scholarly journals Relationship between Persistent Dizziness and Markers of Alzheimer's disease – Mayo Clinic Study of Aging

Author(s):  
RAZAN AL FAKIR

Abstract Persistent dizziness or lightheadedness ranks among the most frequent complaints in primary care. Persistent dizziness is frequently described as a consequence or side effect of defined entities such as cardiovascular, infectious, neurological, and otological disease. Persistent dizziness is potentially disabling and has a distinct impact on participation, psychosocial interaction, and quality of life. We examined the relationship between persistent dizziness or lightheadedness and Alzheimer's disease (AD) markers among 924 individuals aged ≥50 years (52.3% male, mean age 74 years) selected from 5707 individuals who participated in the population-based Mayo Clinic Study of Aging in Olmsted County, Minnesota. Neuropsychiatric symptoms (depression and anxiety), cognitive evaluation (overall and across multiple domains), magnetic resonance imaging for AD-signature "regional thickness," and 11Carbon-Pittsburgh compound B positron emission tomography (11C-PiB PET) for Amyloid deposition are all investigated. Significant contributing factors to persistent dizziness in older adults were found and include [age, sex (male), lower education, high comorbidity index, high-density lipoprotein, balance problems, neuropsychiatric symptoms, cognitive impairments, and AD-signature” regional thickness]. After adjusting for age, sex, education, medical comorbidities, and other variables, a statistically significant association between persistent dizziness/lightheadedness and neuropsychiatric symptoms, and Amyloid-β deposition. This finding implies that the underlying AD biology may drive both the neuropsychiatric symptoms and persistent dizziness or lightheadedness, even before the onset of cognitive impairments and dementia. Further studies are needed to support the findings.

2006 ◽  
Vol 14 (7S_Part_22) ◽  
pp. P1156-P1156
Author(s):  
Danni Li ◽  
Clinton E. Hagen ◽  
David S. Knopman ◽  
Clifford R. Jack ◽  
Ronald C. Petersen ◽  
...  

2012 ◽  
Vol 43 (5) ◽  
pp. 911-920 ◽  
Author(s):  
I. H. G. B. Ramakers ◽  
F. R. J. Verhey ◽  
P. Scheltens ◽  
H. Hampel ◽  
H. Soininen ◽  
...  

BackgroundAnxiety, apathy and depression are common in subjects with mild cognitive impairment (MCI) and may herald Alzheimer's disease (AD). We investigated whether these symptoms correlated with cerebrospinal fluid (CSF) markers for AD in subjects with MCI.MethodSubjects with MCI (n=268) were selected from the ‘Development of screening guidelines and criteria for pre-dementia Alzheimer's disease’ (DESCRIPA) and Alzheimer's Disease Neuroimaging Initiative (ADNI) studies. We measured amyloid β(1-42)protein (Aβ42) and total tau (t-tau) in CSF. Neuropsychiatric symptoms were measured with the Neuropsychiatric Inventory.ResultsDepressive symptoms were reported by 55 subjects (21%), anxiety by 35 subjects (13%) and apathy by 49 subjects (18%). The presence of anxiety was associated with abnormal CSF Aβ42 [odds ratio (OR) 2.3, 95% confidence interval (CI) 1.6–3.3] and t-tau (OR 2.6, 95% CI 1.9–3.6) concentrations and with the combination of abnormal concentrations of both Aβ42 and t-tau (OR 3.1, 95% CI 2.0–4.7). The presence of agitation and irritability was associated with abnormal concentrations of Aβ42 (agitation: OR 1.6, 95% CI 1.1–2.3; irritability: OR 2.2, 95% CI 1.5–3.3). Symptoms of depression and apathy were not related to any of the CSF markers.ConclusionsIn subjects with MCI, symptoms of anxiety, agitation and irritability may reflect underlying AD pathology, whereas symptoms of depression and apathy do not.


RSC Advances ◽  
2019 ◽  
Vol 9 (64) ◽  
pp. 37127-37135
Author(s):  
Yao Bai ◽  
Lingling Chen ◽  
Yao Chen ◽  
Xinmeng Chen ◽  
Yilong Dong ◽  
...  

