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The area of the brain most damaged in early Huntington's disease is the dorsal striatum made up of the caudate nucleus and the putamen. Initially, damage to the brain is regionally specific with the dorsal striatum in the subcortical basal ganglia being primarily affected, followed later by cortical involvement in all areas.
Huntingtin (Htt) is the protein coded for in humans by the HTT gene, also known as the IT15 ("interesting transcript 15") gene. [5] Mutated HTT is the cause of Huntington's disease (HD), and has been investigated for this role and also for its involvement in long-term memory storage.
Transmissible spongiform encephalopathies (TSEs), also known as prion diseases, [1] are a group of progressive, incurable, and fatal conditions that are associated with the prion hypothesis and affect the brain and nervous system of many animals, including humans, cattle, and sheep.
The human brain contains 86 billion neurons, with 16 billion neurons in the cerebral cortex. [ 2 ] [ 1 ] Neuron counts constitute an important source of insight on the topic of neuroscience and intelligence : the question of how the evolution of a set of components and parameters (~10 11 neurons, ~10 14 synapses) of a complex system leads to ...
Neurodegenerative diseases include amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease, Alzheimer's disease, Huntington's disease, multiple system atrophy, tauopathies, and prion diseases. Neurodegeneration can be found in the brain at many different levels of neuronal circuitry, ranging from molecular to systemic. [4]
Huntington's disease is a degenerative neurological disorder that is inherited. Degeneration of neuronal cells occurs throughout the brain, especially in the striatum. There is a progressive decline that results in abnormal movements. [31] Statistics show that Huntington's disease may affect 10 per 100,000 people of Western European descent.
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Huntington's disease is also associated with problems in odor identification, detection, discrimination, and memory. The problem is prevalent once the phenotypic elements of the disorder appear, although it is unknown how far in advance the olfactory loss precedes the phenotypic expression.