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Journal articles on the topic 'Such as Alzheimer's disease (AD)'

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Published: 5 June 2025

Last updated: 2 August 2025

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1

BAR, Hassan. "Various Infections and Alzheimer's Disease." Virology & Immunology Journal 7, no. 3 (2023): 1–3. http://dx.doi.org/10.23880/vij-16000317.

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Alzheimer's disease (AD) is a major contributor to the worldwide prevalence of dementia. Extracellular-amyloid (A) senile plaques (SP) and intracellular neurofibrillary tangles (NFT) are the neuropathological hallmarks of Alzheimer's disease. Currently, it is believed that both hereditary and environmental variables interact to contribute to the pathophysiology of AD. Despite significant investments in neurological research, the precise molecular basis of AD pathogenesis remains unknown. Multiple studies point to the possibility that pathogenic microorganisms contribute to the development of A

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2

Heckmann, Bradlee. "Beyond amyloid: What's next for Alzheimers disease therapeutics?" Open Access Government 38, no. 1 (2023): 116–17. http://dx.doi.org/10.56367/oag-038-10770.

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Beyond amyloid: What's next for Alzheimers disease therapeutics? Bradlee Heckmann, PhD, from USF Health Neuroscience Institute, Byrd Alzheimer's Center & Asha Therapeutics, in this discussion goes beyond amyloid, asking what's next for Alzheimer's Disease therapeutics. The recent approvals of aducanumab and lecanamab, targeting amyloid beta, a key pathogenic hallmark of Alzheimer's Disease (AD), represent an impressive step forward in developing new treatment options for one of the most devastating neurological diseases. AD impacts over 5 million individuals in the United States and an est

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3

Koberskaya, N. N. "Alzheimer's disease." Neurology, Neuropsychiatry, Psychosomatics 11, no. 3S (2019): 52–60. http://dx.doi.org/10.14412/2074-2711-2019-3s-52-60.

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Despite progress made in laboratory methods, genetic studies, and modern neuroimaging, the diagnosis of diseases that cause dementia makes difficulties. The review presents an update on the epidemiology, risk factors, pathogenesis, clinical presentation, diagnosis, and treatment of Alzheimer's disease (AD). It discusses the issues of symptomatic and pathogenetic treatments and combination therapy for AD. The efficacy of memantine (akatinol memantine) and the expediency of its use at different stages of the disease in patients with AD are noted. Non-pharmacological treatments for this disease,

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Vyshnavi Ramineni, Vyshnavi Ramineni, and Goo-Rak Kwon Goo-Rak Kwon. "An Implementation of Effective CNN Model for AD Detection." Korean Institute of Smart Media 13, no. 6 (2024): 90–97. http://dx.doi.org/10.30693/smj.2024.13.6.90.

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This paper focuses on detecting Alzheimer’s Disease (AD). The most usual form of dementia is Alzheimer's disease, which causes permanent cause memory cell damage. Alzheimer's disease, a neurodegenerative disease, increases slowly over time. For this matter, early detection of Alzheimer's disease is important. The purpose of this work is using Magnetic Resonance Imaging (MRI) to diagnose AD. A Convolution Neural Network (CNN) model, Reset, and VGG the pre-trained learning models are used. Performing analysis and validation of layers affects the effectiveness of the model. T1-weighted MRI images

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G., J. Avhale* R. S. Mohan R. M. Kawade. "Alzheimer's Diseases." International Journal in Pharmaceutical Sciences 1, no. 11 (2023): 507–16. https://doi.org/10.5281/zenodo.10207202.

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Alzheimer's disease (AD) is a disorder that causes degeneration of the cells in the brain and it is the main cause of dementia, which is characterized by a decline in thinking and independence in personal daily activities. AD is considered a multifactorial disease: two main hypotheses were proposed as a cause for AD, cholinergic and amyloid hypotheses. Additionally, several risk factors such as increasing age, genetic factors, head injuries, vascular diseases, infections, and environmental factors play a role in the disease. Currently, there are only two classes of approved drugs to treat AD,

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Lokshina, A. B., D. A. Grishina, and A. V. Obukhova. "Early-onset Alzheimer's disease." Neurology, Neuropsychiatry, Psychosomatics 14, no. 2 (2022): 110–16. http://dx.doi.org/10.14412/2074-2711-2022-2-110-116.

