"Pharmacological Modulation of Neuroinflammation in Alzheimer's Disease: Current Advances, Emerging Therapeutic Targets, and Future Perspectives"

Abstract

The gradual degeneration of brain cells, known as synapses and neurones, is the main cause of memory loss and cognitive dysfunction in Alzheimer's disease (AD), a neurodegenerative disorder. Chronic neuroinflammation is an important factor in the development and advancement of the illness, with characteristic pathological characteristics including amyloid-beta plaques and tau-protein tangles. As part of this inflammatory reaction, glial cells, mostly microglia and astrocytes, are activated and pro-inflammatory cytokines like TNF-α, IL-1β, and IL-6 are released. The present therapeutic approaches utilise cytokine inhibitors, microglial modulators, non-steroidal anti-inflammatory medicines (NSAIDs), and anti-inflammatory chemicals derived from plants in an effort to decrease this inflammation and safeguard neuronal integrity. Delays in treatment initiation, inadequate drug penetration across the blood-brain barrier, and low bioavailability are among the reasons that may explain the contradictory clinical results compared to the promising preclinical data. New methods are being developed to improve the efficacy of treatments. These include gene-based therapeutics, monoclonal antibodies, and drug delivery systems driven by nanotechnology. In the future, patient outcomes may be improved by the use of inflammatory biomarkers to drive personalised therapy options. In order to develop better treatments that can halt or slow cognitive loss, our knowledge of neuroinflammation's function in AD must expand.