Alzheimer’s disease (AD) is a gradually advancing neurodegenerative condition that results in cognitive decline, memory impairment, and neuronal loss. The condition is characterized by hallmark pathological features, including extracellular amyloid-beta (Aβ) plaque accumulation, intracellular τ protein tangles, synaptic malfunction, and chronic neuroinflammation. While the precise aetiology of AD remains blurred, rising indications suggest a significant interplay between the central nervous system and the gut microbiome, collectively known as the gut-brain axis. Dysbiosis, or an imbalance in gut-microbiota, has been linked to increased neuroinflammation, oxidative stress, and blood-brain barrier disruption, all of which contribute to AD pathogenesis. Recent investigations have emphasized on the potential influence of gut microbiota modulation in neuroprotection. Prebiotics and probiotics, which influence gut microbiota composition and function, have emerged as promising interventions for delaying or mitigating AD progression. Prebiotics, non-digestible dietary fibres, selectively promote the growth of beneficial gut bacteria, leading to the production of neuroactive metabolites such as short-chain fatty acids (SCFAs). SCFAs help regulate neuroinflammatory pathways, improve gut barrier integrity, and reduce oxidative stress, thereby mitigating neurodegenerative processes. Probiotics, live microorganisms that confer health benefits, play a crucial role in restoring microbial balance. They enhance neurotransmitter synthesis, regulate immune responses, and modulate metabolic pathways, potentially reducing Aβ aggregation and inflammation associated with AD. Preclinical and early clinical studies suggest that probiotic supplementation may improve cognitive function, strengthen neuronal plasticity, and decrease neurodegenerative markers. These findings underscore the therapeutic potential of microbiota-targeted approaches in AD management.

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Prebiotics and Probiotics in Alzheimer’s Disease

  • Soumya Mitra,
  • Rakesh Kumar Dolai,
  • Amit Kumar Halder,
  • Nilanjan Ghosh,
  • Subhash Chandra Mandal

摘要

Alzheimer’s disease (AD) is a gradually advancing neurodegenerative condition that results in cognitive decline, memory impairment, and neuronal loss. The condition is characterized by hallmark pathological features, including extracellular amyloid-beta (Aβ) plaque accumulation, intracellular τ protein tangles, synaptic malfunction, and chronic neuroinflammation. While the precise aetiology of AD remains blurred, rising indications suggest a significant interplay between the central nervous system and the gut microbiome, collectively known as the gut-brain axis. Dysbiosis, or an imbalance in gut-microbiota, has been linked to increased neuroinflammation, oxidative stress, and blood-brain barrier disruption, all of which contribute to AD pathogenesis. Recent investigations have emphasized on the potential influence of gut microbiota modulation in neuroprotection. Prebiotics and probiotics, which influence gut microbiota composition and function, have emerged as promising interventions for delaying or mitigating AD progression. Prebiotics, non-digestible dietary fibres, selectively promote the growth of beneficial gut bacteria, leading to the production of neuroactive metabolites such as short-chain fatty acids (SCFAs). SCFAs help regulate neuroinflammatory pathways, improve gut barrier integrity, and reduce oxidative stress, thereby mitigating neurodegenerative processes. Probiotics, live microorganisms that confer health benefits, play a crucial role in restoring microbial balance. They enhance neurotransmitter synthesis, regulate immune responses, and modulate metabolic pathways, potentially reducing Aβ aggregation and inflammation associated with AD. Preclinical and early clinical studies suggest that probiotic supplementation may improve cognitive function, strengthen neuronal plasticity, and decrease neurodegenerative markers. These findings underscore the therapeutic potential of microbiota-targeted approaches in AD management.