Amyloid-β peptide (Aβ) and tau protein deposits in the human brain are the pathological hallmarks of Alzheimer’s disease (AD). Tau is a class of proteins that are abundant in nerve cells and perform the function of stabilizing microtubules. However, in certain pathological situations, Tau proteins become defective and fail to adequately stabilize microtubules, which can result in the generation of abnormal masses that are toxic to neurons. This process occurs in a number of neurological disorders collectively known as Tauopathies. Tau protein is the major factor of the intracellular filamentous deposits that relate to a number of neurodegenerative diseases which includes the progressive supranuclear palsy (PSP), Pick’s disease, and Parkinsonism. The identification of mutations in Tau established that dysfunction or misregulation of tau protein is sufficient to cause dementia and neurodegeneration. In this review article, we discussed the etiology of the tau formation and role in AD and subsequently therapeutic approach for disassembling and Tau inhibition.
Pleurothotonus, commonly known as Pisa Syndrome (PS), is a rare neurological disorder characterized by lateral bending of the trunk with a tendency to lean to one side. This is typically mobile and resolves in supine position. It often presents as an incapacitating symptom of underlying neurodegenerative conditions like Parkinson’s disease, alzheimer’s disease, multisystem atrophy, dementia with Lewy bodies, progressive supranuclear palsy and even subacute sclerosing panencephalitis. It is known to be associated with neuroleptics, dopaminergic agents, valproic acid and lithium. PS is also seen in neurosurgical disorders like subdural hematoma, normotensive hydrocephalus, or as a late complication of pallidotomy in patients with PD. It can present either as an acute emergency or can develop gradually over time.PS tend to happen in coronal plane and can be controlled and managed if diagnosed in early stage. However, a chronic form known as “camptocormia” occurs often in a combined fashion with anteroposterior flexion which can improve to some extent, remain stable or even get worse. Pathophysiologic mechanism is not completely understood. This review will discuss all the updated literatures published in PS in terms of prevalence, pathophysiology, clinical manifestation, and treatment modalities.
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