Inflammatory and Infectious Processes Serve as Links between Atrial Fibrillation and Alzheimer’s Disease

Atrial fibrillation (AF) is one of the most prevalent forms of arrhythmia that carries an increased risk of stroke which, in turn, is strongly associated with cognitive decline. The majority of dementia cases are caused by Alzheimer’s disease (AD) with obscure pathogenesis. While the exact mechanisms are unknown, the role of inflammatory processes and infectious agents have recently been implicated in both AD and AF, suggesting a common link between these maladies. Here, we present the main shared pathways underlying arrhythmia and memory loss. The overlapping predictive biomarkers and emerging joint pharmacological approaches are also discussed.

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Promoting Conversations About Cognitive Decline Between Older Adults and Primary Care Providers

Innovation in Aging ◽

10.1093/geroni/igaa057.513 ◽

2020 ◽

Vol 4 (Supplement_1) ◽

pp. 157-158

Author(s):

Benjamin Olivari ◽

Christopher Taylor ◽

Nia Reed ◽

Lisa McGuire

Keyword(s):

Alzheimer’S Disease ◽

Primary Care ◽

Alzheimer's Disease ◽

Cognitive Impairment ◽

Cognitive Decline ◽

Chronic Conditions ◽

Memory Loss ◽

Primary Care Providers ◽

Subjective Cognitive Decline ◽

Care Providers

Abstract Alzheimer’s disease and related dementias often begin with symptoms of mild memory loss, eventually leading to more severe cognitive impairment, functional impairment, and ultimately, death. Data from the Behavioral Risk Factor Surveillance System core questions related to chronic diseases and from the cognitive decline optional module on subjective cognitive decline (SCD) from the years 2015-2018 were aggregated across the participating 50 states, D.C., and Puerto Rico for this analysis. Among U.S. adults aged 65 years and older, only 39.8% (95%CI=37.6-42.1) of those experiencing SCD reported discussing their SCD symptoms with a healthcare provider. The prevalence of discussing SCD symptoms with a provider was higher among those with at least one chronic condition than among those with no chronic conditions. 30.7% (28.6-32.8) of those aged 65 years and older reported that their SCD led to functional limitations and 28.8% (26.5-31.2) needed assistance with day-to-day activities. For patients aged 65 years and older, Welcome to Medicare visits and Medicare Annual Wellness Visits are critically underutilized primary care access points. Primary care providers can manage chronic conditions, cognitive health, and initiate referrals for testing. Efforts to promote the use of toolkits and diagnostic codes that are available to primary care providers to initiate conversations about memory loss with patients may be utilized to improve detection, diagnosis, and planning for memory problems. Discussions may lead to earlier detection and diagnosis of cognitive impairment, such as Alzheimer’s disease, or other treatable conditions such as delirium or pressure in the brain and avoid costly hospitalizations.

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Isovitexin modulates autophagy in Alzheimer’s disease via miR-107 signalling

Translational Neuroscience ◽

10.1515/tnsci-2020-0109 ◽

2020 ◽

Vol 11 (1) ◽

pp. 391-401

Author(s):