PGM ameliorates AD-like pathology and cognitive impairments by enhancing microglial amyloid-β clearance.


2020 ◽  
Author(s):  
Wei Xu ◽  
Chen-Chen Tan ◽  
Xi-Peng Cao ◽  
Jin-Tai Yu ◽  
Lan Tan

Abstract Background: Both progranulin (PGRN) and neuroinflammatory activities increased over the course of Alzheimer’s disease (AD). In this study, we set out to determine if cerebrospinal fluid (CSF) PGRN could be a marker of neuroinflammation, and if so, how it contributed to AD pathogenesis and cognitive impairments. Methods: A total of 965 participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) were grouped within the framework of A-T-N biomarker profile and clinical stage. Causal mediation analyses with 10,000 bootstrapped iterations were conducted to explore the mediation effects of neuroinflammatory markers on the associations of PGRN with amyloid burden indicated by CSF β-amyloid (Aβ) levels. The longitudinal influences of PGRN on cognition were tested. Results: Increases of CSF PGRN and multiple neuroinflammatory markers (sTNFR1, sTNFR2, TGF-β1, VCAM1, and ICAM1) were associated with tau-related neurodegeneration, but not with Aβ pathology. PGRN was positively linked with these neuroinflammatory markers only in the presence of tau pathologies (TN+). In TN+ profile, PGRN was associated with higher CSF Aβ42 via mediating neuroinflammatory markers and could also predict slower cognitive decline. The abovementioned associations became non-significant in TN- profile. Conclusions: PGRN could protect against Aβ pathology and cognitive impairments via modulating neuroinflammation that occurs with neuronal injuries.


Author(s):  
Pallavi Singh Chauhan ◽  
Meerambika Mishra ◽  
Bhupendra Koul ◽  
Mayank Sharma ◽  
Dhananjay Yadav

: Sleep disorders has been shown to increase the risk of dementia. This particular aspect may affect the cognition of the patient, leading to behavioral disorders, and depression. In early symptomatic Alzheimer’s disease (AD), default mode network (DMN) disruption occurs and progresses along with the course of the disease. This review mainly focuses on the leading causes of AD along with management of conditions like insomnia, obstructive sleep apnea, nighttime sleep duration, circadian rhythm disorder (CRD), neuroendocrine alternation and impaired sleep to prevent the use of drugs that can cause complications, especially falls or additional cognitive deficits. Moreover, this study highlights identification of molecular mechanisms like effect of impaired sleep on amyloid β (Aβ) and Tau dynamics, impaired proteostasis along with appropriate measures to treat few contributing factors lead to insomnia in AD or mild cognitive impairment (MCI).


2015 ◽  
Vol 40 (5-6) ◽  
pp. 268-275 ◽  
Author(s):  
Thais Bento Lima-Silva ◽  
Valéria Santoro Bahia ◽  
Viviane Amaral Carvalho ◽  
Henrique Cerqueira Guimarães ◽  
Paulo Caramelli ◽  
...  

Background/Aims: We aimed to compare caregiver burden and distress in behavioral-variant frontotemporal dementia (bvFTD) and Alzheimer's disease (AD) and to investigate which factors contribute to caregivers' burden and distress. Methods: Fifty patients and their caregivers were invited to participate. Among the patients, 20 had a diagnosis of bvFTD and 30 had AD. Caregivers and patients were statistically equivalent for age, sex, education and dementia severity according to Clinical Dementia Rating. The protocol included the Short Zarit Burden Inventory, the Neuropsychiatric Inventory (NPI), Disability Assessment for Dementia (DAD), the Cornell Scale for Depression in Dementia (CSDD), Addenbrooke's Cognitive Examination-Revised, the Executive Interview with 25 Items, Direct Assessment of Functional Status and the Geriatric Anxiety Inventory (GAI). Results: In the NPI, caregivers of bvFTD patients reported a higher presence and severity of neuropsychiatric symptoms and caregiver distress compared to caregivers of AD patients. There was no significant difference in the perceived burden. In bvFTD, DAD and GAI scores were significantly correlated with burden, whereas in AD, burden was correlated with CSDD and NPI scores. Psychiatric symptoms were associated with distress in both groups. Conclusions: Caregivers of bvFTD patients experienced higher levels of distress than caregivers of AD patients. Patients' functional limitations were associated with burden of caregivers of bvFTD patients, whereas neuropsychiatric symptoms were associated with caregiver strain in both groups.


