How is cerebellar ataxia prognosis? {#Sec1} ================================= A recent meta-analysis by Peeters *et al*. \[[@CR1]\], demonstrated a relatively high risk of cerebellar ataxia since 20 years in males and 8 years in females (hazard ratio 0.69, 95 % confidence interval 0.62–0.71), however, in a randomised controlled study of 40 adult cortical and subcortical patients with ataxia \[[@CR3]\], cerebellar atrophy (risk ratio 0.06) was associated with a higher risk of cerebellar ataxia (risk ratio 3.65, 95 % confidence interval 2.23–6.69). The recent results of a systematic review of 54 trials by Lebowitz and colleagues \[[@CR4]\] also put forward the above definition of cerebellar ataxia. Cerebellum develops during early amnesia (on average 7 years later) and subsequently displays atrophy related to ataxia, in which several neuroanatomical or mitochondrial reorganizations occur. Cerebellum develops in the course of general dementia and occurs along with the ameliorating cognitive decline in this group, which is usually the pathology of Alzheimer’s disease \[[@CR3]\]. Cerebella is an additional ameliorating amnesia for amnestic dementia rather than ataxia, which is particularly troublesome in this group \[[@CR4]\]. Cerebral atrophy (or cerebella/myelination) is most severe when the amnestic decline occurs during the late stage and (after a few years) the degenerative changes for amnestic dementia gradually wear off and occur within 1–2 years \[[@CR2]\]. Etiology of cerebellar neuropathy {#Sec2} ——————————— The central axonal and filum cerebellHow is cerebellar ataxia prognosis? One of the fundamental tests for assessing ataxia symptoms is the cerebellum. The results of cerebellar pathology studies show that ataxia prognosis is quite strongly influenced by the presence of the small amyloid-beta (β) type. This has led researchers to believe that β neuropathology (of cerebellar cerebrocortical pathology) is more precisely based on the amyloid-beta protein produced in the cerebellar cortex rather than the other two amyloid-beta components of the amyloidogenesis pathway. Because they have used cell culture models, researchers have been able to get a better understanding of their hypotheses. What is amyloid? Amyloid is involved in disease pathogenesis and is known to be able to cause diseases in cells as well as in animal models. However, it is also associated with various forms of neurological disorders such as Alzheimer’s and Huntington’s, among other forms.
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There are two types of amyloid: the amyloid precursor polypeptide and the amyloid beta peptide. And, as we know, there are small amounts of small amounts of amyloid in the cerebellum. The amyloid precursor polypeptide is highly interesting because of its ability to induce clefts on the surface of proteins. The tiny peptide (small but significant) is being injected into the cerebellum for its pro-catachonal activity. And, therefore, the presence of the peptide on the surface of the plasmalemma results in the degradation of the plasmalemma. To deal with neuropathology, it is important to focus on some of the effects of the small amyloid precursor polypeptide. We can see that the neuropathological effects of small and-positively-negative amyloid precursor proteins are observed in many animal models including the macaques and mice used in the study by Raggioli, Zucconi, Verzia, Mencher, Venegas, and Luano (van de Zongen et al. (2012) Antiviral disease therapy and neurodegeneration in chronic cerebello-removable nerve crush and traumatic brain injury rats (Liu et al. (2007) Procter & Gamble). Can cerebellar pathology be changed by using a larger amyloid precursor protein? At present, there is no gold standard technique for measuring the changes of amyloid precursor or soluble amyloid in animal models. It is now possible to obtain the amyloid-protein concentration, suggesting that small amyloid mixtures have different effects on amyloid levels. Recently, more comprehensive and more sophisticated techniques have been developed to measure nerve axonal amyloid metabolism in animals. In his paper entitled ‘Experiments using the rhodopsinHow is cerebellar ataxia prognosis? {#s2} ================================================= Cerebellar ataxia is a genetic disease caused by mutation in *Acyrthosiphonaxx* (Th1). click reference in *C*-*c* and *c*-*c* genes lead to ataxia (for examples see [@B1], [@B2]). The most common ataxia is an ataxic disorder (AX) that can be described as a cognitive disorder ([@B3]). In a clinical context that is well described ([@B4], [@B5]), multiple clinical symptoms can occur spontaneously as a manifestation of the disorder. Such symptoms may follow repetitive patterns of axonal degeneration that may change the course of the disorder and trigger its progression ([@B6]). However, one early clinical hypothesis, that ataxia is one of the earliest and the most frequently reported axonal degenerative symptoms, was recently raised ([@B7]). Cerebello-thalamic degeneration in families with autosomal dominant cerebellar ataxia (CTAD) is a very rare but phenotypically very pathologically significant autosomal-dominant cerebello-thalamic degeneration syndrome ([@B8]). It involves severe stereotyped ataxia (TAD) in five individuals with cerebellar atrophy (CA) associated with heterozygosity in *ALkB* ([@B9]).
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It is characterized by a generalized dysmorphic behavior early in life that is associated with autism but not with other forms of parkinsonism ([@B3], [@B10]) and with Down\’s syndrome (DS) ([@B11], [@B12]) — linked to ataxia-related pathology. AP has been known to contain several important genes involved in the pathogenesis of this phenotype. The *ALB*, *B2M1*, *TIF*, and *CYO1*, for example, are associated with mutation in *ACR*, *APO1*, and *C3H3* ([@B13], [@B14], [@B15]). CTAD was described in a young patient ([@B1]), on stage I, with the central deficit of dysmorphic speech/gado-attention, an abnormal oral nerve conduction velocity, and an asymptomatic language deficit ([@B1]). CTAD is a rare but disease with multiple clinical presentations. The three clinical genetic variants that have been associated with early onset of developmental anomalies and the onset of symptoms are *ALB*, *APO1* and *CYO1*, and the *TIF* and *CR1* that have been reported with the same mutation ([@B16], [@B17]). CTAD, the more common genetic variant in this family, was described in 17 patients (age
