scholarly journals Seizure in Alzheimer’s Disease: An Underestimated Phenomenon

2018 ◽  
Vol 34 (2) ◽  
pp. 81-88 ◽  
Author(s):  
Marjan Asadollahi ◽  
Musa Atazadeh ◽  
Maryam Noroozian
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Treatment Options ◽  
Cognitive Domains ◽  
Inhibitory Circuits ◽  
Epileptiform Discharges ◽  
Cerebrospinal Fluid Biomarkers ◽  
Clinical Presentations ◽  
Underlying Mechanisms ◽  
Electroencephalogram Eeg

Alzheimer’s disease (AD) is considered as a potential risk factor for the development of seizure due to neurodegeneration and imbalance between stimulatory and inhibitory circuits in the brain. Seizure could occur in any point during the course of AD, and its presentation varies from fluctuation in cognitive domains to more typical seizures. The clinical diagnosis of seizure in patients with dementia may be challenging due to difficulty in history taking and clinical assessment. No paraclinic methods other than electroencephalogram (EEG) could provide arguments for the diagnosis of AD-related seizures (neither imaging modalities nor cerebrospinal fluid biomarkers). Standard 30-minute EEG may not be sufficiently sensitive to detect epileptiform discharges. In the present study, we aim to review different aspects of seizure in AD, including seizure prevalence, risk factors, underlying mechanisms, electroencephalographic findings, clinical presentations, impact of seizures on AD, and treatment options.

scholarly journals Electrophysiological Biomarkers of Epileptogenicity in Alzheimer’s Disease

2021 ◽  
Vol 15 ◽  
Author(s):  
Tingting Yu ◽  
Xiao Liu ◽  
Jianping Wu ◽  
Qun Wang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
High Frequency ◽  
Cortical Network ◽  
Accurate Identification ◽  
New Approach ◽  
Epileptiform Discharges ◽  
Scalp Electroencephalogram ◽  
Electroencephalogram Eeg

Cortical network hyperexcitability is an inextricable feature of Alzheimer’s disease (AD) that also might accelerate its progression. Seizures are reported in 10–22% of patients with AD, and subclinical epileptiform abnormalities have been identified in 21–42% of patients with AD without seizures. Accurate identification of hyperexcitability and appropriate intervention to slow the compromise of cognitive functions of AD might open up a new approach to treatment. Based on the results of several studies, epileptiform discharges, especially those with specific features (including high frequency, robust morphology, right temporal location, and occurrence during awake or rapid eye movement states), frequent small sharp spikes (SSSs), temporal intermittent rhythmic delta activities (TIRDAs), and paroxysmal slow wave events (PSWEs) recorded in long-term scalp electroencephalogram (EEG) provide sufficient sensitivity and specificity in detecting cortical network hyperexcitability and epileptogenicity of AD. In addition, magnetoencephalogram (MEG), foramen ovale (FO) electrodes, and computational approaches help to find subclinical seizures that are invisible on scalp EEGs. We performed a comprehensive analysis of the aforementioned electrophysiological biomarkers of AD-related seizures.

scholarly journals “Brain Fog” by COVID-19 or Alzheimer’s Disease? A Case Report

2021 ◽  
Vol 12 ◽  
Author(s):  
Jordi A. Matias-Guiu ◽  
Cristina Delgado-Alonso ◽  
Miguel Yus ◽  
Carmen Polidura ◽  
Natividad Gómez-Ruiz ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Older Patients ◽  
Early Stage ◽  
Acute Infection ◽  
Cognitive Symptoms ◽  
Cerebrospinal Fluid Biomarkers ◽  
Detailed Assessment ◽  
Underlying Mechanisms

Cognitive symptoms after COVID-19 have been increasingly recognized several months after the acute infection and have been designated as “brain fog.” We report a patient with cognitive symptoms that started immediately after COVID-19, in which cerebrospinal fluid biomarkers were highly suggestive of Alzheimer’s disease. Our case highlights the need to examine patients with cognitive symptoms following COVID-19 comprehensively. A detailed assessment combining clinical, cognitive, and biomarker studies may help disentangle the underlying mechanisms associated with cognitive dysfunction in each case. The investigation of neurodegenerative processes in an early stage, especially in older patients, is probably warranted.

