scholarly journals Impact of coronary heart disease on cognitive decline in Alzheimer’s disease: a prospective longitudinal cohort study in primary care

2016 ◽  
Vol 67 (655) ◽  
pp. e111-e117 ◽  
Author(s):  
Markus Bleckwenn ◽  
Luca Kleineidam ◽  
Michael Wagner ◽  
Frank Jessen ◽  
Siegfried Weyerer ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Coronary Heart Disease ◽  
Cohort Study ◽  
Heart Disease ◽  
Cognitive Decline ◽  
Late Onset ◽  
Cardiovascular Prevention ◽  
Clinical Dementia Rating ◽  
Prospective Longitudinal

BackgroundArteriosclerotic disorders increase the risk of dementia. As they have common causes and risk factors, coronary heart disease (CHD) could influence the course of dementia.AimTo determine whether CHD increases the speed of cognitive decline in Alzheimer’s disease, and to discuss the potential for secondary cardiovascular prevention to modify this decline.Design and settingProspective multicentre cohort study in general practices in six cities in Germany.MethodParticipants were patients with probable mild-to-moderate Alzheimer’s dementia or mixed dementia (n = 118; mean age 85.6 [±3.4] years, range 80–96 years). The authors assessed the presence of CHD according to the family physicians’ diagnosis. Cognitive performance was measured during home visits for up to 3 years in intervals of 6 months, using Mini Mental State Examination (MMSE) and Clinical Dementia Rating Sum of Boxes (CDR-SoB). The authors also recorded whether patients died in the observation period.ResultsAt baseline, 65 patients (55%) had CHD and/or a heart condition following a myocardial infarction. The presence of CHD accelerated cognitive decline (MMSE, P<0.05) by about 66%, and reduced cognitive-functional ability (CDR-SoB, P<0.05) by about 83%, but had no impact on survival.ConclusionThe study shows that CHD has a significant influence on cognitive decline in older patients with late-onset dementia. The dementia process might therefore be positively influenced by cardiovascular prevention, and this possible effect should be further investigated.

Pharmacogenetics of Angiotensin-Converting Enzyme Inhibitors in Patients with Alzheimer's Disease Dementia

2018 ◽  
Vol 15 (4) ◽  
pp. 386-398 ◽  
Author(s):  
Fabricio Ferreira de Oliveira ◽  
Elizabeth Suchi Chen ◽  
Marilia Cardoso Smith ◽  
Paulo Henrique Ferreira Bertolucci
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Angiotensin Converting Enzyme ◽  
Cognitive Decline ◽  
Enzyme Inhibitors ◽  
Late Onset ◽  
Amyloid Β ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitors ◽  
Alzheimer’S Disease Dementia

Background: While the angiotensin-converting enzyme degrades amyloid-β, angiotensinconverting enzyme inhibitors (ACEis) may slow cognitive decline by way of cholinergic effects, by increasing brain substance P and boosting the activity of neprilysin, and by modulating glucose homeostasis and augmenting the secretion of adipokines to enhance insulin sensitivity in patients with Alzheimer’s disease dementia (AD). We aimed to investigate whether ACE gene polymorphisms rs1800764 and rs4291 are associated with cognitive and functional change in patients with AD, while also taking APOE haplotypes and anti-hypertensive treatment with ACEis into account for stratification. Methods: Consecutive late-onset AD patients were screened with cognitive tests, while their caregivers were queried for functional and caregiver burden scores. Prospective pharmacogenetic correlations were estimated for one year, considering APOE and ACE genotypes and haplotypes, and treatment with ACEis. Results: For 193 patients, minor allele frequencies were 0.497 for rs1800764 – C (44.6% heterozygotes) and 0.345 for rs4291 – T (38.9% heterozygotes), both in Hardy-Weinberg equilibrium. Almost 94% of all patients used cholinesterase inhibitors, while 155 (80.3%) had arterial hypertension, and 124 used ACEis. No functional impacts were found regarding any genotypes or pharmacological treatment. Either for carriers of ACE haplotypes that included rs1800764 – T and rs4291 – A, or for APOE4- carriers of rs1800764 – T or rs4291 – T, ACEis slowed cognitive decline independently of blood pressure variations. APOE4+ carriers were not responsive to treatment with ACEis. Conclusion: ACEis may slow cognitive decline for patients with AD, more remarkably for APOE4- carriers of specific ACE genotypes.