Jiang Cheng ◽

Guowei Wang ◽

Na Zhang ◽

Fang Li ◽

Lina Shi ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Memory Loss ◽

The Elderly ◽

Tnf Α ◽

Autophagic Process ◽

Molecular Signals ◽

Ad Mouse Model ◽

Mtor Signalling

AbstractBackground:Alzheimer’s disease (AD) is an ultimately fatal, degenerative brain disease in the elderly people. In the current work, we assessed the defensive capability of isovitexin (IVX) through an intracerebroventricular injection of streptozotocin (STZ)-induced AD mouse model.Methods:Mice were separated into four cohorts: sham-operated control mice; STZ-intoxicated Alzheimer’s mice; IVX cohort, IVX + STZ; and Ant-107 cohort, antagomiR-107 + IVX/STZ as in the IVX cohort.Results:The outcomes indicated that IVX administration ameliorated spatial memory loss and blunted a cascade of neuro-noxious episodes – including increased amyloid-beta (Aβ) and degraded myelin basic protein burden, neuroinflammation (represented by elevated caspase-1, TNF-α and IL-6 levels) and autophagic dysfunction (represented by altered LC3-II, Atg7 and beclin-1 expressions) – via the inhibition of PI3K/Akt/mTOR signalling axis. We considered the question of whether the epigenetic role of microRNA-107 (miR-107) has any impact on these events, by using antagomiR-107.Conclusion:This probing underscored that miR-107 could be a pivotal regulatory button in the activation of molecular signals linked with the beneficial autophagic process and anti-inflammatory activities in relation to IVX treatment. Hence, this report exemplifies that IVX could guard against Aβ toxicity and serve as an effectual treatment for patients afflicted with AD.

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Subjective cognitive decline: The first clinical manifestation of Alzheimer's disease?

Dementia & Neuropsychologia ◽

10.1590/s1980-5764-2016dn1003002 ◽

2016 ◽

Vol 10 (3) ◽

pp. 170-177 ◽

Cited By ~ 22

Author(s):

Adalberto Studart Neto ◽

Ricardo Nitrini

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Cognitive Impairment ◽

Mild Cognitive Impairment ◽

Cognitive Decline ◽

Clinical Manifestation ◽

Neurodegenerative Disorder ◽

Subjective Cognitive Decline ◽

Subjective Memory ◽

Increased Risk

ABSTRACT Background: Mild cognitive impairment is considered as the first clinical manifestation of Alzheimer's disease (AD), when the individual exhibits below performance on standardized neuropsychological tests. However, some subjects before having a lower performance on cognitive assessments already have a subjective memory complaint. Objective: A review about subjective cognitive decline, the association with AD biomarkers and risk of conversion to dementia. Methods: We performed a comprehensive non-systematic review on PubMed. The keywords used in the search were terms related to subjective cognitive decline. Results: Subjective cognitive decline is characterized by self-experience of deterioration in cognitive performance not detected objectively through formal neuropsychological testing. However, various terms and definitions have been used in the literature and the lack of a widely accepted concept hampers comparison of studies. Epidemiological data have shown that individuals with subjective cognitive decline are at increased risk of progression to AD dementia. In addition, there is evidence that this group has a higher prevalence of positive biomarkers for amyloidosis and neurodegeneration. However, Alzheimer's disease is not the only cause of subjective cognitive decline and various other conditions can be associated with subjective memory complaints, such as psychiatric disorders or normal aging. The features suggestive of a neurodegenerative disorder are: onset of decline within the last five years, age at onset above 60 years, associated concerns about decline and confirmation by an informant. Conclusion: These findings support the idea that subjective cognitive complaints may be an early clinical marker that precedes mild cognitive impairment due to Alzheimer's disease.

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Polymorphisms inHSD17B1: Early Onset and Increased Risk of Alzheimer’s Disease in Women with Down Syndrome

Current Gerontology and Geriatrics Research ◽

10.1155/2012/361218 ◽

2012 ◽

Vol 2012 ◽

pp. 1-8 ◽

Cited By ~ 8

Author(s):