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Alzheimer's disease (AD) is the most common cause of cognitive impairment in adults. There are two main forms of AD: early-onset (onset before 65 years) and late-onset (onset after 65 years). Early-onset AD accounts for at least 5% of all disease cases. The risk of early-onset AD increases in the presence of a family burden and a history of traumatic brain injury. However, it is less associated with cerebrovascular disease, diabetes mellitus, and obesity compared to late-onset AD. The article provides a review of current publications on the diagnostic and treatment problems in early forms of A

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G.V., Srivani* Kothagadi Veena Thakur Vaishnavi Poddutoori Manaswini Sangem Varsha S. K. Kovid. "Alzheimer's Disease: An Overview." International Journal of Pharmaceutical Sciences 3, no. 1 (2025): 1169–76. https://doi.org/10.5281/zenodo.14651398.

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Alzheimer’s disease (AD), the most common form of dementia, is a striking example of the connection between neurophysiological abnormalities and higher-order cognitive deficiencies. Since its initial description in 1906, research into the pathophysiology and etiology of AD has led to the illumination of an incredibly complex set of genetic and molecular mechanisms for the disease’s progression, characterized by much more than the neuropathological hallmarks of beta- amyloid (Aβ) plaques and neurofibrillary tangles (NFTs) Aging is the most obvious risk factor for developing AD.

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8

Angale, Ruth. "The Role of Mitochondria in Alzheimer's disease: Neurodegenerative Disease and Future Therapeutic Options." Neuroscience and Neurological Surgery 2, no. 1 (2018): 01–03. http://dx.doi.org/10.31579/2578-8868/026.

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Mitochondria are cytoplasmic organelles responsible for life and death. Extensive evidence from animal and clinical studies suggests that mitochondria play a critical role in aging, cancer, diabetes and neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and Huntington's disease. Several lines of research suggest that mitochondrial oxidative damage is an important cellular change in most late-onset neurodegenerative diseases. Further, emerging evidence suggests that structural changes in mitochondria, including increased mitochondrial fragmentation and decreased mitoc

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9

Shah, Rahul, and Sankha Bhattacharya. "Advanced Nanoparticular Approaches to Combat Alzheimer's Disease." Pharmaceutical Nanotechnology 9, no. 5 (2021): 308–16. http://dx.doi.org/10.2174/2211738509666211123091913.

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: Alzheimer's disease (AD) is a neurological disease that affects many of the world's rapidly ageing population. In the etiology of Alzheimer’s disease (AD), the involvement of amyloid β (Aβ) plaque accumulation and oxidative stress in the brain have important roles. Various drugs have been proposed to prevent and treat AD, but delivering these therapeutic agents to the brain is difficult. Over the last decade, nanoparticle-mediated drug delivery represents one promising strategy to increase the CNS penetration of several therapeutic moieties successfully. Different nanocarriers are being inve

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10

Amaducci, L., and A. Lippi. "Epidemiology of Alzheimer's disease (AD)." Journal of Neural Transmission - Parkinson's Disease and Dementia Section 1, no. 1-2 (1989): 2. http://dx.doi.org/10.1007/bf02312183.

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11

VanDongen, Antonius M. "Arc: A new target for treating alzheimer's disease." Open Access Government 43, no. 1 (2024): 160–61. http://dx.doi.org/10.56367/oag-043-11454.

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Arc: A new target for treating alzheimer's disease Antonius M. VanDongen, Associate Professor from Duke University, walks us through Arc, a new target for treating Alzheimer’s disease. Alois Alzheimer is a German psychiatrist credited with identifying the first case of the debilitating disease named after him. In 1906, he described neurofibrillary tangles and amyloid plaques in his patient’s brain as unique hallmarks of her dementia. Advances in neuroimaging, genetics, and molecular biology have expanded our understanding of the mechanisms underlying Alzheimer’s disease (AD) significantly. But

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Zarrouk, Amira, Meryam Debbabi, Maryem Bezine, et al. "Lipid Biomarkers in Alzheimer's Disease." Current Alzheimer Research 15, no. 4 (2018): 303–12. http://dx.doi.org/10.2174/1567205014666170505101426.

