Vascular risk factor detection and control may prevent Alzheimer's disease

2010 ◽  
Vol 9 (3) ◽  
pp. 218-225 ◽  
Author(s):  
Jack C. de la Torre
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Vascular Risk Factor ◽  
Vascular Risk ◽  
And Control

scholarly journals Vascular risk burden is a key player in the early progression of Alzheimer's disease

2021 ◽  
Author(s):  
João Pedro Ferrari-Souza ◽  
Wagner S. Brum ◽  
Lucas A. Hauschild ◽  
Lucas U. Da Ros ◽  
Pâmela C. L. Ferreira ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Cognitive Decline ◽  
Vascular Risk Factor ◽  
Vascular Risk Factors ◽  
Vascular Risk ◽  
Preclinical Alzheimer’S Disease ◽  
Risk Factor Burden

Understanding whether vascular risk factors synergistically potentiate Alzheimer's disease progression is important in the context of emerging treatments for preclinical Alzheimer's disease. The existence of a synergistic relationship could suggest that the combination of therapies targeting Alzheimer's disease pathophysiology and vascular risk factors might potentiate treatment outcomes. In the present retrospective cohort study, we tested whether vascular risk factor burden interacts with Alzheimer's disease pathophysiology to accelerate neurodegeneration and cognitive decline in cognitively unimpaired subjects. We evaluated 503 cognitively unimpaired participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) study. Baseline vascular risk factor burden was calculated considering the history of cardiovascular disease, hypertension, diabetes mellitus, hyperlipidemia, stroke or transient ischemic attack, smoking, atrial fibrillation, and left ventricular hypertrophy. Alzheimer's disease pathophysiology was evaluated using cerebrospinal fluid (CSF) amyloid-β1-42 (Aβ1-42) reflecting brain amyloidosis (A) and tau phosphorylated at threonine 181 (p-tau181) reflecting brain tau pathology (T). Individuals were dichotomized as having an elevated vascular risk factor burden (V+ if having two or more vascular risk factors) and as presenting preclinical Alzheimer's disease [(AT)+ if having abnormal CSF p-tau181 and Aβ1-42 levels]. Neurodegeneration was assessed with plasma neurofilament light (NfL) and global cognition with the modified version of the Preclinical Alzheimer's Cognitive Composite. Linear mixed-effects models revealed that an elevated vascular risk factor burden synergistically interacted with Alzheimer's disease pathophysiology to drive longitudinal increases in plasma NfL levels (β = 5.08, P = 0.016) and cognitive decline (β = -0.43, P = 0.020). Additionally, we observed that vascular risk factor burden was not associated with CSF Aβ1-42 or p-tau181 changes over time. Survival analysis demonstrated that individuals with preclinical Alzheimer's disease and elevated vascular risk factor burden [(AT)+V+] had a significantly greater risk of clinical progression to cognitive impairment (adjusted Hazard Ratio = 3.5, P < 0.001). Our results support the notion that vascular risk factor burden and Alzheimer's disease pathophysiology are independent processes; however, they synergistically lead to neurodegeneration and cognitive decline. These findings can help in providing the blueprints for the combination of vascular risk factor management and Alzheimer's disease pathophysiology treatment in preclinical stages. Moreover, we observed plasma NfL as a robust marker of disease progression that may be used to track therapeutic response in future trials.

scholarly journals Interactions between sleep disturbances and Alzheimer’s disease on brain function: a preliminary study combining the static and dynamic functional MRI

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Kaicheng Li ◽  
Xiao Luo ◽  
Qingze Zeng ◽  
Yerfan Jiaerken ◽  
Shuyue Wang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Sleep Disturbance ◽  
Brain Function ◽  
Sleep Disturbances ◽  
Brain Activity ◽  
Vascular Risk Factor ◽  
Underlying Mechanism ◽  
Amyloid Pet

AbstractThough sleep disturbance constitutes the risk factor for Alzheimer’s disease (AD), the underlying mechanism is still unclear. This study aims to explore the interaction between sleep disturbances and AD on brain function. We included 192 normal controls, 111 mild cognitive impairment (MCI), and 30 AD patients, with either poor or normal sleep (PS, NS, respectively). To explore the strength and stability of brain activity, we used static amplitude of low-frequency fluctuation (sALFF) and dynamic ALFF (dALFF) variance. Further, we examined white matter hyperintensities (WMH) and amyloid PET deposition, representing the vascular risk factor and AD-related hallmark, respectively. We observed that sleep disturbance significantly interacted with disease severity, exposing distinct effects on sALFF and dALFF variance. Interestingly, PS groups showed the dALFF variance trajectory of initially increased, then decreased and finally increased along the AD spectrum, while showing the opposite trajectory of sALFF. Further correlation analysis showed that the WMH burden correlates with dALFF variance in PS groups. Conclusively, our study suggested that sleep disturbance interacts with AD severity, expressing as effects of compensatory in MCI and de-compensatory in AD, respectively. Further, vascular impairment might act as important pathogenesis underlying the interaction effect between sleep and AD.

scholarly journals Trends in Vascular Risk Factor Treatment and Control in US Stroke Survivors

2013 ◽  
Vol 6 (3) ◽  
pp. 270-277 ◽  
Author(s):  
Nilay S. Shah ◽  
Mark D. Huffman ◽  
Hongyan Ning ◽  
Donald M. Lloyd-Jones
Keyword(s):  
Risk Factor ◽  
Vascular Risk Factor ◽  
Stroke Survivors ◽  
Vascular Risk ◽  
And Control

scholarly journals Prior Intra-operative Hypotension is not a Risk Factor for Development of Alzheimer’s Disease