Smell identification test as a progression marker in Alzheimer's disease

2011 ◽  
Vol 26 (S2) ◽  
pp. 502-502
Author(s):  
L. Velayudhan ◽  
M. Pritchard ◽  
S. Lovestone
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Late Onset ◽  
Linear Regression Analysis ◽  
Rapid Progressors ◽  
Progression Marker ◽  
Identification Test ◽  
Smell Identification

IntroductionFactors influencing or predicting progression in Alzheimer's disease (AD) is not well understood. Olfactory dysfunction, impaired smell identification in particular, is known to occur in AD. Mesial temporal lobe, important for memory function is also critical for the processing of olfactory information. In view of the common anatomical substrate, we hypothesized that olfaction dysfunction worsens faster in people with AD with rapid cognitive decline compared to those with slower cognitive decline.AimsTo test whether smell identification test can be used as a predictor for illness progression in AD patients.MethodsForty one participants with late onset mild to moderate AD were recruited from mental health services for older adults. Subjects were classified as ‘Rapid Progressors’ defined on ‘a-priori’ with a loss of 2 or more points in Mini-Mental State Examination (MMSE) within six months. Assessments included MMSE, Neuropsychiatric Inventory, Bristol Activities of Daily Living, and the University of Pennsylvania Smell Identification Test (UPSIT), at baseline and after 3 months.ResultsTwenty subjects were ‘Rapid Progressors’, and had lower UPSIT scores compared to ‘Non-Rapid Progressors’ both at the baseline (p = 0.02) and at follow up after 3 months (p = 0.05). Baseline UPSIT correlated with follow up UPSIT (r = 0.5, p < 0.01) and MMSE (r = 0.4, p = 0.04). Also it was the baseline UPSIT score that best predicted (p < 0.05) the follow up smell and cognitive function on linear regression analysis.ConclusionsSmell identification function could be useful as a clinical measure to assess and predict progression in AD.

scholarly journals Comparison of cognitive decline between dementia with Lewy bodies and Alzheimer's disease: a cohort study

BMJ Open ◽  
2012 ◽  
Vol 2 (1) ◽  
pp. e000380 ◽  
Author(s):  
Zuzana Walker ◽  
Ian McKeith ◽  
Joanne Rodda ◽  
Tarik Qassem ◽  
Klaus Tatsch ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cohort Study ◽  
Cognitive Decline ◽  
Dementia With Lewy Bodies ◽  
Lewy Bodies

scholarly journals Predictors of rapid cognitive decline in Alzheimer's disease: results from the Australian Imaging, Biomarkers and Lifestyle (AIBL) study of ageing

2011 ◽  
Vol 24 (2) ◽  
pp. 197-204 ◽  
Author(s):  
Alessandro Sona ◽  
Ping Zhang ◽  
David Ames ◽  
Ashley I. Bush ◽  
Nicola T. Lautenschlager ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Rating Scale ◽  
Cognitive Status ◽  
Imaging Biomarkers ◽  
Clinical Dementia Rating ◽  
Factors Associated ◽  
Biological Variables ◽  
Rapid Cognitive Decline

ABSTRACTBackground: The AIBL study, which commenced in November 2006, is a two-center prospective study of a cohort of 1112 volunteers aged 60+. The cohort includes 211 patients meeting NINCDS-ADRDA criteria for Alzheimer's disease (AD) (180 probable and 31 possible). We aimed to identify factors associated with rapid cognitive decline over 18 months in this cohort of AD patients.Methods: We defined rapid cognitive decline as a drop of 6 points or more on the Mini-Mental State Examination (MMSE) between baseline and 18-month follow-up. Analyses were also conducted with a threshold of 4, 5, 7 and 8 points, as well as with and without subjects who had died or were too severely affected to be interviewed at 18 months and after, both including and excluding subjects whose AD diagnosis was “possible” AD. We sought correlations between rapid cognitive decline and demographic, clinical and biological variables.Results: Of the 211 AD patients recruited at baseline, we had available data for 156 (73.9%) patients at 18 months. Fifty-one patients were considered rapid cognitive decliners (32.7%). A higher Clinical Dementia Rating scale (CDR) and higher CDR “sum of boxes” score at baseline were the major predictors of rapid cognitive decline in this population. Furthermore, using logistic regression model analysis, patients treated with a cholinesterase inhibitor (CheI) had a higher risk of being rapid cognitive decliners, as did males and those of younger age.Conclusions: Almost one third of patients satisfying established research criteria for AD experienced rapid cognitive decline. Worse baseline functional and cognitive status and treatment with a CheI were the major factors associated with rapid cognitive decline over 18 months in this population.

