The cerebellum in mild cognitive impairment and Alzheimer’s disease – A structural MRI study

Thomann, Philipp A.; Schläfer, Christine; Seidl, Ulrich; Santos, Vasco Dos; Essig, Marco; Schröder, Johannes

doi:10.1016/j.jpsychires.2007.12.002

Cited by 97 publications

(75 citation statements)

References 24 publications

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“…This loss of gray and white matter significantly impacts the connectivity between the cortex and the cerebellum [77]. In addition, atrophy of the posterior cerebellar hemispheres was found in manifest AD patients, with more atrophy corresponding to poorer cognitive performance [78]. Specifically, amyloid plaques (a representative feature of AD pathology) were found in the cerebellum of AD brains, as well as Purkinje and granule cell death (contributing to the lower cerebellar volumes) [79].…”

Section: Cerebellar Dysfunction In Neurodegenerationmentioning

confidence: 99%

Neurodegeneration and the Cerebellum

Samson

Claassen²

2017

Neurodegener Dis

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Background: The cerebellum modulates diverse neuronal networks, regulating motor, cognitive, behavioral, and limbic circuits. Structural and functional changes to the cerebellum that occur with neurodegenerative conditions have not been systematically reviewed. Objective: We synthesize the current understanding of cerebellar somatotopy and function with previously described cerebellar changes in neurodegenerative diseases not associated with primary cerebellar pathology. Methods: A thorough literature review defines the role of the cerebellum in normal function and neurodegeneration, and we additionally provide exemplar cases of cerebellar dysfunction in neurodegenerative disorders. Results: Comparisons between normal function and neurodegenerative disease states emphasize how normal organization of the cerebellum is altered in neurodegenerative disease states. We illustrate key anatomic structures using novel cerebellar segmentation tools and images. Conclusions: Altered cerebellum in neurodegeneration can provide important diagnostic and pathologic insights into both predicting disease progression and network dysfunction.

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Section: Cerebellar Dysfunction In Neurodegenerationmentioning

confidence: 99%

Neurodegeneration and the Cerebellum

Samson

Claassen²

2017

Neurodegener Dis

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“…Additionally, Braak et al [57] and Yamaguchi et al [58] described the presence of diffuse amyloid plaques in the molecular layer of the cerebellar cortex of AD subjects and Wegiel et al [59] reported a volumetric loss in both the molecular and granular layers. Shrinkage of the posterior cerebellar region of AD has been associated with poorer cognitive performance [60]. Furthermore, elevated levels of 8-hydroxyguanine and FapyG were observed in the CER of DC subjects, consistent with FTD associated loss of the Purkinje cells [61] and detection of α-synuclein positive Purkinje cells in DLB subjects [62].…”

Section: Conflict Of Interestmentioning

confidence: 59%

Increased Oxidative Damage in RNA in Alzheimer’s Disease Progression

Lovell¹

2014

J Anal Bioanal Tech

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“…Consistent with frequent cerebellar symptoms, abundant amyloid deposits in the cerebellum and loss of Purkinje cells was described in 2 patients [43,45]. However, in contrast to its relatively rare clinical manifestations, cerebellar pathology is consistently described in both sporadic [68,69,70,71,72] and familial AD cases [35,67,73,74,75]. Cerebellar damage is thought to characterize a late event in the sequence of amyloid deposition in distinct brain regions [76].…”

Section: Discussionmentioning

confidence: 99%

Phenotypic Variability in Autosomal Dominant Familial Alzheimer Disease due to the S170F Mutation of Presenilin-1

et al. 2018

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Background: In rare cases, patients with Alzheimer disease (AD) present at an early age and with a family history suggestive of an autosomal dominant mode of inheritance. Mutations of the presenilin-1 (PSEN1) gene are the most common causes of dementia in these patients. Early-onset and particularly familial AD patients frequently present with variable non-amnestic cognitive symptoms such as visual, language or behavioural changes as well as non-cognitive, e.g. motor, symptoms. Objective: To investigate the phenotypic variability in carriers of the PSEN1 S170F mutation. Methods: We report a family with 4 patients carrying the S170F mutation of whom 2 underwent detailed clinical examinations. We discuss our current findings in the context of previously reported S170F cases. Results: The clinical phenotype was consistent regarding initial memory impairment and early onset in the late twenties found in all S170F patients. There were frequent non-amnestic cognitive changes and, at early stages of the disease, indications of a more pronounced disturbance of visuospatial abilities as compared to face and object recognition. Non-cognitive symptoms most often included myoclonus and cerebellar ataxia. A review of the available case reports indicates some phenotypic variability associated with the S170F mutation including different constellations of symptoms such as parkinsonism and delusions. Conclusion: The variable clinical findings associated with the S170F mutation highlight the relevance of atypical phenotypes in the context of research and under a clinical perspective. CSF sampling and detection of Aβ species may be essential to indicate AD pathology in unclear cases presenting with cognitive and motor symptoms at a younger age.

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The cerebellum in mild cognitive impairment and Alzheimer’s disease – A structural MRI study

Cited by 97 publications

References 24 publications

Neurodegeneration and the Cerebellum

Neurodegeneration and the Cerebellum

Increased Oxidative Damage in RNA in Alzheimer’s Disease Progression

Phenotypic Variability in Autosomal Dominant Familial Alzheimer Disease due to the S170F Mutation of Presenilin-1

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