Parkinsons Vs Huntingtons:
However, unlike for cognition, the scores on the Mini Mental State Examination and Montreal Cognitive Assessment were unexpectedly low at 23 and 22. An examination of his eye movement revealed delayed saccadic initiation without any gaze limitation. Based on these findings, genetic analysis for HD was done, which demonstrated heterozygous expansion you can try here of 50 CAG repeats on the Huntingtin gene. Both diseases have no cures, therefore therapy focuses on easing symptoms and managing any mental health issues that may arise, especially in the case of Huntington’s disease. The progressive loss of cells in the substantia nigra causes decreased dopamine production in Parkinson’s disease.
Then, a homologous protein called CDNF was discovered with a protective role for dopaminergic neurons. Several studies evidence the protective role of CDNF and MANF in dopaminergic neurons against the injury caused by a-syn oligomers (Latge et al., 2015). The intrastriatal injection of CDNF prevents the loss of TH-positive neurons in a 6-OHDA-lesioned rat model of PD (Lindholm et al., 2007), and protected dopaminergic neurons in 6-OHDA and MPTP mouse models of PD (Lindholm et al., 2007; Voutilainen et al., 2009).
Though studies on Huntington’s and Parkinson’s disease are ongoing, prevention is unlikely. Eating a healthy diet and exercising to strengthen muscles can also be a part of the treatment plan for Parkinson’s. Though Huntington’s and Parkinson’s share some symptoms, they have a distinct set of symptoms that differentiate them.
The disease affects about 1 million people in the United States, and 10 million globally. Causes of Parkinson’s disease are generally unknown, although research suggests that genetics and environmental factors likely play a role. Parkinson’s is caused by the death of cells in a part of your brain called the substantia nigra. When these cells die, levels of the neurotransmitter dopamine drop in your brain. This reduction leads to symptoms such as tremors, impaired balance, rigid muscles, and difficulty walking.
DBS is a procedure that involves doctors surgically implanting electrodes in the part of the brain that controls movement. The electrodes connect to a pacemaker-like device, or neurostimulator, which is under the skin on the upper chest. The device then sends electrical impulses along a wire into the brain via the electrodes.
Currently, considerable therapeutic advances have been achieved seeking a more efficacious and durable therapeutic effect. Here, we will focus on the new advances of several therapeutic approaches for PD and HD, starting with the available pharmacological treatments to alleviate the motor symptoms in both diseases. Then, we describe therapeutic strategies that aim to restore specific neuronal populations or their activity.
The information we present is intended for educational purposes only and should not be construed as offering diagnoses or recommendations. We operate as a not-for-profit public service organization, and our funding is entirely from private sources. The following chapter aims to compare Huntington’s disease to other neurological diseases such as Alzheimer’s disease and Parkinson’s disease. Huntington’s disease, like Alzheimer’s disease, can produce severe cognitive difficulties, albeit this is not a prominent hallmark of Parkinson’s disease. Doctors may give selective serotonin reuptake inhibitors (SSRIs) or tricyclic antidepressants (TCAs) if the person is suffering from mental health issues such as anxiety, depression, or OCD. Starting an action, such as getting out of bed, may be challenging for a person.
Nevertheless, this does not explain the effect of SCS on gait and postural dysfunction. The participation of the brainstem, specifically the pedunculopontine nucleus (PPN), has been suggested, given its connection with different structures involved in the motor system, summarized by Chambers et al. (2019). This case was an adult patient with HD in the fourth decade of life who presented with generalized parkinsonism and showed only a short-lasting and modest response to levodopa. In addition, preexisting rapid eye movement sleep behavior disorder-like phenotype and levodopa responsiveness can masquerade as young-onset Parkinson’s disease (PD). However, unlike PD, this patient showed symmetric akinetic rigidity with early postural instability. Moreover, the presynaptic dopaminergic neuronal density in the striatum was diffusely and symmetrically decreased in the caudate and putamen, which differs markedly from PD showing dorsal-to-ventral and posterior-to-anterior gradients of striatal denervation.
Medical professionals classify both conditions as neurodegenerative diseases ‘ conditions in which a person’s brain or nerve cells gradually degrade. A diagnosis of Huntington’s or Parkinson’s disease can be upsetting and create challenges in your life. Staying informed, talking to your physician about treatment options to manage symptoms, as well as connecting with others who are going through similar experiences, can help you live well with either disease.
The results of the sensitivity analysis ‘ in which the requirement for full medication coverage was removed across all cohorts ‘ largely reflected those of the primary analysis. Of the prespecified comorbidities, depression and anxiety were the most frequently reported during the analysis period, and were more common in people with HD (45.8% and 37.2%, respectively) or PD (38.0% and 35.1%) versus GP controls (18.5% and 17.7%). Compared with PD controls, dementia was more common in the HD cohort during the analysis period (2.83 [2.18’3.68]). Depression (1.38 [1.15’1.65]) and anxiety (1.09 [0.91’1.31]) were also more common in HD versus PD, though the magnitude of these differences were reduced compared with the primary analysis. In the broader panel of comorbidities, dementia remained more common in HD versus PD during the analysis period (4.59 [3.23’6.52]) and lack of coordination was more common versus GP controls (23.96 [10.51’54.62]). These and other studies have demonstrated that the reduction of mHTT using RNAi in the brain of HD mice decreases both mHTT mRNA and protein levels, which is accompanied by improved motor behavior.
Alice has obtained her BSc and MSc at King’s College London, and presented and published her research at international neuroscience conferences and peer-reviewed journals. For improved mobility, PD patients are often referred to physiotherapists and massage therapists to improve balance and loosen tension in their muscles. The progression of PD is very slow, and often these treatments allow a patient to maintain their former independence for many years. Since both diseases have a genetic component, this also varies greatly across regions. Through a combination of conversations and tests, your doctor may diagnose you with Parkinson’s or Huntington’s. While having a progressive disease may be life-changing, once you know the cause of your symptoms, you and your care team can work together to treat them.
According to a 2018 review, this healthy habit may help maintain the brain’s dopamine levels. The expansion of the cytosine-adenine-guanine (CAG) trinucleotide in the HTT gene leads to the production of atypical protein. The higher the number you could try this out of CAG repeats, the earlier the age of onset and the greater the severity of the disease. They both involve a brain structure known as the basal ganglia and can affect a person’s movement, mental health, and cognitive (thinking) ability.
Reports published between 1987 and 1989 showed that blocking the activity of the STN produces hyperkinetic motor symptoms. Similar results are observed when the GABAergic inputs from the striatum are blocked, favoring the inhibitory (GABAergic) modulation of the GPe over the STN (Crossman, 1987; Crossman et al., 1988; Robertson et al., 1989). internet On the other hand, hypokinetic disorders like akinesia and bradykinesia have been described in PD. These symptoms, unlike hyperkinetic movements, are treated with DA agonists as L-dopa (Cotzias et al., 1967, 1969). However, today no clinical trials are studying the safety and efficacy of IGF2 as a possible treatment for PD or HD.