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Background: There are now significant evidences that lipid metabolism is affected in numerous neurodegenerative diseases including Alzheimer’s disease. These dysfunctions lead to abnormal levels of certain lipids in the brain, cerebrospinal fluid and plasma. It is consequently of interest to establish lipid profiles in neurodegenerative diseases. This approach, which can contribute to identify lipid biomarkers of Alzheimers' disease, can also permit to identify new therapeutic targets. It was therefore of interest to focus on central and peripheral biomarkers in Alzheimer's disease. Methods: A

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13

Pia, Lorenzo, and Paul M. Conway. "Anosognosia and Alzheimer's Disease." Brain Impairment 9, no. 1 (2008): 22–27. http://dx.doi.org/10.1375/brim.9.1.22.

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AbstractNeurological patients can be entirely unaware of their disease; this phenomenon is called anosognosia and it has been shown in different sensory-motor and cognitive domains. Lack of awareness has been investigated in Alzheimer's disease (AD) and within different domains of it. In the present article we review the literature on anosognosia for AD that had been indexed on the Medline database until the end of 2004. Historical introduction to the subject is followed by a brief description of the anatomy and clinical characteristics of AD. An analysis of a number of studies that focus on t

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Koberskaya, N. N. "Dysphagia in Alzheimer's disease." Neurology, Neuropsychiatry, Psychosomatics 14, no. 5 (2022): 83–89. http://dx.doi.org/10.14412/2074-2711-2022-5-83-89.

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The article highlights the problem of dysphagia, which is often present in patients with Alzheimer's disease (AD), as a rule, at advanced stages of the disease and significantly complicates the management of this group of patients. Issues of age-related physiologic swallowing changes are considered. Mechanisms of dysphagia development in the elderly and in AD patients are discussed. It is noted that in AD areas of the cerebral cortex, involved in the act of normal swallowing are affected. The most dangerous complication of dysphagia is aspiration, which increases the risk of pneumonia and deat

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Thriveni, Ankam, Kolukulapally Radhika,, Achina Anuhya, Dr M. Vijaya bhargavi, and M. Sumakanth,. "Role of Genomics and Proteomics in Alzheimer’s Disease." INTERANTIONAL JOURNAL OF SCIENTIFIC RESEARCH IN ENGINEERING AND MANAGEMENT 09, no. 04 (2025): 1–9. https://doi.org/10.55041/ijsrem44128.

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Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized by progressive cognitive decline, and its underlying mechanisms involve intricate interactions between genetic and proteomic factors. Genomics and proteomics play a crucial role in understanding Alzheimer’s disease by identifying genetic risk factors. Recent advancements in genomics and proteomics have enabled researchers to develop deeper into the molecular pathways implicated in AD. Genomic studies have uncovered various genetic variants associated with increased risk for AD, particularly in genes such as APP, APO

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Villain, Nicolas, and Bruno Dubois. "Alzheimer's Disease Including Focal Presentations." Seminars in Neurology 39, no. 02 (2019): 213–26. http://dx.doi.org/10.1055/s-0039-1681041.

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AbstractAlzheimer's disease (AD) is the commonest neurodegenerative disease and the most frequent cause of dementia. It affects 30 million people worldwide. Current research criteria focus on biomarkers' status for amyloid and tau using positron emission tomography and cerebrospinal fluid analysis, independent of clinical status. Current epidemiological data, which mostly rely on biomarker-undetermined AD cases, have highlighted ApoE4 and age as the main risk factors. Rare autosomal dominant mutations also account for a small fraction of early-onset AD. The main clinical phenotype at presentat

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Leszek, Jerzy, Elizaveta V. Mikhaylenko, Dmitrii M. Belousov, et al. "The Links between Cardiovascular Diseases and Alzheimer's Disease." Current Neuropharmacology 19, no. 2 (2020): 152–69. http://dx.doi.org/10.2174/1570159x18666200729093724.

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: The root cause of non-inherited Alzheimer’s disease (AD) remains unknown despite hundreds of research studies performed to attempt to solve this problem. Since proper prophylaxis remains the best strategy, many scientists have studied the risk factors that may affect AD development. There is robust evidence supporting the hypothesis that cardiovascular diseases (CVD) may contribute to AD progression, as the diseases often coexist. Therefore, a lack of well-defined diagnostic criteria makes studying the relationship between AD and CVD complicated. Additionally, inflammation accompanies the pa

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18

Wolozin, B. "Cholesterol and Alzheimer's disease." Biochemical Society Transactions 30, no. 4 (2002): 525–29. http://dx.doi.org/10.1042/bst0300525.