scholarly journals Late Onset Alzheimer’s Disease Risk Variants in Cognitive Decline: The PATH Through Life Study

2017 ◽  
Vol 57 (2) ◽  
pp. 423-436 ◽  
Author(s):  
Shea J. Andrews ◽  
Debjani Das ◽  
Kaarin J. Anstey ◽  
Simon Easteal
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Disease Risk ◽  
Late Onset ◽  
Life Study ◽  
Risk Variants

Associations of Blood Pressure with Functional and Cognitive Changes in Patients with Alzheimer's Disease

2016 ◽  
Vol 41 (5-6) ◽  
pp. 314-323 ◽  
Author(s):  
Fabricio Ferreira de Oliveira ◽  
Elizabeth Suchi Chen ◽  
Marilia Cardoso Smith ◽  
Paulo Henrique Ferreira Bertolucci
Keyword(s):  
Alzheimer’S Disease ◽  
Blood Pressure ◽  
Alzheimer's Disease ◽  
Rating Scale ◽  
Late Onset ◽  
Angiotensin Receptor Blockers ◽  
Channel Blockers ◽  
Clinical Dementia Rating ◽  
Cognitive Changes ◽  
Converting Enzyme Inhibitors

Background: Midlife hypertension followed by late life hypotension resulting from neurodegeneration increases amyloidogenesis and tauopathy. Methods: Consecutive outpatients with late-onset Alzheimer's disease (AD) at various stages and their respective caregivers were assessed for score variations in 1 year of tests assessing caregiver burden, functionality and cognition according to blood pressure (BP) variations and APOE haplotypes, while also taking into account differential effects of angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, β-blockers, calcium channel blockers, diuretics, or no antihypertensive medication on score changes. The diagnosis and treatment of arterial hypertension followed the JNC 7 report. Results: Variations in systolic BP (-11.76 ± 17.1 mm Hg), diastolic BP (-4.92 ± 10.3 mm Hg) and pulse pressure (-6.84 ± 12.6 mm Hg) were significant after 1 year (n = 191; ρ < 0.01). For APOE4+ carriers, rises in systolic or diastolic BP improved Clinical Dementia Rating Scale Sum of Boxes scores (ρ < 0.04), with marginally significant improvements in Mini-Mental State Examination scores resulting from risen systolic (ρ = 0.069) or diastolic BP (ρ = 0.079), and in basic independence only regarding risen diastolic BP (ρ = 0.055). APOE4- carriers resisted any functional or cognitive effects of BP variations. No differences were found regarding any antihypertensive class for variations in BP or any test scores, regardless of APOE haplotypes. Conclusions: Targeting mild BP elevations brings better functional and cognitive results for APOE4+ carriers with AD.

scholarly journals DL-3-n-butylphthalide Delays Cognitive Decline in Patients With Mild to Moderate Alzheimer's Disease Already Receiving Donepezil: A Multicenter, Prospective Cohort Study

2020 ◽  
Author(s):  
Jin Wang ◽  
Xiaojuan Guo ◽  
Wenhui Lu ◽  
Jie Liu ◽  
Hong Zhang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Logistic Regression ◽  
Regression Analysis ◽  
Cohort Study ◽  
Activities Of Daily Living ◽  
Cognitive Decline ◽  
Prospective Cohort Study ◽  
Prospective Cohort ◽  
Daily Living

