Most people agree that animals have at least some moral status — that is why it is wrong to abuse pets or needlessly hurt other animals. This alone represents a shift from a past view where animals had no moral status and treating an animal well was more about maintaining human standards of dignity than respecting any innate rights of the animal. In modern times, the question has shifted from whether animals have moral status to how much moral status they have and what rights come with that status. The strongest pro animal rights answer to this question would be that non-human animals have exactly the same moral status as humans and are entitled to equal treatment.
Regions of the brain have differing amounts and reliance on these types of neurons, and are affected accordingly.
The remaining variation is attributed to environment and other genes that modify the mechanism of HD. In some cases the onset may be so late that symptoms are never noticed.
Inheritance is independent of gender, and the phenotype does not skip generations.
This probability is sex-independent. Individuals with both genes affected are rare. For some time HD was thought to be the only disease for which possession of a second mutated gene did not affect symptoms and progression,  but it has since been found that it can affect the phenotype and the rate of progression.
Early damage is most evident in the striatumbut as the disease progresses, other areas of the brain are also more conspicuously affected. Early symptoms are attributable to functions of the striatum and its cortical connections—namely control over movement, mood and higher cognitive function.
Huntingtin HTT is expressed in all cells. The highest concentrations are found in the brain and testeswith moderate amounts in the liverheartand lungs. It interacts with proteins which are involved in transcription, cell signalingand intracellular transporting. Caspasean enzyme which plays a role in catalyzing apoptosis, is thought to be activated by the mutated gene through damaging the ubiquitin-protease system.
It also acts as an anti-apoptotic agent preventing programmed cell death and controls the production of brain-derived neurotrophic factora protein which protects neurons and regulates their creation during neurogenesis. HTT also facilitates vesicular transport and synaptic transmission and controls neuronal gene transcription.
Over time, the aggregates accumulate to form inclusion bodies within cells, ultimately interfering with neuron function. Inclusion bodies have been found in both the cell nucleus and cytoplasm. Mutant Huntingtin protein has been found to play a key role in mitochondrial dysfunction.
Excitotoxins may cause damage to numerous cellular structures. Although glutamine is not found in excessively high amounts, it has been postulated that because of the increased vulnerability, even normal amounts glutamine can cause excitotoxins to be expressed.
The most prominent early effects are in a part of the basal ganglia called the neostriatumwhich is composed of the caudate nucleus and putamen. Their functions are not fully understood, but current theories propose that they are part of the cognitive executive system  and the motor circuit.
To initiate a particular movement, the cerebral cortex sends a signal to the basal ganglia that causes the inhibition to be released. Damage to the basal ganglia can cause the release or reinstatement of the inhibitions to be erratic and uncontrolled, which results in an awkward start to motion or motions to be unintentionally initiated, or a motion to be halted before, or beyond, its intended completion.
The accumulating damage to this area causes the characteristic erratic movements associated with HD. Thus, the glutamines on CBP interact directly with the increased numbers of glutamine on the HTT chain and CBP gets pulled away from its typical location next to the nucleus.Huntington's disease (HD), also known as Huntington's chorea, is an inherited disorder that results in death of brain cells.
Huntington's disease, particularly the application of the genetic test for the disease, has raised several ethical issues. The issues for genetic testing include defining how mature an individual should be before. Assessment and management by speech-language pathologists with experience in Huntington's disease is recommended.
People with Huntington's disease may see a physical therapist for non-invasive and non-medication-based ways of managing the physical symptoms.
Physical therapists may implement fall risk assessment and prevention, as well as strengthening, stretching, and cardiovascular exercises. While all cases of Huntington's disease have some common characteristics, there is wide variation among patients. Even a brother and a sister can be very different: one calm, isolated, and compliant and the other agitated, with severe chorea, and prone to self-injurious behaviors.
Genetic Issues in HD –page 2 Genetic Issues in Huntington’s Disease HDSA Center of Excellence UC Davis Medical Center Mara Sifry-Platt, M.S. – Genetic Counselor Huntington’s Disease(HD) is a genetic condition of the brain where symptoms usually.
Huntington’s Disease PSYCH (4 Pages | Words) Current Ethical Issue Paper XMGT Discuss a contemporary information technology issue for which our society’s moral guidelines seem to be nonexistent or unclear. Ethical, social and legal issues in Huntington disease: the nurse's role.
Rohs G, Klimek ML. The nurse's role will be discussed in relation to the issues which may present as the result of our ability to use predictive tests for neurodegenerative disease.