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Accumulation of a 40–42-amino acid peptide, termed amyloid-β peptide (Aβ), is associated with Alzheimer's disease (AD), and identifying medicines that inhibit Aβ could help patients with AD. Recent evidence suggests that a class of medicines that lower cholesterol by blocking the enzyme 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-CoA reductase), termed statins, can inhibit Aβ production. Increasing evidence suggests that the enzymes that generate Aβ function best in a high-cholesterol environment, which might explain why reducing cholesterol would inhibit Aβ production. Studies using both ne

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Kyrtata, Natalia, Ben Dickie, Hedley Emsley, and Laura Parkes. "Glucose transporters in Alzheimer's disease." BJPsych Open 7, S1 (2021): S265—S266. http://dx.doi.org/10.1192/bjo.2021.707.

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BackgroundPhysiological brain function depends on tight glucose regulation, including transport and phosphorylation, the first step in its metabolism. Impaired glucose regulation is increasingly implicated in the pathophysiology of Alzheimer's disease (AD). Glucose hypometabolism in AD may be at least partly due to impaired glucose transport at the blood-brain barrier (BBB). Glucose transporters (GLUTs) are an integral component of the BBB. There is evidence of a significant reduction in vascular and non-vascular forms of GLUT1 and GLUT3 in AD brains compared to age-matched controls. Glucose t

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Finch, Caleb E., and Alexander M. Kulminski. "The Alzheimer's Disease Exposome." Alzheimer's & Dementia 15, no. 9 (2019): 1123–32. https://doi.org/10.5281/zenodo.14819064.

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(Uploaded by Plazi for the Bat Literature Project) Abstract Introduction Environmental factors are poorly understood in the etiology of Alzheimer's disease (AD) and related dementias. The importance of environmental factors in gene environment interactions (GxE) is suggested by wide individual differences in cognitive loss, even for carriers of AD‐risk genetic variants. Results and Discussion We propose the "AD exposome" to comprehensively assess the modifiable environmental factors relevant to genetic underpinnings of cognitive aging and AD. Analysis of endogenous and exogenous environmental

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Fisman, M., M. I. Laskey, and H. E. Enesco. "Liver Polyploidy in Alzheimer's Disease." Canadian Journal on Aging / La Revue canadienne du vieillissement 6, no. 4 (1987): 264–70. http://dx.doi.org/10.1017/s0714980800007558.

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ABSTRACTThe amount of liver polyploidy in a group of patients with Alzheimer's disease (AD) was compared with that of an age-matched control group. There was great variability in the percentage of cells in each ploidy class from one individual to the next in both control and AD subjects. AD patients had a lower percentage of 2N cells, and a higher percentage of 4N cells than the controls. There was no difference in the percentage of 8N or 16N cells in AD, indicating that there was no shift to higher ploidy classes in AD. The most stringent statistical analysis failed to reveal statistically si

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Jain, Bhomik, Aarav Sharma, Anjali Sharma, and Kiranpreet Kaur. "Disease detection for Alzheimer’s using Machine Learning Techniques." INTERANTIONAL JOURNAL OF SCIENTIFIC RESEARCH IN ENGINEERING AND MANAGEMENT 07, no. 11 (2023): 1–11. http://dx.doi.org/10.55041/ijsrem27262.

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THIS PAPER PRESENTS A COMPREHENSIVE REVIEW OF RECENT ADVANCEMENTS IN THE PREDICTION OF ALZHEIMER’S DISEASE (AD) USING MACHINE LEARNING TECHNIQUES.WE ANALYZE TWO PIVOTAL STUDIES: ONE EMPLOYING DEEP LEARNING MODELS FOR ALZHEIMER'S DETECTION FROM RETINAL PHOTOGRAPHS AND ANOTHER USING MACHINE LEARNING TECHNIQUES ALONGSIDE PRINCIPAL COMPONENT ANALYSIS (PCA) FOR AD PROGRESSION CLASSIFICATION. THE FIRST STUDY DEMONSTRATES THE POTENTIAL OF DEEP LEARNING ALGORITHMS IN ANALYZING RETINAL IMAGES, ACHIEVING HIGH ACCURACY, SENSITIVITY, AND SPECIFICITY. THE SECOND STUDY EXPLORES THE EFFICACY OF SVM, RELM, AN

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Madhuri, Badole, Rane Siddhesh, Bharne Atharv, and Karpe Mayur. "Personalized Alzheimer's Disease Progression Prediction with Machine Learning." Personalized Alzheimer's Disease Progression Prediction with Machine Learning 9, no. 1 (2024): 6. https://doi.org/10.5281/zenodo.10567352.