Abstract Background：Vascular factors and mitochondria dysfunction contributeto thepathogenesis of Alzheimer’s Disease (AD).DL-3-n-butylphthalide (NBP)has an effect in protecting mitochondria and improving microcirculation. We investigated the effect of NBP in patients with mild-moderate AD already receiving donepezil.Methods: It was a prospective cohort study. 92 mild-moderate AD patients were classified into the donepezil alone group (n=43) or the donepezil combined NBP group (n=49) for 48 weeks. The primary outcome was change of Alzheimer’s disease assessment scale-cognitive subscale (ADAS-cog) from baseline after treatment 48 weeks. All patients were also evaluated with clinician’s interview-based impression of change plus caregiver input (CIBIC-plus), Alzheimer's disease cooperative study-activities of daily living (ADCS-ADL) and neuropsychiatric inventory (NPI) every 12 weeks. All patients were monitored for adverse events (AEs). The efficacy was analyzed using logistic regression analysis.Results:The univariate analysis showed that age wasolder in donepezil alone group(P=0.005), prevalence of hypertension was higher in donepezil alone group(P=0.026).The ADAS-cog score change from baseline in thedonepezil alone group was significant than that in the donepezil combined NBP group at 48 weeks(1.82±5.20 vs -0.38±4.46, P=0.048). The multivariate logistic regression analysis showed that between the 2 groups, there were significant differencesin changes on the ADAS-cog(OR=0.879,95% CI:[0.785,0.984],P=0.026),MMSE(OR=1.270,95% CI:[1.036,1.557],P=0.021), and ADCS-ADL(OR=1.067,95% CI:[1.002,1.136],P=0.042) but no significant differences for changes on the NPI(OR=0.955,95% CI:[0.901，1.013],P=0.125)and CIBIC-plus (OR=0.356,95% CI:[0.093,1.364],P=0.132). The occurrence of AEs was similar in the 2 groups.Conclusions:Over the 48-week treatment period, donepezil combined NBP group had slower cognitive decline and better activities of daily living in patients with mild to moderate AD. These indicated that the multi-target therapeutic effect of NBP may be a new choice for AD treatment.Trial registration:Clinical trial registration URL:https://clinicaltrials.gov/ct2/show/NCT02711683?term=NCT02711683&draw=2&rank=1ClinicalTrials.gov Identifier: NCT02711683. Date of registration: March 14,2016.

scholarly journals Benfotiamine and Cognitive Decline in Alzheimer’s Disease: Results of a Randomized Placebo-Controlled Phase IIa Clinical Trial

2020 ◽  
Vol 78 (3) ◽  
pp. 989-1010
Author(s):  
Gary E. Gibson ◽  
José A. Luchsinger ◽  
Rosanna Cirio ◽  
Huanlian Chen ◽  
Jessica Franchino-Elder ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Placebo Group ◽  
Cognitive Decline ◽  
Controlled Trial ◽  
Amyloid Β ◽  
Cognitive Outcomes ◽  
Disease Assessment ◽  
Clinical Dementia Rating ◽  
Positron Emission

Background: In preclinical models, benfotiamine efficiently ameliorates the clinical and biological pathologies that define Alzheimer’s disease (AD) including impaired cognition, amyloid-β plaques, neurofibrillary tangles, diminished glucose metabolism, oxidative stress, increased advanced glycation end products (AGE), and inflammation. Objective: To collect preliminary data on feasibility, safety, and efficacy in individuals with amnestic mild cognitive impairment (aMCI) or mild dementia due to AD in a placebo-controlled trial of benfotiamine. Methods: A twelve-month treatment with benfotiamine tested whether clinical decline would be delayed in the benfotiamine group compared to the placebo group. The primary clinical outcome was the Alzheimer’s Disease Assessment Scale-Cognitive Subscale (ADAS-Cog). Secondary outcomes were the clinical dementia rating (CDR) score and fluorodeoxyglucose (FDG) uptake, measured with brain positron emission tomography (PET). Blood AGE were examined as an exploratory outcome. Results: Participants were treated with benfotiamine (34) or placebo (36). Benfotiamine treatment was safe. The increase in ADAS-Cog was 43% lower in the benfotiamine group than in the placebo group, indicating less cognitive decline, and this effect was nearly statistically significant (p = 0.125). Worsening in CDR was 77% lower (p = 0.034) in the benfotiamine group compared to the placebo group, and this effect was stronger in the APOE ɛ4 non-carriers. Benfotiamine significantly reduced increases in AGE (p = 0.044), and this effect was stronger in the APOE ɛ4 non-carriers. Exploratory analysis derivation of an FDG PET pattern score showed a treatment effect at one year (p = 0.002). Conclusion: Oral benfotiamine is safe and potentially efficacious in improving cognitive outcomes among persons with MCI and mild AD.

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