Culprits of Neurodegeneration in Alzheimer’s Diseases: Bench to Bedside Impression

Abstract

Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease of the brain and around 60% of dementia cases are associated with sporadic AD. Dementia particularly beyond 65 years of age, is the chief problem; therefore, it is called the senile dementia of Alzheimer’s type (SDAT). Besides SDAT, patients manifest anxiety, delusion, aggression, memory loss and cognitive impairment. To understand the pathophysiology of the disease various animal models of Alzheimer’s disease like streptozotocin, polyC, amyloid beta, hp-tau and APOE 4 Tg mice are widely used in the discovery of potential targets for AD treatment. The actual pathophysiology of the disease is not known yet. Hypotheses proposed for the onset of AD are proteinopathies like tauopathy and amyloid-beta deposits, neuroinflammation, oxidative stress, cholinergic deficit and impaired insulin signaling. To date, there are no therapeutic interventions available; only a few drugs are recommended to AD patients; only to harness temporary symptomatic relief. Understanding the actual culprits of the disease is necessary to retain lost neurons in the brain by stimulating NPCs present in the brain with some non-invasive techniques. Neurogenesis could be a potential compensatory pathway for neurodegeneration and related global brain atrophy in Alzheimer’s disease, which can retain functional deficits.