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One of the most prevalent diseases in the world is Alzheimer’s (AD). It is a neurological condition that can lead to cognitive decline and memory loss. Both the senior population and the prevalence of diseases affecting them have dramatically increased in recent years. It is critical to categorize the progression of Alzheimer’s disease. Alzheimer's disease (AD) is a complicated neurological ailment that progresses in different ways for each individual. In this study, we present a novel approach to personalised Alzheimer's disease progression prediction using machine learning techni

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Berriel Pinho, Victor Hugo, João Paulo Lima Daher, Salim Kanaan, and Thalia Medeiros. "Extracellular vesicles in Alzheimer's disease." Arquivos de Neuro-Psiquiatria 82, no. 03 (2024): 001–8. http://dx.doi.org/10.1055/s-0044-1779296.

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AbstractExtracellular vesicles (EVs) are small vesicles released by cells that facilitate cell signaling. They are categorized based on their biogenesis and size. In the context of the central nervous system (CNS), EVs have been extensively studied for their role in both normal physiological functions and diseases like Alzheimer's disease (AD). AD is a neurodegenerative disorder characterized by cognitive decline and neuronal death. EVs have emerged as potential biomarkers for AD due to their involvement in disease progression. Specifically, EVs derived from neurons, astrocytes, and neuron pre

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Claassen, Jurgen AHR, and Rong Zhang. "Cerebral autoregulation in Alzheimer's disease." Journal of Cerebral Blood Flow & Metabolism 31, no. 7 (2011): 1572–77. http://dx.doi.org/10.1038/jcbfm.2011.69.

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Cerebral autoregulation aims to stabilize blood flow to the brain during variations in perfusion pressure, thus protecting the brain against the risks of low or high systemic blood pressure. This vital mechanism is severely impaired in the transgenic mouse model of Alzheimer's disease (AD) that abundantly produces amyloid-β peptide β1-42. These observations have been extrapolated to human AD, wherein impairment of autoregulation could have important implications for the clinical management and prevention of AD. Research on cerebral autoregulation in human AD, however, has only recently become

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Reisberg, Barry, and Alistair Burns. "Diagnosis of Alzheimer's Disease." International Psychogeriatrics 9, S1 (1997): 5–7. http://dx.doi.org/10.1017/s1041610297004651.

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This issue on the diagnosis of Alzheimer's disease (AD) is the product of a special meeting of the International Psychogeriatric Association with the cosponsorship of Alzheimer's Disease International, the European Federation of Neurological Societies, the World Health Organization, and the World Psychiatric Association. The meeting was held in Geneva, Switzerland, from November 10 to 12, 1996. Participants included many of the leading experts on the various aspects of AD diagnosis as well as clinical experts, general experts in the field of AD, organizational representatives, and outstanding

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Ferreira, Pricilla Costa, Kamila de Almeida Piai, Angela Maria Magosso Takayanagui, and Susana Inés Segura-Muñoz. "Aluminum as a risk factor for Alzheimer's disease." Revista Latino-Americana de Enfermagem 16, no. 1 (2008): 151–57. http://dx.doi.org/10.1590/s0104-11692008000100023.

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The purpose of the study was to condense existing scientific evidence about the relation between aluminum (Al) exposure and risk for the development of Alzheimer's Disease (AD), evaluating its long-term effects on the population's health. A systematic literature review was carried out in two databases, MEDLINE and LILACS, between 1990 and 2005, using the uniterms: "Aluminum exposure and Alzheimer Disease" and "Aluminum and risk for Alzheimer Disease". After application of the Relevance Test, 34 studies were selected, among which 68% established a relation between Al and AD, 23.5% were inconclu

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Nefedova, A. "MICROGLIAL PHAGOCYTOSIS IN RATS WITH DIFFERENT MODELS OF ALZHEIMER'S DISEASE." Biotechnologia Acta 16, no. 1 (2023): 57–66. http://dx.doi.org/10.15407/biotech16.01.057.

