scholarly journals Action of anti-TNF-α drugs on the progression of Alzheimer's disease: A case report

2015 ◽  
Vol 9 (2) ◽  
pp. 196-200 ◽  
Author(s):  
Carlos Henrique Ferreira Camargo ◽  
Filipe Fernandes Justus ◽  
Giuliano Retzlaff ◽  
Marcelo Rezende Young Blood ◽  
Marcelo Derbli Schafranski
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Drug Class ◽  
Cognitive Response ◽  
Cognitive Improvement ◽  
Tnf Α ◽  
Patient Reported ◽  
Previously Treated ◽  
The Subject

The aim of this study was to describe a clinical case of a patient with Alzheimer's disease (AD) in use of an anti-TNF-α agent for rheumatoid arthritis (RA). The patient reported is an 81-year-old Caucasian man and retired teacher, diagnosed with RA in 2008 and AD in 2011. Treatment with donepezil was started in 2011 and the use of etanercept introduced in 2012. He was previously treated with adalimumab in 2010 for 18 months. In 2013, the subject was engaged in a clinical trial to assess a complementary non-pharmacological approach for AD, presenting significant cognitive improvement during the follow-up period. We propose the hypothesis of a synergistic effect of anti-TNF-α medication used for the treatment of RA as the cause of the improvement in cognitive response observed. These findings could suggest a possible use of this drug class in the therapeutic management of AD.

scholarly journals Effect of a Cognitive Training Program on the Platelet APP Ratio in Patients with Alzheimer’s Disease

2020 ◽  
Vol 21 (14) ◽  
pp. 5110
Author(s):  
Tiziana Casoli ◽  
Cinzia Giuli ◽  
Marta Balietti ◽  
Paolo Fabbietti ◽  
Fiorenzo Conti
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Synaptic Plasticity ◽  
Cognitive Training ◽  
Control Group ◽  
Word Fluency ◽  
Clinical Dementia Rating ◽  
Cognitive Improvement ◽  
App Ratio

In patients with Alzheimer’s disease (AD), synaptic plasticity seems to be involved in cognitive improvement induced by cognitive training. The platelet amyloid precursor protein (APP) ratio (APPr), i.e., the ratio between two APP isoforms, may be a useful peripheral biomarker to investigate synaptic plasticity pathways. This study evaluates the changes in neuropsychological/cognitive performance and APPr induced by cognitive training in AD patients participating in the “My Mind Project”. Neuropsychological/cognitive variables and APPr were evaluated in the trained group (n = 28) before a two-month experimental protocol, immediately after its termination at follow-up 1 (FU1), after 6 months at follow-up 2 (FU2), and after 24 months at follow-up 3 (FU3). The control group (n = 31) received general psychoeducational training for two months. Some memory and attention parameters were significantly improved in trained vs. control patients at FU1 and FU2 compared to baseline (Δ values). At FU3, APPr and Mini Mental State Examination (MMSE) scores decreased in trained patients. Δ APPr correlated significantly with the Δ scores of (i) MMSE at FU1, (ii) the prose memory test at FU2, and (iii) Instrumental Activities of Daily Living (IADL), the semantic word fluency test, Clinical Dementia Rating (CDR), and the attentive matrices test at FU3. Our data demonstrate that the platelet APPr correlates with key clinical variables, thereby proving that it may be a reliable biomarker of brain function in AD patients.

Exercise-Mediated Alteration of miR-192-5p Is Associated with Cognitive Improvement in Alzheimer’s Disease

2021 ◽  
pp. 1-8
Author(s):  
Zhaomei Qin ◽  
Xingjun Han ◽  
Jing Ran ◽  
Shanshan Guo ◽  
Lina Lv
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Physical Exercise ◽  
Protective Effect ◽  
Exercise Intervention ◽  
Neuroprotective Effect ◽  
Voluntary Exercise ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cognitive Improvement ◽  
Tnf Α

<b><i>Introduction:</i></b> Physical exercise is an important component of managing Alzheimer’s disease (AD). miRNAs can be modulated by exercise intervention. <b><i>Objective:</i></b> The study explored the involvement and potential mechanism of miR-192-5p in the protective effect of physical exercise on AD. <b><i>Methods:</i></b> Ninety AD patients were enrolled, in which 45 cases accepted cycling training for continuous 3 months. The expression changes of miR-192-5p before and after exercise were analyzed by reverse transcription-quantitative PCR. 8-month-old APP/PS1 double Tg mice were used as the AD animal model. Mice in the voluntary exercise (VE) group received VE for 4 weeks. Morris water maze (MWM) test was used to evaluate the learning and memory function. Enzyme-linked immunosorbent assay was used to calculate the level of IL-1β, IL-6, and TNF-α. <b><i>Results:</i></b> AD patients showed elevated MMSE scores, decreased ADAS-cog and NPI-Q scores after 3 months of exercise. miR-192-5p was downregulated in the serum of AD patients and correlated with the levels of MMSE score, ADAS-cog, and NPI-Q score. A positive association was detected between serum miR-192-5p with TNF-α, IL-6, and IL-1β levels. MiR-192-5p is downregulated in the hippocampus tissues of mice after VE. Overexpression of miR-192-5p reversed the neuroprotective effect of exercise on AD in mice and promoted the inflammatory response of AD mice. <b><i>Conclusion:</i></b> MiR-192-5p can be modulated by the exercise intervention and involved in the protective effect of exercise on AD.

