Amyloid plaques in cerebellar cortex and the integrity of Purkinje cell dendrites
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Altered microglia and neurovasculature in the Alzheimer's disease cerebellum
2019, Neurobiology of DiseaseCitation Excerpt :These findings provide evidence that AD-related molecular changes occur within non-neuronal cells of the neocerebellum, which may contribute to the symptomatology and pathophysiology of AD. Our study of neocerebellar neuropathology using TMAs revealed a considerable increase in amyloid-β expression and load within AD cases, which is in general agreement with earlier studies of AD neuropathology (Braak et al., 1989; Joachim et al., 1989; Dickson et al., 1990; Li et al., 1994; Fukutani et al., 1997; Wegiel et al., 1999; Wang et al., 2002). Furthermore, no tau-positive neurofibrillary tangles were identified in AD neocerebellar TMA cores, which is in line with previous observations (Joachim et al., 1989; Li et al., 1994; Wegiel et al., 1999; Yamamoto and Hirano, 1985).
Accumulation of amyloid-β in the cerebellar cortex of essential tremor patients
2015, Neurobiology of DiseaseCitation Excerpt :The concept of Aβ accumulation in the cerebellum is not new. By the use of microscopic, biochemical or mass spectrometry approaches, significant levels of Aβ have been reported in the cerebellum of subject with Down's syndrome or AD, typically with an higher incidence in patients with an early onset diagnosis and longer disease duration (Braak et al., 1989; Cole et al., 1989, 1993; Joachim et al., 1989; Yamaguchi et al., 1989; Mann et al., 1990, 1996; Jellinger, 1993; Li et al., 1994; Tamaoka et al., 1995; Lemere et al., 1996; Mann and Iwatsubo, 1996; Fukutani et al., 1997; Wang et al., 2002; Verdile et al., 2004; Portelius et al., 2010; Sepulveda-Falla et al., 2011; Rohn et al., 2013). Here we corroborated the cerebellar Aβ accumulation observed in these studies using samples from our cohort of neuropathologically diagnosed AD patients.
Isolation and characterization of patient-derived, toxic, high mass Amyloid β-protein (Aβ) assembly from Alzheimer disease brains
2009, Journal of Biological ChemistryCitation Excerpt :Furthermore, in AD patients with severe pathology, significantly higher amounts of native ASPD were detected in the frontal or temporal cortices (7.2 ± 1.5 nmol/g brain tissue, n = 3, Scheffé post hoc test p = 0.0012) than in the cerebellum (0.14 ± 0.1 nmol/g brain tissue). The result is consistent with previous findings that the cerebellum in AD is pathologically less affected (44, 45). The above observations suggest the involvement of native ASPDs in neurodegeneration of AD brains.
Comparisons of telomere lengths in peripheral blood and cerebellum in Alzheimer's disease
2009, Alzheimer's and DementiaCitation Excerpt :Here we examined the association between PBL and cerebellum telomere lengths in AD, and also compared telomere lengths in the cerebella of AD patients and control subjects. We chose the cerebellum because whereas it may suffer limited pathology in AD, including atrophy of the molecular and granular layers [31], it does not experience gliosis [31–33]. Thus, the measurement of cerebellar telomere length should not be complicated by telomerase expression in proliferating glial cells.