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Neuroinflammation is a key feature of Alzheimer's disease (AD), a progressive neurodegenerative disorder. Microglia, the resident immune cells of the central nervous system, play a crucial role in the pathogenesis of AD and are active participants in neuroinflammation. Adequate reproduction of neuroinflammation in animal models is one of the main methodological approaches for studying AD pathogenesis and pathophysiology. The aim of the study was to conduct a comparative assessment of the phagocytic activity of microglia in rats with AD induced by intrahippocampal administration of beta-amyloid

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Korten, A. E., A. F. Jorm, A. S. Henderson, G. A. Broe, H. Creasey, and E. McCusker. "Assessing the risk of Alzheimer's disease in first-degree relatives of Alzheimer's disease cases." Psychological Medicine 23, no. 4 (1993): 915–23. http://dx.doi.org/10.1017/s0033291700026386.

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SynopsisFamily history of Alzheimer's disease (AD) was investigated using a telephone re-interview of 99 cases and 116 controls selected from a case–control study of 170 matched pairs. It was found that the family history method used in the initial interview was satisfactory in identifying first-degree relatives and assessing their ages of birth and death, but the number of first-degree relatives suffering from AD was probably under-estimated. Family history of AD was confirmed as a risk factor for AD. Higher estimates of cumulative incidence were obtained among case relatives than among contr

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Can, Eda, and Gülmira Kuruoğlu. "Pragmatic Knowledge in Alzheimer's Disease." Psycholinguistics in a Modern World 17 (December 9, 2022): 41–47. http://dx.doi.org/10.31470/2706-7904-2022-17-41-47.

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Alzheimer's disease (AD) consists of disorders of the memory and language changes which is mostly in syntactical functions and pragmatic-semantic functions. Via conversational analysis, it is easy to evaluate AD patients’ pragmatic skills. In this respect, the aim of this study is to analyse the pragmatic knowledge of AD patients by using a picture description test. In the evaluation, only the maxim of relation in Grice’s cooperative principle was considered. Speech samples were solicited from patients with AD (n=20) and age‐matched healthy people (n=20). Two extra raters made blind ratings on

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Ahmad, Syed S., Shahzad Khan, Mohammad A. Kamal та Umam Wasi. "The Structure and Function of α, β and γ-Secretase as Therapeutic Target Enzymes in the Development of Alzheimer’s Disease: A Review". CNS & Neurological Disorders - Drug Targets 18, № 9 (2020): 657–67. http://dx.doi.org/10.2174/1871527318666191011145941.

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: Alzheimer's disease is a progressive neurodegenerative disorder that affects the central nervous system. There are several factors that cause AD, like, intracellular hyperphosphorylated Tau tangles, collection of extracellular Amyloid-β42 and generation of reactive oxygen species due to mitochondrial dysfunction. This review analyses the most active target of AD and both types of AD-like early-onset AD and late-onset AD. BACE1 is a β-secretase involved in the cleavage of amyloid precursor protein and the pathogenesis of Alzheimer's disease. The presenilin proteins play a critical role in the

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CADIEUX, NICOLE L., and KEVIN W. GREVE. "Emotion processing in Alzheimer's disease." Journal of the International Neuropsychological Society 3, no. 5 (1997): 411–19. http://dx.doi.org/10.1017/s1355617797004116.

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Emotion processing deficits may have an important effect on the quality of life of Alzheimer's disease (AD) patients and their families, yet there are few studies in this area and little is known about the cause of such deficits in AD. This study sought to determine if some AD patients have a disruption in a specific right hemisphere emotion processing system, and to determine if the processing of emotional facial expression is more vulnerable to the pathology of AD than is the perception of emotional prosody. It was specifically hypothesized that patients with greater right hemisphere dysfunc

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Dr., Lawrence Broxmeyer MD. "Are the Infectious Roots of Alzheimer's Buried Deep in the Past?" Journal of MPE Molecular Pathological Epidemiology 3, No. S2:2 (2017): 19. https://doi.org/10.5281/zenodo.894141.

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Recent literature shows a controversial new push to tie microorganisms to Alzheimer's disease (AD). Study after study, in which scientists have injected human Alzheimer-diseased brain tissue into mice and other laboratory animals that later developed the disease have left little doubt that Alzheimer's disease (AD) arises from an infectious process. By 2013 Mawanda and Wallace's " Can Infections Cause Alzheimer's Disease " struck down some of the commonly entertained pathogens for AD such as herpes simplex virus type 1, Chlamydia pneumoniae, and several types of spirochetes. Instead they pointe

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Zhao, Zhenyi. "Emerging Treatments for Alzheimer's Disease." Highlights in Science, Engineering and Technology 54 (July 4, 2023): 280–86. http://dx.doi.org/10.54097/hset.v54i.9778.