Longitudinal Changes in Individual BrainAGE in Healthy Aging, Mild Cognitive Impairment, and Alzheimer’s Disease

GeroPsych ◽  
2012 ◽  
Vol 25 (4) ◽  
pp. 235-245 ◽  
Author(s):  
Katja Franke ◽  
Christian Gaser
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Healthy Aging ◽  
Brain Aging ◽  
Elderly Subjects ◽  
Additional Increase ◽  
Longitudinal Changes ◽  
Novel Method ◽  
The Brain

We recently proposed a novel method that aggregates the multidimensional aging pattern across the brain to a single value. This method proved to provide stable and reliable estimates of brain aging – even across different scanners. While investigating longitudinal changes in BrainAGE in about 400 elderly subjects, we discovered that patients with Alzheimer’s disease and subjects who had converted to AD within 3 years showed accelerated brain atrophy by +6 years at baseline. An additional increase in BrainAGE accumulated to a score of about +9 years during follow-up. Accelerated brain aging was related to prospective cognitive decline and disease severity. In conclusion, the BrainAGE framework indicates discrepancies in brain aging and could thus serve as an indicator for cognitive functioning in the future.

Elucidating the risk factors for progression from amyloid-negative amnestic mild cognitive impairment to dementia

2020 ◽  
Vol 17 ◽  
Author(s):  
Hyung-Ji Kim ◽  
Jae-Hong Lee ◽  
E-nae Cheong ◽  
Sung-Eun Chung ◽  
Sungyang Jo ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Amnestic Mild Cognitive Impairment ◽  
Amyloid Pet ◽  
Clinical Progression ◽  
Amnestic Mci

Background: Amyloid PET allows for the assessment of amyloid β status in the brain, distinguishing true Alzheimer’s disease from Alzheimer’s disease-mimicking conditions. Around 15–20% of patients with clinically probable Alzheimer’s disease have been found to have no significant Alzheimer’s pathology on amyloid PET. However, a limited number of studies had been conducted this subpopulation in terms of clinical progression. Objective: We investigated the risk factors that could affect the progression to dementia in patients with amyloid-negative amnestic mild cognitive impairment (MCI). Methods: This study was a single-institutional, retrospective cohort study of patients over the age of 50 with amyloidnegative amnestic MCI who visited the memory clinic of Asan Medical Center with a follow-up period of more than 36 months. All participants underwent brain magnetic resonance imaging (MRI), detailed neuropsychological testing, and fluorine-18[F18]-florbetaben amyloid PET. Results: During the follow-up period, 39 of 107 patients progressed to dementia from amnestic MCI. In comparison with the stationary group, the progressed group had a more severe impairment in verbal and visual episodic memory function and hippocampal atrophy, which showed an Alzheimer’s disease-like pattern despite the lack of evidence for significant Alzheimer’s disease pathology. Voxel-based morphometric MRI analysis revealed that the progressed group had a reduced gray matter volume in the bilateral cerebellar cortices, right temporal cortex, and bilateral insular cortices. Conclusion: Considering the lack of evidence of amyloid pathology, clinical progression of these subpopulation may be caused by other neuropathologies such as TDP-43, abnormal tau or alpha synuclein that lead to neurodegeneration independent of amyloid-driven pathway. Further prospective studies incorporating biomarkers of Alzheimer’s diseasemimicking dementia are warranted.

