Abstract

Alzheimer’s disease effects a large percentage of elderly dementia patients and is diagnosed on the basis of amyloid plaques and neurofibrillary tangles (NFTs) present in the brain. Urinary incontinence (UI) is often found in the elderly populations and multiple studies have shown that it is more common in Alzheimer’s disease patients than those with normal cognitive function. However, the link between increased UI and Alzheimer’s disease is still unclear. Amyloid plaques and NFTs present in micturition centers of the brain could cause a loss of signal to the bladder, resulting in the inability to properly void. Additionally, as Alzheimer’s disease progresses, patients become less likely to recognize the need or understand the appropriate time and place to void. There are several treatments for UI targeting the muscarinic and β3 adrenergic receptors, which are present in the bladder and the brain. While these treatments may aid in UI, they often have effects on the brain with cognitive impairment side-effects. Acetylcholine esterase inhibitors are often used in treatment of Alzheimer’s disease and directly oppose effects of anti-muscarinics used for UI, making UI management in Alzheimer’s disease patients difficult. There are currently over 200 pre-clinical models of Alzheimer’s disease, however, little research has been done on voiding disfunction in these models. There is preliminary data suggesting these models have similar voiding behavior to Alzheimer’s disease patients but much more research is needed to understand the link between UI and Alzheimer’s disease and discover better treatment options for managing both simultaneously.

Highlights

  • It is estimated that there are 35 million people living with dementia globally and by the year 2030, that number is predicted to double (Lee et al, 2017)

  • Alzheimer’s disease (AD) diagnosis is based on the presence of protein aggregates found in the brain, including amyloid plaques and neurofibrillary tangles (NFTs), which are referred to as neurologic lesions (Hall and Roberson, 2012)

  • This study suggests that while the urge to urinate still exists in AD patients, lesions in the frontal cortex may be causing a loss of inhibitory signal to the bladder, which may drive Urinary incontinence (UI) (Lee et al, 2017)

Read more

Summary

INTRODUCTION

It is estimated that there are 35 million people living with dementia globally and by the year 2030, that number is predicted to double (Lee et al, 2017). Bladder dysfunction is the costliest lower urinary tract disorder and one of the top three negative effectors on quality-oflife, behind stroke and AD (Coyne et al, 2009) Both UI and dementia increases the likelihood of placement in a nursing home (Orme et al, 2015). As AD progresses, patients decline in both cognitive and physical abilities such as memory loss, changes in personality, confusion, and inability to complete daily tasks such as toileting (Jung et al, 2017) These progressing impairments caused by AD can lead to an increasing risk of UI as it is difficult to identify when or where to void and patients’ ability to access the toilet becomes difficult (Lee et al, 2017). The only treatments used for fecal incontinence is increased fiber intake, laxatives, enemas, and increasing quality of care to ensure a toilet schedule is followed (Leung and Rao, 2009)

DAMAGE TO MICTURITION CENTERS IN THE BRAIN
Reversibly binds to AChE and inhibits the hydrolysis of ACh
DISCUSSION
Findings
AUTHOR CONTRIBUTIONS
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call