Potential Causes of Parkinson’s Identified by Scientists

Parkinson’s disease has the reputation of being a mainstream ailment of some sort, with famous figures like Muhammad Ali and Michael J. Fox having suffered from it to the attention of the public. Its debilitating effects on movement, balance, and coordination are well-known, often beginning with subtle symptoms such as a slight tremor in one hand or a barely noticeable stiffness in the limbs. The visibility of these symptoms in well-known individuals has brought Parkinson’s disease to the forefront of public awareness, highlighting the urgent need for understanding its causes. Here are 15 causes of the disease

Genetic Mutations

Several gene mutations have been identified that are linked to the development of the disease. For example, mutations in the LRRK2, PARK7, PINK1, and SNCA genes can contribute to the disease. These genes are responsible for multiple cellular processes and the regulation of dopamine production. Inherited mutations in these genes can disrupt these processes, leading to the degeneration of dopamine-producing neurons in the brain.

Source: National Institute of Health

Environmental Toxins

Pesticides and herbicides containing paraquat and rotenone as active ingredients have been particularly implicated in being a causative agent of Parkinson’s disease. Such chemicals can induce oxidative stress and mitochondrial dysfunction in neurons, leading to neuronal demise. People living in rural areas or those working in farming occupations may have higher exposure to these substances. 

Source: National Institute of Health

Age-Related Degeneration

While aging alone does not cause Parkinson’s, it significantly heightens the susceptibility to the disease due to the cumulative impact of various degenerative processes. As people age, there is a natural decline in dopamine-producing neurons in the brain. The build-up of cellular damage over time can impair the brain’s ability to produce and regulate dopamine, leading to the motor symptoms characteristic of Parkinson’s disease.

Source: National Institute of Health

Oxidative Stress and Inflammation

Oxidative stress results from a disproportion between free radicals and antioxidants, leading to cellular damage. In the brain, oxidative stress can damage neurons, particularly those that produce dopamine. The brain’s immune cells, called microglia, become overactive in response to these stressors, releasing inflammatory cytokines that can damage neurons and support the progression of Parkinson’s disease.

Source: National Institute of Health

Mitochondrial Dysfunction

Mitochondria are the energy powerhouse within cells, and their proper function is vital for cell survival. In Parkinson’s disease, the mitochondria in dopamine-producing neurons become impaired, leading to reduced energy production and increased production of reactive oxygen species. The resulting energy deficit can cause the death of neurons, particularly those in the substantia nigra region of the brain, which is critical for movement control.

Source: National Institute of Health

Lewy Bodies

A key pathological hallmark of Parkinson’s disease is the occurrence and build-up of Lewy bodies, which are abnormal aggregates of the protein alpha-synuclein. For a Parkinson’s disease patient, this protein misfolds and accumulates in neurons, forming these harmful aggregates. When this misfolded alpha-synuclein accumulates, it then disrupts normal cellular functions, including synaptic transmission and intracellular transport.

Source: National Institute of Health

Gut-Brain Axis

Recent research has highlighted the role of the gut-brain axis in Parkinson’s disease. The gut microbiome, which has trillions of microbes residing in the digestive system, can influence brain health through various mechanisms. A lopsidedness in the gut microbiome has been linked to Parkinson’s disease. Abnormal gut bacteria can produce harmful metabolites and trigger inflammation, which can spread to the brain via the vagus nerve. 

Source: National Institute of Health

Traumatic Brain Injury (TBI)

Individuals who have experienced moderate to severe head injuries are more prone to developing the disease later in life. TBI can cause immediate damage to brain tissue and induce chronic inflammation, both of which can contribute to the degeneration of dopamine-producing neurons. Repeated head trauma, as seen in athletes and individuals with certain occupations, can exacerbate this risk. 

Source: Mayo Clinic

Neuroinflammation

Chronic inflammation in the brain can result from various causes, including infections, autoimmune responses, and exposure to neurotoxins. Activated microglia, the brain’s resident immune cells, release inflammatory inhibitors such as cytokines and chemokines in response to perceived threats. While this response is initially protective, sustained microglial activation can lead to a harmful inflammatory environment that damages neurons. 

Source: Frontiers

Autophagy Dysfunction

Autophagy is a physiological process that involves the degradation and recycling of damaged cellular components. Proper autophagy is needed to maintain cellular health and function. However, in Parkinson’s disease, there is evidence that autophagy is impaired, leading to the accumulation of damaged proteins such as alpha-synuclein within neurons. This impairment can result from genetic mutations and other environmental and physiological factors.

Source: National Institute of Health

Diet and Nutrition

Certain dietary patterns and nutrient deficiencies have been linked to an increased risk. For example, diets high in saturated fats and low in antioxidants can result in oxidative stress and inflammation in the brain, exacerbating neuronal damage. Additionally, deficiencies in essential nutrients such as vitamin D, omega-3 fatty acids, and some vitamins in the B complex can impair neuroprotective mechanisms. 

Source: Parkinson’s Foundation

Sleep Disorders

Sleep disorders, particularly REM sleep behavior disorder (RBD), have been identified as potential early indicators and risk factors for Parkinson’s disease. RBD involves acting out dreams due to a lack of normal muscle paralysis during REM sleep. The underlying mechanisms linking sleep disturbances to Parkinson’s are not fully understood, but they may involve disruptions in the brainstem regions that regulate sleep and motor control. 

Source: Cleveland Clinic

Heavy Metal Exposure

Occupational exposure to heavy metals in industries such as mining, welding, and manufacturing can significantly elevate the risk of Parkinson’s disease due to prolonged and high levels of contact with these harmful substances. Culprits, such as lead, mercury, and cadmium, have been identified as particularly note-worthy. For instance, lead exposure can disrupt the normal functioning of the blood-brain barrier, allowing more toxins to enter the brain and damage neurons.

Source: John Hopkins Medicine

Viral Infections

Viruses can induce neuroinflammation and directly infect neurons, leading to their dysfunction and death. For instance, there is evidence suggesting that viral ailments such as influenza and herpes viruses may aggravate the risk of developing Parkinson’s disease. The mechanisms may involve the virus crossing the blood-brain barrier and causing direct neuronal damage or triggering an autoimmune response that targets the brain. 

Source: National Institute of Health

Hormonal Changes

There is evidence that low levels of estrogen in postmenopausal women can increase the risk of developing Parkinson’s. Estrogen is thought to have neuroprotective properties, and its decline may leave neurons more vulnerable to damage. In a similar vein, hypothyroidism has also been linked with heightened development of Parkinson’s disease.

Source: National Institute of Health