Parkinsons Vs Huntingtons:
Also in the 1960s, tetrabenazine was introduced as an antipsychotic but also showed beneficial effects for the treatment of hyperkinetic motor symptoms, like chorea in HD patients (Dalby, 1969; Huntington Study Group, 2006). To date, it is known that these drugs do not reverse disease progression and in many cases do not have the desired effects. This has brought the idea that local production of DA and GABA, and therefore the replacement of the neurons that produce it, would be the ideal treatment for these diseases.
In total, according to the Parkinson’s Foundation, more than 10 million people live with Parkinson’s disease worldwide [11]. Parkinson’s disease can also cause changes in the way a person walks, referred to as changes in gait [1]. Trouble with balance and coordination, and falls, known as postural instability, are common symptoms of Parkinson’s disease [3]. Some people with Parkinson’s disease may have “flat” facial expressions [1].
Lifestyle changes such as eating a balanced diet, exercising regularly, and undergoing physical therapy can also keep symptoms under control and improve your quality of life. Parkinson’s disease is a neurological condition that gets progressively worse over time and causes trouble with movement. HD is caused by a mutation in the Huntington gene, which lies on chromosome 4.
Generally, medications for these symptoms are considered when non-medicated alternatives have failed and/or these symptoms put the AD patients, or others, in danger. Though Huntington’s, Parkinson’s, and Alzheimer’s disease are caused by unique cellular processes, all three diseases are facilitated by the inability of neurons to communicate with each other. Gradual neuron death in people with HD hinders the ability of neurons to communicate. For people with PD, neurons die, causing an imbalance of dopamine and acetylcholine and the uncontrolled firing of nerve cells. Finally, in people with AD, plaques and tangles inhibit neurons’ ability to communicate. In Alzheimer’s disease, neurons in the brain and the spaces between them become clogged with protein deposits called beta amyloid plaques and neurofibrillary tangles.
Parkinson’s disease was named for James Parkinson, an English physician, whose work ‘An Essay on the Shaking Palsy’ published in 1817 described six individuals with symptoms of the disease. Huntington’s disease was named for George Huntington, an American physician, who published an article entitled ‘On Chorea’ in 1872 that described the disease. Parkinson’s disease and Huntington’s disease both have similar motor symptoms, characterized by uncontrolled or involuntary movements. However, PD motor symptoms are referred to as ‘tremors,’ while Huntington’s symptoms are twitching movements. Both will experience rigidity in the limbs with the progression of the disease, but cognitive decline and memory loss experienced by Huntington’s patients is far more pronounced. Although both diseases cause involuntary movements, their motor symptoms differ, and so do their causes.
Similarly, Parkinson’s disease patients experience uncontrollable movements due to the disease’s effects on a specific area of the basal ganglia called the substantia nigra. The substantia nigra produces a chemical called dopamine, which is a neurotransmitter. Neurotransmitters are special chemicals that help neurons communicatewith each other.
Although challenging, in vivo cell reprogramming appears as the most promising therapy candidate for cellular replacement for PD and HD patients. The first studies in which dopaminergic neurons were generated by reprogramming human and mouse fibroblasts using lineage-specific factors for the pop over to these guys conversion to dopaminergic neurons (Caiazzo et al., 2011; Kim et al., 2011). The converted neurons were positive for several dopaminergic markers and expressed genes related to the dopaminergic lineage rather than with the fibroblast of origin (Caiazzo et al., 2011; Kim et al., 2011).
Nowadays, there are several gene silencing/editing technologies, including RNA interference (RNAi), antisense oligonucleotides (ASO), and clustered interspaced short palindromic repeats (CRISPR/cas9), which can be used as therapies for the treatment of PD and HD. For a more in-depth knowledge of gene therapy delivery systems and other cellular targets, reviews are published elsewhere (Sudhakar and Richardson, 2019; Chen et al., 2020). Although the contribution of BDNF on PD and HD pathology is robust, no clinical trials are currently testing its safety and efficacy for the treatment of these diseases. A study with 42 HD patients revealed that BDNF serum concentrations were significantly lower in patients compared to healthy controls (Ciammola et al., 2007). However, a later study analyzed 398 blood samples, indicating that mRNA and protein levels of BDNF between HD and healthy controls were not significantly different, questioning its potential as a biomarker for early diagnosis of HD (Zuccato et al., 2011).
