Cerebrovascular disease and gait and balance impairment in mild to moderate Alzheimer's disease

Inzitari, Marco; Giné-Garriga, María; Martinez, Bruno Prata; Pérez-Fernández, María; Barranco-Rubia, E.; Lleó, Alberto; Salvà, Antoni

doi:10.1007/s12603-012-0091-3

Cited by 6 publications

(4 citation statements)

References 23 publications

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“…38 However, this may be due to risk factors such as hypertension, stroke, and arthritis. 4,37 Although in our study, we didn't find a relationship between gait disturbance and comorbid diseases, this relationship has been valued by Inzitari et al 39 We found worst scores on the disability scale RDRS in patients presenting gait disturbance. Patients with greater disability in the early stages of the disease reach gait disturbance sooner, so it could be a good predictor of gait disturbance.…”

Section: Discussioncontrasting

confidence: 48%

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Gait Disorder in a Cohort of Patients With Mild and Moderate Alzheimer’s Disease

Castrillo

Olmos²,

Rodríguez

et al. 2015

Am J Alzheimers Dis Other Demen

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Gait disturbance results in an increase in the risk of falls in patients with Alzheimer's disease (AD). The falls are events that might be related to an increase in the number of fractures, loss of mobility, being bedridden, early institutionalization, and increased use of medication. Therefore, the reduction in the number of falls is important for the maintenance of the functional independence of the patients as well as for the prevention of sequelae resulting from those events. Alterations in the gait occur very frequently in AD, and the gait disturbance occurs relatively early in the course of the disease. This study has important implications for public health and clinical practice. This study and previous studies have reported that abnormal gait predicts greater risk of falls, dementia, institutionalization, and death. The high prevalence and incidence of abnormal gait and its association with multiple adverse outcomes in older adults require urgent attention. Our results allow us to identify the risk factors.

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Section: Discussioncontrasting

confidence: 48%

“…38 However, this may be due to risk factors such as hypertension, stroke, and arthritis. 4,37 Although in our study, we didn’t find a relationship between gait disturbance and comorbid diseases, this relationship has been valued by Inzitari et al 39…”

Section: Discussionmentioning

confidence: 52%

Gait Disorder in a Cohort of Patients With Mild and Moderate Alzheimer’s Disease

Castrillo

Olmos²,

Rodríguez

et al. 2015

Am J Alzheimers Dis Other Demen

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“…This progressive decline of gait parameters paralleling the evolution of dementia confirms the findings of previous studies . Different factors have been suggested to explain this parallel decline between cognition and gait: the progressive decline of the frontal lobe functions , the involvement of the basal ganglia or the accumulation of vascular lesions . The progressive gait degradation with the course of dementia has been associated with poor clinical outcomes such as falls , institutionalization and mortality .…”

Section: Discussionmentioning

confidence: 99%

Gait phenotype from mild cognitive impairment to moderate dementia: results from the GOOD initiative

Allali

Annweiler

Blumen

et al. 2015

Euro J of Neurology

116

122

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Background The differences in gait abnormalities from the earliest to the latter stages of dementia and in the different subtypes of dementia have not been fully examined. This study aims to compare spatio-temporal gait parameters in cognitively healthy individuals, patients with amnestic (aMCI) and non-amnestic (naMCI) MCI, and patients with mild and moderate stages of Alzheimer’s disease (AD) and non-Alzheimer’s disease (non-AD). Methods Based on a cross-sectional design, 1719 participants (77.4±7.3 years, 53.9% female) were recruited from cohorts from seven countries participating in the “Gait, cOgnitiOn & Decline” initiative. Mean values and coefficients of variation of spatio-temporal gait parameters were measured during normal pace walking with the GAITRite system at all sites. Results Performance of spatio-temporal gait parameters declined in parallel to the stage of cognitive decline from MCI status to moderate dementia. Gait parameters of patients with naMCI were more disturbed compared to patients with aMCI, and MCI subgroups performed better than demented patients. Patients with non-AD dementia had worse gait performance than those with AD dementia. This degradation of the gait parameters was similar between mean values and coefficients of variation of spatio-temporal gait parameters in the earliest stages of cognitive decline, but different in the most advanced stages, especially in the non-AD subtypes. Conclusions Spatio-temporal gait parameters were more disturbed in the advanced stages of dementia, and more affected in the non-AD dementias than in AD. These findings suggest that quantitative gait parameters could be used as a surrogate marker for improving the diagnosis of dementia.

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“…AD is characterized by loss of neurons and dendritic spins with degeneration of neurofibrils, mainly in the hippocampus and cerebellum ( Mavroudis et al, 2010 ) Cerebellum modulates coordination of movement, and cerebellar dysfunction lacks coordination of voluntary movement and then causes gait disturbance ( Taroni and DiDonato, 2004 ). Several studies suggested that AD induces motor impairments, including dysfunction of gait and balance ( Inzitari et al, 2013 ; Kuwabara et al, 2014 ). In the present study, Aβ 25–35 -induced AD rats showed disturbance of coordination and balance in the rota-rod test.…”

Section: Discussionmentioning

confidence: 99%

Treadmill exercise improves motor coordination through ameliorating Purkinje cell loss in amyloid beta23-35-induced Alzheimer’s disease rats

Lee

Shin

et al. 2014

J Exerc Rehabil

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Alzheimer’s disease (AD) is a most common age-related neurodegenerative disease. AD is characterized by a progressive loss of neurons causing cognitive dysfunction. The cerebellum is closely associated with integration of movement, including motor coordination, control, and equilibrium. In the present study, we evaluated the effect of tread-mill exercise on the survival of Purkinje neurons in relation with reactive astrocyte in the cerebellum using Aβ25–35–induced AD rats. AD was induced by a bilateral intracerebroventricular (ICV) injection of Aβ25–35. The rats in the exercise groups were forced to run on a motorized treadmill for 30 min once a day for 4 weeks, starting 2 days after Aβ25–35 injection. In the present results, ICV injection of Aβ25–35 deteriorated motor coordination and balance. The number of calbindin-positive cells in the cerebellar vermis was decreased and glial fibrillary acidic protein (GFAP) expression in the cerebellar vermis was increased in the Aβ25–35-induced AD rats. Treadmill exercise improved motor coordination and balance. Treadmill exercise increased the number of Purkinje neurons and suppressed GFAP expression in the cerebellar vermis. The present study demonstrated that treadmill exercises alleviated dysfunction of motor coordination and balance by reduction of Purkinje cell loss through suppressing reactive astrocytes in the cerebellum of AD rats. The present study provides the possibility that treadmill exercise might be an important therapeutic strategy for the symptom improvement of AD patients.

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Cerebrovascular disease and gait and balance impairment in mild to moderate Alzheimer's disease

Abstract: In our sample, AD with cerebrovascular disease had worse gait and balance than AD without cerebrovascular disease. If confirmed, these results may have clinical implications, since cerebrovascular disease can be potentially prevented.

Cited by 6 publications

References 23 publications

Gait Disorder in a Cohort of Patients With Mild and Moderate Alzheimer’s Disease

Gait Disorder in a Cohort of Patients With Mild and Moderate Alzheimer’s Disease

Gait phenotype from mild cognitive impairment to moderate dementia: results from the GOOD initiative

Treadmill exercise improves motor coordination through ameliorating Purkinje cell loss in amyloid beta23-35-induced Alzheimer’s disease rats

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