scholarly journals The “Counseling+” Roles of the Speech-Language Pathologist Serving Older Adults With Mild Cognitive Impairment and Dementia From Alzheimer's Disease

2021 ◽  
pp. 1-16
Author(s):  
Alyssa M. Lanzi ◽  
James M. Ellison ◽  
Matthew L. Cohen
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Health Care Professionals ◽  
Systematic Research ◽  
Complex Nature ◽  
Cognitive Screening ◽  
Speech Language Pathologist ◽  
Age Related

Purpose Persons with dementia and mild cognitive impairment (MCI) are major consumers of services provided by speech-language pathologists (SLPs). These services include not only direct assessment and treatment of communication and swallowing but also counseling, collaboration, prevention, and wellness. These “counseling+” activities can be especially challenging for SLPs to deliver because of the lack of evidence, as well as the complex nature of Alzheimer's disease (AD) and other conditions that cause MCI and dementia. Method This tutorial is written by a speech-language pathologist, a neuropsychologist, and a geriatric psychiatrist to provide education, resources, and recommendations for SLPs delivering counseling+ activities to patients with MCI and dementia from AD and related disorders. Results and Conclusions We describe counseling+ activities across the continuum of care ranging from educating and conducting cognitive screenings with adults experiencing age-related cognitive decline to supporting end-of-life wishes. Because of their expertise in communication, SLPs can provide an array of important leading and supporting services to patients, their family, and other health care professionals on the care team, such as providing patients with appropriate feedback following a cognitive screening and helping caregivers identify the communicative intent of a responsive behavior. The demand for SLP services for patients with MCI and dementia will grow significantly over the next few decades, necessitating more systematic research and clinical evidence in this area.

scholarly journals Physician Perceptions about the Barriers to Prompt Diagnosis of Mild Cognitive Impairment and Alzheimer’s Disease

2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Davneet Judge ◽  
Jenna Roberts ◽  
Rezaul Khandker ◽  
Baishali Ambegaonkar ◽  
Christopher M. Black
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Primary Care Physicians ◽  
Online Survey ◽  
Waiting Lists ◽  
Financial Strain ◽  
Age Related ◽  
Prompt Diagnosis

Prior studies have identified numerous barriers to the prompt diagnosis of patients with suspected Alzheimer’s disease (AD). The aim of the study was to evaluate physician’s perceptions of the importance of previously identified barriers to diagnosis, but with a specific focus on the presentation of mild cognitive impairment (MCI), which may be indicative of neurodegenerative disorders such as AD. A second aim was to evaluate how the perspective of primary care physicians (PCPs) may differ from that of specialists. A cross-sectional online survey of PCPs and specialists who routinely manage patients with complaints of age-related cognitive impairment was conducted. Participants were asked to identify barriers to prompt diagnosis from prespecified lists of known diagnostic challenges categorized into 4 domains: patient-related, physician-related, setting-related, and those relating to the clinical profile of AD. Physicians report a range of barriers when attempting to diagnose MCI and AD. Major themes included patients seeing cognitive decline as a normal part of aging and not disclosing symptoms, long waiting lists, and a lack of treatment options and definitive biomarker tests. Generally, PCPs and specialists showed broad agreement; however, PCPs were more likely to identify burdens on the healthcare system, such as long waiting lists and inadequate time to evaluate patients. Substantial barriers continue to hinder early diagnosis of MCI and AD. There are numerous areas where improvements might be made but the implementation of potential interventions will likely be associated with financial strain for many healthcare systems.

Association of Androgens and Gonadotropins with Amnestic Mild Cognitive Impairment and Probable Alzheimer’s Disease in Chinese Elderly Men

2020 ◽  
Vol 78 (1) ◽  
pp. 277-290
Author(s):  
Yan Li ◽  
Sha Li ◽  
Shunjiang Xu ◽  
Hong Yu ◽  
Longmei Tang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Area Under The Curve ◽  
Amnestic Mild Cognitive Impairment ◽  
Elderly Men ◽  
Age Related ◽  
Potential Biomarker ◽  
Amci Group