Formononetin Ameliorates Cognitive Disorder via PGC-1α Pathway in Neuroinflammation Conditions in High-Fat Diet-Induced Mice

2019 ◽  
Vol 18 (7) ◽  
pp. 566-577 ◽  
Author(s):  
Xinxin Fu ◽  
Tingting Qin ◽  
Jiayu Yu ◽  
Jie Jiao ◽  
Zhanqiang Ma ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
High Fat Diet ◽  
Trifolium Pratense ◽  
Amyloid Β ◽  
Cognitive Disorder ◽  
Mechanism Study ◽  
High Fat ◽  
Neuroprotective Effects ◽  
Underlying Mechanisms

Background: Alzheimer’s disease is one of the most common neurodegenerative diseases in many modern societies. The core pathogenesis of Alzheimer’s disease includes the aggregation of hyperphosphorylated Tau and abnormal Amyloid-β generation. In addition, previous studies have shown that neuroinflammation is one of the pathogenesis of Alzheimer’s disease. Formononetin, an isoflavone compound extracted from Trifolium pratense L., has been found to have various properties including anti-obesity, anti-inflammation, and neuroprotective effects. But there are very few studies on the treatment of Alzheimer’s disease with Formononetin. Objective: The present study focused on the protective activities of Formononetin on a high-fat dietinduced cognitive decline and explored the underlying mechanisms. Methods: Mice were fed with HFD for 10 weeks and intragastric administrated daily with metformin (300 mg/kg) and Formononetin (20 and 40 mg/kg). Results: We found that Formononetin (20, 40 mg/kg) significantly attenuated the learning and memory deficits companied by weight improvement and decreased the levels of blood glucose, total cholesterol and triglyceride in high-fat diet-induced mice. Meanwhile, we observed high-fat diet significantly caused the Tau hyperphosphorylation in the hippocampus of mice, whereas Formononetin reversed this effect. Additionally, Formononetin markedly reduced the levels of inflammation cytokines IL-1β and TNF-α in high-fat diet-induced mice. The mechanism study showed that Formononetin suppressed the pro-inflammatory NF-κB signaling and enhanced the anti-inflammatory Nrf-2/HO-1 signaling, which might be related to the regulation of PGC-1α in the hippocampus of high-fat diet -induced mice. Conclusion: Taken together, our results showed that Formononetin could improve the cognitive function by inhibiting neuroinflammation, which is attributed to the regulation of PGC-1α pathway in HFD-induced mice.

scholarly journals Unique Sleep and Circadian Rhythm Dysfunction Neuroinflammatory and Immune Profiles in Alzheimer’s Disease with Mild Cognitive Impairment

2021 ◽  
pp. 1-6
Author(s):  
Jagan A. Pillai ◽  
James Bena ◽  
Lynn M. Bekris ◽  
Nancy Foldvary-Schaefer ◽  
Catherine Heinzinger ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Circadian Rhythm ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Humoral Immune ◽  
Humoral Immune Responses ◽  
Cerebrospinal Fluid Biomarkers ◽  
Circulating Markers

Sleep dysfunction has been identified in the pathophysiology of Alzheimer’s disease (AD); however, the role and mechanism of circadian rhythm dysfunction is less well understood. In a well-characterized cohort of patients with AD at the mild cognitive impairment stage (MCI-AD), we identify that circadian rhythm irregularities were accompanied by altered humoral immune responses detected in both the cerebrospinal fluid and plasma as well as alterations of cerebrospinal fluid biomarkers of neurodegeneration. On the other hand, sleep disruption was more so associated with abnormalities in circulating markers of immunity and inflammation and decrements in cognition.