Cognitive Improvement by Photic Stimulation in a Mouse Model of Alzheimer’s Disease

2015 ◽  
Vol 12 (9) ◽  
pp. 860-869 ◽  
Author(s):  
Yu Zhang ◽  
Furong Wang ◽  
Xianwen Luo ◽  
Li Wang ◽  
Peng Sun ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Photic Stimulation ◽  
Cognitive Improvement ◽  
Model Of Alzheimer’S Disease

Lower perception of pharmacological treatment increases risk of non-adherence to medication

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
CB Graversen ◽  
JB Valentin ◽  
ML Larsen ◽  
S Riahi ◽  
T Holmberg ◽  
...  
Keyword(s):  
Pharmacological Treatment ◽  
Poisson Regression ◽  
Drug Class ◽  
Angiotensin Receptor Blockers ◽  
Adverse Outcomes ◽  
Adherence To Medication ◽  
Increased Risk ◽  
Patient Reported ◽  
High Level

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): The Danish Heart Foundation Background A large proportion of patients fail to reach optimal adherence to medication following incident ischemic heart disease (IHD) despite amble evidence of the beneficial effect of medication. Non-adherence to medication increases risk of disease-related adverse outcomes but none has explored how perception about pharmacological treatment detail on non-adherence using register-based follow-up data. Purpose To investigate the association between patients’ perception of pharmacological treatment and risk of non-initiation and non-adherence to medication in a population with incident IHD. Methods This cohort study followed 871 patients until 365 days after incident IHD. The study combined patient-reported survey data on perception about pharmacological treatment (categorised by ‘To a high level’, ‘To some level’, and ‘To a lesser level’) with register-based data on reimbursed prescription of cardiovascular medication (antithrombotics, statins, ACE-inhibitors/angiotensin receptor blockers, and β-blockers). Non-initiation was defined as no pick-up of medication in the first 180 days following incident IHD and analysed by Poisson regression. Two different measures evaluated non-adherence in patients initiating treatment: 1) proportion of days covered (PDC) analysed by Poisson regression, and 2) risk of discontinuation analysed by Cox proportional hazard regression. All analyses were adjusted for confounding variables (age, sex, ethnicity, income, educational level, civil status, occupation, charlson comorbidity index, supportive relatives, and individual consultation in medication) identified by directed acyclic graph and obtained from national registers and the survey. Item non-response was handled by multiple imputation and item consistency was evaluated by McDonalds omega. Results Lower perceptions about pharmacological treatment was associated with increased risk of non-initiation and non-adherence to medication irrespectively of drug class and adherence measure in the multiple adjusted analyses (please see figure illustrating results on antithrombotics). A dose-response relationship was observed both at 180- and 365-days of follow-up, but the steepest decline in adherence differed when comparing the two adherence measures (results not shown). Moderate internal consistency was found for the summed measure of perception (McDonalds omega = 0.67). Conclusion Lower perception of pharmacological treatment was associated with subsequent non-initiation and non-adherence to medication, irrespectively of measurement method and drug class. Abstract Figure. Figre: Multiple adjusted analyses

scholarly journals Cortical plasticity is correlated with cognitive improvement in Alzheimer’s disease patients after rTMS treatment

2021 ◽  
Vol 14 (3) ◽  
pp. 503-510 ◽  
Author(s):  
Xingxing Li ◽  
Gangqiao Qi ◽  
Chang Yu ◽  
Guomin Lian ◽  
Hong Zheng ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cortical Plasticity ◽  
Cognitive Improvement

scholarly journals Shotgun lipidomics of liver and brain tissue of Alzheimer’s disease model mice treated with acitretin

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Anna A. Lauer ◽  
Daniel Janitschke ◽  
Malena dos Santos Guilherme ◽  
Vu Thu Thuy Nguyen ◽  
Cornel M. Bachmann ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Disorder ◽  
Amyloid Β ◽  
Lipid Homeostasis ◽  
Medical Surveillance ◽  
Shotgun Lipidomics ◽  
App Processing ◽  
Cognitive Improvement ◽  
The Impact

AbstractAlzheimer’s disease (AD) is a very frequent neurodegenerative disorder characterized by an accumulation of amyloid-β (Aβ). Acitretin, a retinoid-derivative and approved treatment for Psoriasis vulgaris, increases non-amyloidogenic Amyloid-Precursor-Protein-(APP)-processing, prevents Aβ-production and elicits cognitive improvement in AD mouse models. As an unintended side effect, acitretin could result in hyperlipidemia. Here, we analyzed the impact of acitretin on the lipidome in brain and liver tissue in the 5xFAD mouse-model. In line with literature, triglycerides were increased in liver accompanied by increased PCaa, plasmalogens and acyl-carnitines, whereas SM-species were decreased. In brain, these effects were partially enhanced or similar but also inverted. While for SM and plasmalogens similar effects were found, PCaa, TAG and acyl-carnitines showed an inverse effect in both tissues. Our findings emphasize, that potential pharmaceuticals to treat AD should be carefully monitored with respect to lipid-homeostasis because APP-processing itself modulates lipid-metabolism and medication might result in further and unexpected changes. Moreover, deducing effects of brain lipid-homeostasis from results obtained for other tissues should be considered cautiously. With respect to acitretin, the increase in brain plasmalogens might display a further positive probability in AD-treatment, while other results, such as decreased SM, indicate the need of medical surveillance for treated patients.

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