This is largely because the bradykinesia in PD is very characteristic and developed late in life, making it unlikely to be HD [33, 34]. Patients are typically diagnosed correctly following attempts at treatment, where the parkinsonian-like symptoms do not respond to L-DOPA [29, 33], as well as comprehensive genetic testing for Huntington’s disease. Non-motor symptoms of Parkinson’s disease include memory problems, loss of smell, constipation, trouble urinating, temperature sensitivity, excessive sweating or salivating, sleep disorders, mood disorders, and changes in handwriting or voice [1]. Both Parkinson’s and Huntington’s diseases cause involuntary movements when neurons in the brain stop working or die. While there is some symptom overlap, like muscle rigidity and trouble balancing, some of the involuntary movements are distinguishable.
Because diagnosing Huntington’s and Parkinson’s can be complex, patients may want to seek out a neurologist who specializes in movement disorders for a diagnosis. There are a wide variety of medications and therapies that are available to help people with Huntingtons Disease. It is important to practice patience and perseverance visit the website when beginning a new medication as it takes time to figure out how these medications interact with your body and with each other. It may take weeks or months to figure out the correct combination and dosage of medications. Early drugs targeted the large amyloid plaques found in the brains of people with the disease.
There are people with a low number of repeats that have mild abnormal movements later in life and progression is slow whereas others with a large repeat length who are severely affected at a young age. The purpose of all medicines for Parkinson’s disease is to help control tremor, movement, and balance to maintain daily activities. One of the mechanisms targeted by Parkinson’s medications includes the interactions of dopamine, a neurotransmitter (chemical messenger) that affects brain processes by allowing nerve cells to communicate with one another in the brain.
A new study strongly suggests that the brains of people who have died of Huntington’s disease and Parkinson’s disease show a similar response to a lifetime of neurodegeneration, despite being two very distinct diseases. It “opens the path” to finding the initial event that leads to diseases like Alzheimer’s and Parkinson’s, says Corinne Lasm’zas, who studies neurodegenerative diseases at the Wertheim UF Scripps Institute in Jupiter, Florida. The finding involves Huntington’s disease, a rare, inherited brain disorder that cut short the life of songwriter Woody Guthrie. But the study has implications for other degenerative brain diseases, including Alzheimer’s. During the conduct of the work and most of the manuscript development, LI was employed by F. DO is an employee of Genesis Research, which received consulting fees from Roche.
But these drugs didn’t work, perhaps because the plaques they sought to eliminate are just the charred remains of a forest that has already burned. They used genetic tweaks to create hundreds of versions of a protein segment called PolyQ, which becomes via toxic in Huntington’s. These data highlight the prevalence of psychiatric, cognitive, communication, swallowing, and mobility problems in people with Huntington’s disease, underscoring the need for holistic expert care of these individuals.
In addition, delayed saccadic initiation and subclinical cognitive dysfunction gave diagnostic clues for HD.9 Targeted panel sequencing and whole-exome sequencing are now popular, but because these tests might miss triplet repeats, suspicion of HD is important. As discussed elsewhere in this website, HD is a progressively debilitating disease with no known cure. The person with Huntington’s disease may be able to maintain a job for several years after diagnosis, despite the increase in disability. Loss of cognitive functions and increase in motor and behavioral symptoms eventually prevent the person with HD from continuing employment. Progressive weakness of respiratory and swallowing muscles leads to increased respiratory infection and choking, the most common causes of death. (For more information about the complications of HD, click here.) However, not all patients with Huntington’s disease progress at the same pace and are equally affected.