Neurodegenerative diseases are categorized mostly by protein deposits or
known hereditary mechanisms, despite recent studies showing overlap and intraindividual variations in these symptoms. A synergistic interaction between pathological
proteins advises extensive pathogenic pathways. Animal models and other studies have
uncovered the fundamental mechanisms underlying neurodegeneration and cell death,
opening up new avenues for future prevention and therapy plans. A multidomain
therapy approach that emphasizes the underlying reasons why diseases alike
Parkinson's, Alzheimer's, etc. occur. Neurodegenerative diseases like Parkinson's
disease (PD) and Alzheimer's disease (AD) are becoming far more common in the
Western world. Neuronal inflammation, gut microbiota, extracellular misfolded protein
accumulation, hallmarks of various neurodegenerative nephropathies, and failure of the
systemic and cerebral immune systems are some of the elements that affect the
immunopathogenesis of neurodegenerative diseases. Deficits in the ubiquitin
proteasome autophagy system, abnormal protein dynamics brought on by oxidative
stress and free radical formation, mitochondrial dysfunction, impaired bioenergetics,
neurotrophins dysfunction, “neuroinflammatory” processes, and (secondary)
distractions of neuronal Golgi apparatus and axonal passage are some of the
fundamental mechanisms that contribute to immunopathogenesis. Long-term
cooperation between these interconnected systems results in programmed cell death. In
this review, we discussed every idea and hypothesis that have been put up on the
pathophysiology of neurodegenerative disorders.
Keywords: Amyloid, Alzheimer's disease, Gut microbiome, Mitochondrial abnormalities, Neuroinflammation, Neuronal dysfunction/death, Oxidative stress, Pathogenic factors, Retinopathies’.