2013 ◽  
Vol 9 ◽  
pp. P635-P635
Author(s):  
Prashanthi Vemuri ◽  
Timothy Lesnick ◽  
Scott Przybelski ◽  
David Knopman ◽  
Mary Machulda ◽  
...  

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Kok Pin Ng ◽  
Hui Chiew ◽  
Pedro Rosa-Neto ◽  
Nagaendran Kandiah ◽  
Zahinoor Ismail ◽  
...  

AbstractThe development of in vivo biomarkers of Alzheimer’s disease (AD) has advanced the diagnosis of AD from a clinical syndrome to a biological construct. The preclinical stage of AD continuum is defined by the identification of AD biomarkers crossing the pathological threshold in cognitively unimpaired individuals. While neuropsychiatric symptoms (NPS) are non-cognitive symptoms that are increasingly recognized as early manifestations of AD, the associations of NPS with AD pathophysiology in preclinical AD remain unclear. Here, we review the associations between NPS and AD biomarkers amyloid-β (Aβ), tau and neurodegeneration in preclinical AD and cognitively-unimpaired individuals in 19 eligible English-language publications (8 cross-sectional studies, 10 longitudinal, 1 both cross-sectional and longitudinal). The cross-sectional studies have consistently shown that NPS, particularly depressive and anxiety symptoms, are associated with higher Aβ. The longitudinal studies have suggested that greater NPS are associated with higher Aβ and cognitive decline in cognitively unimpaired subjects over time. However, most of the studies have either cross-sectionally or longitudinally shown no association between NPS and tau pathology. For the association of NPS and neurodegeneration, two studies have shown that the cerebrospinal fluid total-tau is linked to longitudinal increase in NPS and that the NPS may predict longitudinal metabolic decline in preclinical AD, respectively. However, evidence for the association between atrophy and NPS in preclinical AD is less consistent. Therefore, future longitudinal studies with well-designed methodologies and NPS measurements are required not only to determine the relationship among AT(N) biomarkers, NPS and cognitive decline, but also to elucidate the contribution of comorbid pathology to preclinical AD.


Diagnostics ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 237 ◽  
Author(s):  
Jung-Ju Lee ◽  
Youngki Choi ◽  
Soie Chung ◽  
Dae Hyun Yoon ◽  
Seung Ho Choi ◽  
...  

The increasing prevalence of Alzheimer’s disease (AD) has become a global phenomenon presenting serious social and health challenges. For detecting early molecular changes in the disease, several techniques to measure varied species of amyloid beta in the peripheral blood have been recently developed, but the efforts to associate them with cognitive assessments have yet to produce sufficient data. We prospectively collected participants from the consecutive population who visited our center for brain health screening. In total, 97 participants (F:M = 58:39) aged 69.4 ± 7.52 were assessed. Participants performed the Korean version of the Consortium to Establish a Registry for Alzheimer’s disease (CERAD-K), the clinical dementia rating (CDR), plasma oligomeric amyloid-β (OAβ) level tests, routine blood tests, ApoE genotype, and brain MRI. Among total population, 55.7% had a CDR of 0, and 40.2% had a CDR of 0.5. The results showed that word memory and word recall, and the total scores of the CERAD-K were negatively correlated with the plasma OAβ level. With a cut-off value of 0.78 ng/mL for the OAβ level and a −1.5 standard deviation of age/sex/education adjusted norms for the CERAD-K; naming, word memory, word recall, word recognition, and total score were significantly correlated with the OAβ level. No correlation between the OAβ level and mini-mental status examination was found. Our results demonstrate that the level of plasma OAβ was well correlated with the measure of cognitive function through the CERAD-K in the field data collected from consecutive populations. Studies on longitudinal comparisons with large cohorts will further validate the diagnostic value of plasma OAβ as a useful biomarker for screening AD and predicting progression.


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