Background: Age-related hormone changes play important roles in cognitive decline in older men, and apolipoprotein E ɛ4 (APOE ɛ4) is a risk factor for Alzheimer’s disease (AD). Objective: This study aimed to investigate the interactive role of androgen decline and APOE ɛ4 genotype in the pathogenesis of amnestic mild cognitive impairment (aMCI) and AD. Methods: In total, 576 elderly men over 65 years old from communities in Shijiazhuang were enrolled in this study, including 243 with normal cognition (NC), 271 with aMCI, and 62 with probable AD. Cognitive function was evaluated with a battery of neuropsychological tests. The serum levels of androgen and gonadotropin were detected by ELISA and chemiluminescence immunoassay. Results: The levels of free testosterone (FT) and dihydrotestosterone (DHT) were lower in the aMCI group (p < 0.05), and even lower in the AD group (p < 0.001), but the levels of follicle stimulating hormone (FSH) and luteinizing hormone (LH) were higher in AD group (p < 0.01), comparing with that in NC or aMCI group. The interaction of lower FT or DHT levels with APOE ɛ4 had a risk role in global cognitive impairment (p < 0.05). The area under the curve (AUC) of the ROC curve for predicting aMCI by serum FT levels was 0.745. Conclusion: These results indicated that the interaction of androgen decline and APOE ɛ4 genotype play a role in aMCI and AD. Serum FT levels have a predictive value for aMCI and might be a potential biomarker for prodromal AD.

scholarly journals The Role of Lysosomes in a Broad Disease-Modifying Approach Evaluated across Transgenic Mouse Models of Alzheimer’s Disease and Parkinson’s Disease and Models of Mild Cognitive Impairment

2019 ◽  
Vol 20 (18) ◽  
pp. 4432 ◽  
Author(s):  
Jeannie Hwang ◽  
Candice M. Estick ◽  
Uzoma S. Ikonne ◽  
David Butler ◽  
Morgan C. Pait ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Amyloid Β ◽  
Age Related ◽  
Disease Modifying

Many neurodegenerative disorders have lysosomal impediments, and the list of proposed treatments targeting lysosomes is growing. We investigated the role of lysosomes in Alzheimer’s disease (AD) and other age-related disorders, as well as in a strategy to compensate for lysosomal disturbances. Comprehensive immunostaining was used to analyze brains from wild-type mice vs. amyloid precursor protein/presenilin-1 (APP/PS1) mice that express mutant proteins linked to familial AD. Also, lysosomal modulation was evaluated for inducing synaptic and behavioral improvements in transgenic models of AD and Parkinson’s disease, and in models of mild cognitive impairment (MCI). Amyloid plaques were surrounded by swollen organelles positive for the lysosome-associated membrane protein 1 (LAMP1) in the APP/PS1 cortex and hippocampus, regions with robust synaptic deterioration. Within neurons, lysosomes contain the amyloid β 42 (Aβ42) degradation product Aβ38, and this indicator of Aβ42 detoxification was augmented by Z-Phe-Ala-diazomethylketone (PADK; also known as ZFAD) as it enhanced the lysosomal hydrolase cathepsin B (CatB). PADK promoted Aβ42 colocalization with CatB in lysosomes that formed clusters in neurons, while reducing Aβ deposits as well. PADK also reduced amyloidogenic peptides and α-synuclein in correspondence with restored synaptic markers, and both synaptic and cognitive measures were improved in the APP/PS1 and MCI models. These findings indicate that lysosomal perturbation contributes to synaptic and cognitive decay, whereas safely enhancing protein clearance through modulated CatB ameliorates the compromised synapses and cognition, thus supporting early CatB upregulation as a disease-modifying therapy that may also slow the MCI to dementia continuum.

scholarly journals Cognitive trajectory in mild cognitive impairment due to primary age-related tauopathy

Brain ◽  
2020 ◽  
Vol 143 (2) ◽  
pp. 611-621 ◽  
Author(s):  
Merilee Teylan ◽  
Charles Mock ◽  
Kathryn Gauthreaux ◽  
Yen-Chi Chen ◽  
Kwun C G Chan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cognitive Decline ◽  
Carrier Status ◽  
Neuritic Plaques ◽  
Rates Of Change ◽  
Age Related ◽  
History Of

