definite correlation between the function of neurotransmitters in aberrant neural oscillation and AD-related cognitive impairment. We summarized the AD process to understand the impact of neurotransmitters in the progression and pathogenesis of AD, including the current status of neurotransmitter target drugs, and the latest evidence of neurotransmitters’ function and changes in the AD process.

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“…Pathological perturbations of neurotransmitter systems are believed to play a role in the development of Alzheimer's neuropathology and includes, loss of monoaminergic neurons, decreased monoamine levels, decreased γ‐Aminobutyric acid (GABA) levels, dysfunction of glutamatergic neurons, and loss of cholinergic neurons (Yang et al., 2023). Both animal and human studies have demonstrated a role for monoamine neurotransmitters in the development of Alzheimer's disease (Reddy et al., 2021).…”

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“…The increasing number of individuals suffering from AD is a great concern for healthcare organizations worldwide. Current treatments are palliative and only modulates symptoms or at best slows the progression of disease. − Preventive or long-term strategies are currently lacking . Many studies have highlighted the role of soluble prefibrillar Aβ-oligomers as culprits that disrupt normal neuronal function and structure by damaging cellular components through various pathways .…”