Joseph H. Lee ◽

Susan Gurney ◽

Deborah Pang ◽

Alexis Temkin ◽

Naeun Park ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Down Syndrome ◽

Age At Onset ◽

Nucleotide Polymorphisms ◽

Risk Alleles ◽

Increased Risk ◽

Estrogen Activity ◽

Intron 4

Background/Aims. Genetic variants that affect estrogen activity may influence the risk of Alzheimer's disease (AD). In women with Down syndrome, we examined the relation of polymorphisms in hydroxysteroid-17beta-dehydrogenase (HSD17B1) to age at onset and risk of AD.HSD17B1encodes the enzyme 17β-hydroxysteroid dehydrogenase (HSD1), which catalyzes the conversion of estrone to estradiol.Methods. Two hundred and thirty-eight women with DS, nondemented at baseline, 31–78 years of age, were followed at 14–18-month intervals for 4.5 years. Women were genotyped for 5 haplotype-tagging single-nucleotide polymorphisms (SNPs) in theHSD17B1gene region, and their association with incident AD was examined.Results. Age at onset was earlier, and risk of AD was elevated from two- to threefold among women homozygous for the minor allele at 3 SNPs in intron 4 (rs676387), exon 6 (rs605059), and exon 4 inCOASY(rs598126). Carriers of the haplotype TCC, based on the risk alleles for these three SNPs, had an almost twofold increased risk of developing AD (hazard ratio = 1.8, 95% CI, 1.1–3.1).Conclusion. These findings support experimental and clinical studies of the neuroprotective role of estrogen.

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Clinical Lifestyle Medicine Strategies for Preventing and Reversing Memory Loss in Alzheimer’s

American Journal of Lifestyle Medicine ◽

10.1177/1559827618766468 ◽

2018 ◽

Vol 12 (5) ◽

pp. 391-395 ◽

Cited By ~ 3

Author(s):

Paulina Shetty ◽

Wes Youngberg

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Cognitive Decline ◽

Case Studies ◽

Treatment Guidelines ◽

Memory Loss ◽

Current Approach ◽

Metabolic Parameter ◽

Lifestyle Medicine ◽

Underlying Causes

Alzheimer’s disease (AD) is the most common form of dementia and currently affects over 5 million Americans and 30 million individuals worldwide. Unfortunately, the current approach to treating AD provides nothing more than a marginal, unsustained, symptomatic effect, with little or no effect on disease progression itself. To attain effective improvements in AD, one must determine risk factors, address the underlying causes, and focus on a combination of functional and lifestyle medicine strategies that provide a comprehensive, programmatic, and network-based approach that is sufficient to achieve epigenetic transformation and neurologic healing through its multiple and necessary synergistic components. Rather than normalizing metabolic parameters, the focus is on optimization of each metabolic parameter. Papers published by research neurologist, Dr Dale Bredesen have documented that symptoms of mild cognitive impairment and early AD may often be reversed within 6 months after initiating a comprehensive, functional and lifestyle medicine-focused program. The purpose of this article are as follows: 1. Shed light on a promising clinical protocol that focuses on a comprehensive functional and lifestyle medicine approach to treating mild cognitive decline and Alzheimer’s disease; 2. Identify the Bredesen Protocol testing, diagnostic and treatment guidelines; 3. Review several case studies and discuss the promising results of the program. Although published case studies such as those reported here are relatively few, clinicians applying these comprehensive strategies have reason to expect improvement in their patients. Lifestyle medicine can be a source of greatly needed hope for those suffering with cognitive decline.

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Factors underlying cognitive decline in old age and Alzheimer’s disease: the role of the hippocampus

Reviews in the Neurosciences ◽

10.1515/revneuro-2016-0086 ◽

2017 ◽

Vol 28 (7) ◽

pp. 705-714 ◽

Cited By ~ 20

Author(s):

Wafa Jaroudi ◽

Julia Garami ◽

Sandra Garrido ◽

Michael Hornberger ◽

Szabolcs Keri ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Cognitive Decline ◽

Personality Traits ◽

Old Age ◽

Brain Regions ◽

Personality Factors ◽

Associated Symptoms ◽

Lifestyle Patterns

AbstractThere are many factors that strongly influence the aetiology, development, and progression of cognitive decline in old age, mild cognitive impairment (MCI), and Alzheimer’s disease (AD). These factors include not only different personality traits and moods but also lifestyle patterns (e.g. exercise and diet) and awareness levels that lead to cognitive decline in old age. In this review, we discuss how personality traits, mood states, and lifestyle impact brain and behaviour in older adults. Specifically, our review shows that these lifestyle and personality factors affect several brain regions, including the hippocampus, a region key for memory that is affected by cognitive decline in old age as well as AD. Accordingly, appropriate recommendations are presented in this review to assist individuals in decreasing chances of MCI, dementia, AD, and associated symptoms.

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