1996 ◽  
Vol 23 (1) ◽  
pp. 57-58
Author(s):  
N.I. Bohnen ◽  
E.F.M. Wijdicks ◽  
E. Kokmen ◽  
M.A. Warner ◽  
L.T. Kurland
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Population Based ◽  
Control Group ◽  
Increased Risk ◽  
And Gender ◽  
And Control ◽  
Incident Cases ◽  
Control Study

ABSTRACT:Objective:A retrospective, population-based, case-control study was carried out to evaluate episodes of prior intra-operative hypotension as a potential risk factor for Alzheimer’s disease (AD).Methods:Patients were all incident cases of AD from 1975–1984 who resided for 40 years or more in Olmsted County prior to their onset of dementia (N = 252). One age and gender-matched control for each case was selected from all registrations for care at Mayo Clinic during the year of onset in the incident case. Each case and control group had 252 individuals.Results:Of these, 27 cases and 32 controls had at least one ten minute or longer episode of intra-operative hypotension of a systolic blood pressure of less than 90 mm Hg prior to the year of onset of dementia in the matched AD patient. We did not find a significantly increased risk of AD for hypotensive episodes of less than 75 or 90 mm Hg.Conclusions:It is unlikely that intra-operative hypotensive events of this degree increase the risk of AD.

scholarly journals GENETIC VARIANTS RELATED TO LIPID METABOLISM AS A RISK FACTOR TO LATE-ONSET ALZHEIMER’S DISEASE

2017 ◽  
pp. 1-5
Author(s):  
M.A.S. Pinhel ◽  
A.M. Crestani ◽  
G.F. Sousa-Amorim ◽  
M.L. Gregório ◽  
J.C. Cação ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Genetic Variants ◽  
Cholesterol Metabolism ◽  
Late Onset ◽  
Control Group ◽  
Chi Square ◽  
Genotypic Combination ◽  
And Control

Background: Genetic polymorphisms in genes regulating cholesterol metabolism have been suggested to risk factor of developing Alzheimer’s disease (AD). Objective: to analyze the frequency of polymorphisms apolipoprotein E (APOE-HhaI) and adenosine triphosphate binding cassette transporter 1 (ABCA1-StyI) in patients with late-onset AD. Design: case-control study. Participants: We studied 166 subjects (≥65 years old): Study Group (SG)- 88 patients and Control Group (CG)- 88 without dementia. Setting: The polymorphisms were determined using the polymorphism chain reaction and restriction fragment length polymorphism (PCR-RFLP) methods. It was applied Fisher's exact/chi-square tests (P<0.05). Results: Genotypes with APOE*4 prevailed in SG. The genotypic combination between APOE-HhaI and ABCA1-StyI polymorphisms showed a prevalence of heterozygous genotypes of risk for AD. Conclusion: Although genetic variants for ABCA1-StyI alone does not differentiate patients and controls, the G allele in synergy with APOE*4 allele is highlighted in patients suggesting the influence of ABCA1 in the disease.

SPECIFIC PROPERTIES OF TUBULIN IN THE PREFRONTAL CORTEX IN CONTROL, SCHIZOPHRENIA AND VASCULAR DEMENTIA

2020 ◽  
pp. 65-71
Author(s):  
Burbaeva G.Sh. ◽  
Androsova L.V. ◽  
Vorobyeva E.A. ◽  
Savushkina O.K.
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Prefrontal Cortex ◽  
Vascular Dementia ◽  
Binding Activity ◽  
Nephelometric Method ◽  
Rate Of Polymerization ◽  
Mental Diseases ◽  
And Control ◽  
The Brain

The aim of the study was to evaluate the rate of polymerization of tubulin into microtubules and determine the level of colchicine binding (colchicine-binding activity of tubulin) in the prefrontal cortex in schizophrenia, vascular dementia (VD) and control. Colchicine-binding activity of tubulin was determined by Sherlinе in tubulin-enriched extracts of proteins from the samples. Measurement of light scattering during the polymerization of the tubulin was carried out using the nephelometric method at a wavelength of 450-550 nm. There was a significant decrease in colchicine-binding activity and the rate of tubulin polymerization in the prefrontal cortex in both diseases, and in VD to a greater extent than in schizophrenia. The obtained results suggest that not only in Alzheimer's disease, but also in other mental diseases such as schizophrenia and VD, there is a decrease in the level of tubulin in the prefrontal cortex of the brain, although to a lesser extent than in Alzheimer's disease, and consequently the amount of microtubules.

Repurposing Antihypertensive Drugs for the Management of Alzheimer’s Disease

2020 ◽  
Vol 27 ◽  
Author(s):  
Keng Yoon Yeong ◽  
Christine Law
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Literature Review ◽  
Neurodegenerative Disorder ◽  
Antihypertensive Drugs ◽  
Future Prospects ◽  
Short Term

Alzheimer’s disease (AD) is a neurodegenerative disorder that has affected millions of people worldwide. However, currently there is no treatment to cure the disease. The AD drugs available in the market only manage the disease symptomatically and the effects are usually short-term. Thus, there is a need to look at alternatives AD therapies. Mid-life hypertension has not only been recognised as a risk factor for AD, but its relation with AD has also been well established. Thus, antihypertensives are postulated to be beneficial in managing AD. This literature review aims to shed some light on the potential of repurposing antihypertensives to treat AD, considering recent updates. Four classes of antihypertensives, as well as their potential limitations and future prospects in being utilised as AD therapeutics are discussed in this review.

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