Inflammation and Alzheimer's Disease: Mechanisms and Therapeutic Implications by Natural Products.
Mashoque Ahmad RatherAndleeb KhanSaeed AlshahraniHina RashidMarwa M QadriSummya RashidRana M AlsaffarMohammad Amjad KamalMuneeb U RehmanPublished in: Mediators of inflammation (2021)
Alzheimer's disease (AD) is a neurodegenerative disorder with no clear causative event making the disease difficult to diagnose and treat. The pathological hallmarks of AD include amyloid plaques, neurofibrillary tangles, and widespread neuronal loss. Amyloid-beta has been extensively studied and targeted to develop an effective disease-modifying therapy, but the success rate in clinical practice is minimal. Recently, neuroinflammation has been focused on as the event in AD progression to be targeted for therapies. Various mechanistic pathways including cytokines and chemokines, complement system, oxidative stress, and cyclooxygenase pathways are linked to neuroinflammation in the AD brain. Many cells including microglia, astrocytes, and oligodendrocytes work together to protect the brain from injury. This review is focused to better understand the AD inflammatory and immunoregulatory processes to develop novel anti-inflammatory drugs to slow down the progression of AD.
Keyphrases
- oxidative stress
- induced apoptosis
- cerebral ischemia
- traumatic brain injury
- clinical practice
- cognitive decline
- white matter
- inflammatory response
- anti inflammatory drugs
- multidrug resistant
- cognitive impairment
- lipopolysaccharide induced
- stem cells
- lps induced
- dna damage
- resting state
- signaling pathway
- endoplasmic reticulum stress
- spinal cord injury
- ischemia reperfusion injury
- blood brain barrier
- mesenchymal stem cells
- diabetic rats
- nitric oxide
- functional connectivity
- multiple sclerosis
- cell death
- chemotherapy induced
- replacement therapy
- heat shock protein