Corticobasal Degeneration and Dementia

Armstrong, Richard A.

doi:10.1016/b978-0-12-407824-6.00004-5

Cited by 6 publications

(8 citation statements)

References 46 publications

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“…Brain neurons with CBD react positively with antibodies generated against ubiquitin, hyperphosphorylated tau, phosphorylated neurofilament protein, alpha-B crystal, and synaptophysin. In addition, aggregates of Aβ have been found in some cases of CBD, which are similar to those found in AD (Armstrong, 2015).…”

Section: Neuroinflammation In Several Tauopathiessupporting

confidence: 67%

Neuroinflammation as a Common Feature of Neurodegenerative Disorders

et al. 2019

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Neurodegenerative diseases share the fact that they derive from altered proteins that undergo an unfolding process followed by formation of β-structures and a pathological tendency to self-aggregate in neuronal cells. This is a characteristic of tau protein in Alzheimer’s disease and several tauopathies associated with tau unfolding, α-synuclein in Parkinson’s disease, and huntingtin in Huntington disease. Usually, the self-aggregation products are toxic to these cells, and toxicity spreads all over different brain areas. We have postulated that these protein unfolding events are the molecular alterations that trigger several neurodegenerative disorders. Most interestingly, these events occur as a result of neuroinflammatory cascades involving alterations in the cross-talks between glial cells and neurons as a consequence of the activation of microglia and astrocytes. The model we have hypothesized for Alzheimer’s disease involves damage signals that promote glial activation, followed by nuclear factor NF-kβ activation, synthesis, and release of proinflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, IL-6, and IL-12 that affect neuronal receptors with an overactivation of protein kinases. These patterns of pathological events can be applied to several neurodegenerative disorders. In this context, the involvement of innate immunity seems to be a major paradigm in the pathogenesis of these diseases. This is an important element for the search for potential therapeutic approaches for all these brain disorders.

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Section: Neuroinflammation In Several Tauopathiessupporting

confidence: 67%

Neuroinflammation as a Common Feature of Neurodegenerative Disorders

et al. 2019

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“…The motor symptoms of CBD include parkinsonism, ‘alien hand syndrome’ and apraxia . The parkinsonism usually affects the extremities of the limb, is frequently asymmetric and characterised by rigidity and bradykinesia.…”

Section: Clinical Featuresmentioning

confidence: 99%

“…The disorder has also been referred to as ‘corticoganglionic degeneration’ but CBD remains the most popular descriptive term. Patients with a combination of clinical symptoms suggestive of the disorder are often referred to as having ‘corticobasal syndrome’ (CBS), while CBD is used strictly to describe cases verified at post‐mortem …”

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confidence: 99%

Visual signs and symptoms of corticobasal degeneration

Armstrong

2016

Clinical and Experimental Optometry

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SummaryCorticobasal degeneration is a rare, progressive neurodegenerative disease and a member of the 'parkinsonian' group of disorders which also includes Parkinson's disease, progressive supranuclear palsy, dementia with Lewy bodies, and multiple system atrophy. The most common initial symptom is limb clumsiness, usually affecting one side of the body, with or without accompanying rigidity or tremor.Subsequently, the disease affects gait and there is a slow progression to influence ipsilateral arms and legs. Apraxia and dementia are the most common cortical signs.

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“…the ‘parkinsonian syndromes’. This group includes progressive supranuclear palsy (PSP) [ 19 ], dementia with Lewy bodies (DLB) [ 20 ], multiple system atrophy (MSA) [ 21 ], and corticobasal degeneration (CBD) [ 22 ]. Differential diagnosis of PD within this group can be difficult, especially early in the disease, but where visual signs and symptoms are present they may be useful adjuncts to diagnosis [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

Oculo-Visual Dysfunction in Parkinson’s Disease

Armstrong¹

2015

JPD

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102

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This review describes the oculo-visual problems likely to be encountered in Parkinson’s disease (PD) with special reference to three questions: (1) are there visual symptoms characteristic of the prodromal phase of PD, (2) is PD dementia associated with specific visual changes, and (3) can visual symptoms help in the differential diagnosis of the parkinsonian syndromes, viz. PD, progressive supranuclear palsy (PSP), dementia with Lewy bodies (DLB), multiple system atrophy (MSA), and corticobasal degeneration (CBD)? Oculo-visual dysfunction in PD can involve visual acuity, dynamic contrast sensitivity, colour discrimination, pupil reactivity, eye movement, motion perception, and visual processing speeds. In addition, disturbance of visuo-spatial orientation, facial recognition problems, and chronic visual hallucinations may be present. Prodromal features of PD may include autonomic system dysfunction potentially affecting pupil reactivity, abnormal colour vision, abnormal stereopsis associated with postural instability, defects in smooth pursuit eye movements, and deficits in visuo-motor adaptation, especially when accompanied by idiopathic rapid eye movement (REM) sleep behaviour disorder. PD dementia is associated with the exacerbation of many oculo-visual problems but those involving eye movements, visuo-spatial function, and visual hallucinations are most characteristic. Useful diagnostic features in differentiating the parkinsonian symptoms are the presence of visual hallucinations, visuo-spatial problems, and variation in saccadic eye movement dysfunction.

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Corticobasal Degeneration and Dementia

Cited by 6 publications

References 46 publications

Neuroinflammation as a Common Feature of Neurodegenerative Disorders

Neuroinflammation as a Common Feature of Neurodegenerative Disorders

Visual signs and symptoms of corticobasal degeneration

Oculo-Visual Dysfunction in Parkinson’s Disease

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