A review on factors causing parkinson’s syndrome

Abstract

Parkinson’s disease (PD) was medically reported as a neurological syndrome by James Parkinson, who first explained it in “An Essay on the Shaking Palsy” in 1817.1 He illustrated this disease as started with slow, progressive involuntary tremors, followed by a complication in walking, speech, and swallowing.2 Other than motor symptoms, Parkinson’s disease patients gradually experience remarkable non‒ motor symptoms as well as cognition decline, sensory abnormalities, behavioral changes, fatigue, sleep disturbances, and other autonomic dysfunctions.3‒5 After Alzheimer’s disease (AD), PD is the most common age‒ related neurodegenerative disease. Although the central pathological feature of Parkinson’s disease (PD) was found to be the degradation of neurons in the substantia nigra pars compacta (SNpc), (Figure 1) the loss of SNpc neurons accelerate striatal dopamine (DA) deficiency.6 Which is accountable for the key motor and nonmotor symptoms of PD.4,5 PD tremor decreases the voluntary movement, so naturally, impair the daily life activities. Rigidity refers to the increased resistance (stiffness) to passive movement of a patient’s limbs. Bradykinesia (very slow body movements) could considerably worsen the standared of life as a result of it takes for much longer to perform daily tasks like consumption of food or dressing, hypokinesia (reduction in movement amplitude), and akinesia (absence of normal oblivious movements, like arm swing in walking) evident as a range of symptoms, such as decreased voice volume (hypophonia), paucity of pronormal facial expression (hypomimia), drooling (inability to swallow without pondering it), diminished stride length during walking and slow writing. In addition, PD patients continuously enhance stooped attitude and will lose ordinary postural impulses, resulting in falls and, sometimes, confinement to a wheelchair. Abnormalities and cognition also occur frequently; delayed responses to queries, and slow cognitive process (bradyphrenia).6,7 Many shreds of evidence suggest that phosphatidylinositol‒3 kinase (PI3K)/Akt (protein kinase‒B)/mammalian target of the rapamycin (mTOR) pathway (PI3K/Akt/mTOR) pathway signaling related to dopaminergic neuron degeneration in PD.46‒48 The neuron degeneration concurrently influences the wider region of the brain responsible for dementia. In PD, dementia is not a presenting feature; it develops at least four years after PD motor symptoms start. Among PD patients, who do not primarily experience dementia the yearly occurrence varies from 2.6% to 9.6%, the additive risk of dementia by the age of 85 years was over 65%.8 Dopamine deficiency in the brain is the known causing factor of PD, yet why this initially occurs is less clear. However, the better understanding of the pathology of Parkinson’s disease is helping to identify potential drug targets for disease management.