Lifestyle intervention to prevent Alzheimer’s disease

2020 ◽  
Vol 31 (8) ◽  
pp. 817-824 ◽  
Author(s):  
Yi Ko ◽  
Soi Moi Chye
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lifestyle Intervention ◽  
Social Engagement ◽  
Treatment Options ◽  
Cognitive Stimulation ◽  
Systemic Review ◽  
Lifestyle Interventions ◽  
Alternative Approaches ◽  
The Brain

AbstractAlzheimer’s disease (AD) is the most common neurodegenerative disease that leads to significant morbidities in elderly. The major pathological hallmark of AD is beta-amyloid plaques (Aβ) and intracellular neurofibrillary tangles (NFTs) deposition in hippocampus of the brain. These abnormal protein deposition damages neuronal cells resulting in neurodegeneration and cognitive decline. As a result of limited treatment options available for this disease, there is huge economic burden for patients and social health care system. Thus, alternative approaches (lifestyle intervention) to prevent this disease are extremely important. In this systemic review, we summarized epidemiological evidence of lifestyle intervention and the mechanisms involved in delaying and/or preventing AD. Lifestyle interventions include education, social engagement and cognitive stimulation, smoking, exercise, depression and psychological stress, cerebrovascular disease (CVD), hypertension (HTN), dyslipidaemia, diabetes mellitus (DM), obesity and diet. The methods are based on a literature review of available sources found on the research topic in four acknowledged databases: Web of Science, Scopus, Medline and PubMed. Results of the identified original studies revealed that lifestyle interventions have significant effects and our conclusion is that combination of early lifestyle interventions can decrease the risk of developing AD.

scholarly journals Naringenin improves learning and memory in an Alzheimer's disease rat model: Insights into the underlying mechanisms

2015 ◽  
Vol 764 ◽  
pp. 195-201 ◽  
Author(s):  
Saeed Ghofrani ◽  
Mohammad-Taghi Joghataei ◽  
Simin Mohseni ◽  
Tourandokht Baluchnejadmojarad ◽  
Maryam Bagheri ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Learning And Memory ◽  
Rat Model ◽  
Underlying Mechanisms

Differential Cued-Stroop Performance in Cognitively Asymptomatic Older Adults with Biomarker-Identified Risk for Alzheimer’s Disease: A Pilot Study

2018 ◽  
Vol 15 (9) ◽  
pp. 820-827 ◽  
Author(s):  
Ryan Van Patten ◽  
Anne M. Fagan ◽  
David A.S. Kaufman
Keyword(s):  
Alzheimer’S Disease ◽  
Older Adults ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Stroop Task ◽  
Coefficient Of Variation ◽  
Reaction Times ◽  
Preclinical Alzheimer’S Disease ◽  
Cerebrospinal Fluid Biomarkers ◽  
Accuracy Rates

Background: There exists a need for more sensitive measures capable of detecting subtle cognitive decline due to Alzheimer's disease. Objective: To advance the literature in Alzheimer’s disease by demonstrating that performance on a cued-Stroop task is impacted by preclinical Alzheimer's disease neuropathology. Method: Twenty-nine cognitively asymptomatic older adults completed a computerized, cued-Stroop task in which accuracy rates and intraindividual variability in reaction times were the outcomes of interest. Cerebrospinal fluid biomarkers of Aβ42 and tau were measured and participants were then grouped according to a published p-tau/Aβ42 cutoff reflecting risk for Alzheimer’s disease (preclinical Alzheimer's disease = 14; control = 15). Results: ANOVAs indicated that accuracy rates did not differ between the groups but 4-second delay incongruent color-naming Stroop coefficient of variation reaction times were higher in the preclinical Alzheimer’s disease group compared to the control group, reflecting increased within-person variability. Moreover, partial correlations showed no relationships between cerebrospinal fluid biomarkers and accuracy rates. However, increases in coefficient of variation reaction times correlated with decreased Aβ42 and increases in p-tau and the p-tau/Aβ42 ratio. Conclusion: Results supported the ability of the computerized, cued-Stroop task to detect subtle Alzheimer’s disease neuropathology using a small cohort of cognitively asymptomatic older adults. The ongoing measurement of cued-Stroop coefficient of variation reaction times has both scientific and clinical utility in preclinical Alzheimer’s disease.

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