Abstract Primary age-related tauopathy is increasingly recognized as a separate neuropathological entity different from Alzheimer’s disease. Both share the neuropathological features of tau aggregates and neuronal loss in the temporal lobe, but primary age-related tauopathy lacks the requisite amyloid plaques central to Alzheimer’s disease. While both have similar clinical presentations, individuals with symptomatic primary age-related tauopathy are commonly of more advanced ages with milder cognitive dysfunction. Direct comparison of the neuropsychological trajectories of primary age-related tauopathy and Alzheimer’s disease has not been thoroughly evaluated and thus, our objective was to determine how cognitive decline differs longitudinally between these two conditions after the onset of clinical symptoms. Data were obtained from the National Alzheimer’s Coordinating Center on participants with mild cognitive impairment at baseline and either no neuritic plaques (i.e. primary age-related tauopathy) or moderate to frequent neuritic plaques (i.e. Alzheimer neuropathological change) at subsequent autopsy. For patients with Alzheimer’s disease and primary age-related tauopathy, we compared rates of decline in the sum of boxes score from the CDR® Dementia Staging Instrument and in five cognitive domains (episodic memory, attention/working memory, executive function, language/semantic memory, and global composite) using z-scores for neuropsychological tests that were calculated based on scores for participants with normal cognition. The differences in rates of change were tested using linear mixed-effects models accounting for clinical centre clustering and repeated measures by individual. Models were adjusted for sex, age, education, baseline test score, Braak stage, apolipoprotein ε4 (APOE ε4) carrier status, family history of cognitive impairment, and history of stroke, hypertension, or diabetes. We identified 578 participants with a global CDR of 0.5 (i.e. mild cognitive impairment) at baseline, 126 with primary age-related tauopathy and 452 with Alzheimer’s disease. Examining the difference in rates of change in CDR sum of boxes and in all domain scores, participants with Alzheimer’s disease had a significantly steeper decline after becoming clinically symptomatic than those with primary age-related tauopathy. This remained true after adjusting for covariates. The results of this analysis corroborate previous studies showing that primary age-related tauopathy has slower cognitive decline than Alzheimer’s disease across multiple neuropsychological domains, thus adding to the understanding of the neuropsychological burden in primary age-related tauopathy. The study provides further evidence to support the hypothesis that primary age-related tauopathy has distinct neuropathological and clinical features compared to Alzheimer’s disease.

scholarly journals Deterioration, Compensation and Motor Control Processes in Healthy Aging, Mild Cognitive Impairment and Alzheimer’s Disease

Geriatrics ◽  
2021 ◽  
Vol 6 (1) ◽  
pp. 33
Author(s):  
Gabriel Poirier ◽  
Alice Ohayon ◽  
Adrien Juranville ◽  
France Mourey ◽  
Jeremie Gaveau
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Motor Control ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Motor Function ◽  
Healthy Aging ◽  
Control Processes ◽  
Age Related ◽  
Compensation Mechanisms

Aging is associated with modifications of several brain structures and functions. These modifications then manifest as modified behaviors. It has been proposed that some brain function modifications may compensate for some other deteriorated ones, thus maintaining behavioral performance. Through the concept of compensation versus deterioration, this article reviews the literature on motor function in healthy and pathological aging. We first highlight mechanistic studies that used paradigms, allowing us to identify precise compensation mechanisms in healthy aging. Subsequently, we review studies investigating motor function in two often-associated neurological conditions, i.e., mild cognitive impairment and Alzheimer’s disease. We point out the need to expand the knowledge gained from descriptive studies with studies targeting specific motor control processes. Teasing apart deteriorated versus compensating processes represents precious knowledge that could significantly improve the prevention and rehabilitation of age-related loss of mobility.

Mild Cognitive Impairment: Can We Reliably Detect Alzheimer's Disease Before the Dementia Begins?

2004 ◽  
Vol 10 (6) ◽  
pp. 924-925
Author(s):  
Feggy Ostrosky-Solis
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
New York ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Natural Consequence ◽  
Independent Function ◽  
Oxford University ◽  
Age Related

Mild Cognitive Impairment Aging to Alzheimer's Disease. R.C. Petersen (Ed.), 2003, New York: Oxford University Press. 269 pp., $55.00.People are living longer and along with this phenomenon emerges the concern about the quality of life as the person ages. While dementia is by no means a natural consequence of aging, both its incidence and prevalence increase dramatically with age, from 0.5 percent per year at the age of 65 years to nearly 8%/year after the age of 85 years (Evans et al. 1989). Alzheimer's disease (AD) is the most common cause of dementia. Although the goals of treatment in patients with AD have been to improve or, at least, to slow the deterioration of memory and cognition and to maintain independent function, research is moving from controlling symptoms to early identification and prevention of age-related cognitive disabilities.

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