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The treatment of Alzheimer's disease (AD), a complex neurodegenerative disorder, presents significant challenges. At the same time, addressing these challenges is essential for enhancing patient outcomes. In this paper, pharmacological and non-pharmacological treatments for AD in both current and emerging size are discussed. It discusses the implications of these treatments for AD patients and their families, as well as the potential societal impact of improved treatment. In addition, the author highlights challenges and opportunities in clinical trial design, regulatory and ethical considerat

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N.Jyothi, B.Ramya G.Sai kumar G.Navya 1N.Bramarambha Sumaiya maisara Dr.K. RajeswarDutt Dr. K.N.V Rao Dr.K.Bali reddy N.Shiva krishna K.Nava Jyothi. "A REVIEW ON ALZHEIMER'S DISEASE." INDO AMERICAN JOURNAL OF PHARMACEUTICAL SCIENCES o6, no. 04 (2019): 7396–402. https://doi.org/10.5281/zenodo.2636638.

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<em>Alzheimer’s disease is an irreversible, progressive brain disease that slowly destroys memory and thinking skills. The prevalence is 3% for persons 65-74 years old, 19% for those 75-84 years pld and 47% for those over 85 years  old. Ad is mainly clinically manifested with dementia. The etiology of AD includes cholinergic, amyloid, tau hypothesis. Pathogenesis of AD involves the apperance of extra cellular beta-amyloid plaques and intra cellular neurofibrillary tangles. Drugs mainly includes Anticholinesterases. The recent reserchers using various animal modles are promising a de

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Ugbode, Chris, Yuhan Hu, Benjamin Whalley, Chris Peers, Marcus Rattray, and Mark L. Dallas. "Astrocytic transporters in Alzheimer's disease." Biochemical Journal 474, no. 3 (2017): 333–55. http://dx.doi.org/10.1042/bcj20160505.

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Astrocytes play a fundamental role in maintaining the health and function of the central nervous system. Increasing evidence indicates that astrocytes undergo both cellular and molecular changes at an early stage in neurological diseases, including Alzheimer's disease (AD). These changes may reflect a change from a neuroprotective to a neurotoxic phenotype. Given the lack of current disease-modifying therapies for AD, astrocytes have become an interesting and viable target for therapeutic intervention. The astrocyte transport system covers a diverse array of proteins involved in metabolic supp

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Crehan, Helen, John Hardy, and Jennifer Pocock. "Microglia, Alzheimer's Disease, and Complement." International Journal of Alzheimer's Disease 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/983640.

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Microglia, the immune cell of the brain, are implicated in cascades leading to neuronal loss and cognitive decline in Alzheimer’s disease (AD). Recent genome-wide association studies have indicated a number of risk factors for the development of late-onset AD. Two of these risk factors are an altered immune response and polymorphisms in complement receptor 1. In view of these findings, we discuss how complement signalling in the AD brain and microglial responses in AD intersect. Dysregulation of the complement cascade, either by changes in receptor expression, enhanced activation of different

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Fernandes, Carina, and Jose Manuel Lopes Lima. "Alzheimer's Disease and Signature Execution." Journal of Forensic Document Examination 27 (December 31, 2017): 23–30. http://dx.doi.org/10.31974/jfde27-23-30.

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Alzheimer´s disease (AD) is a progressive and irreversible neurodegenerative disease involving the impairment of several cognitive functions. To determine how AD affects signatures, samples from three groups were analysed: DA1 (17 participants with a medical diagnosis of AD; Mini-Mental State Examination Test (MMSE) 20.12 ± 2.00); DA2 (17 participants with a medical diagnosis of AD; MMSE 11.06 ± 3.93) and a control group (30 healthy matched individuals; MMSE 28.07 ± 1.60). General features (Chi-Square Tests Linear-by-Linear Association, p <0,050) and constructional features (Fischer’s Exact

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Zekanowski, Cezary, Dorota Religa, Caroline Graff, Slawomir Filipek, and Jacek Kuznicki. "Genetic aspects of Alzheimer's disease." Acta Neurobiologiae Experimentalis 64, no. 1 (2004): 19–31. http://dx.doi.org/10.55782/ane-2004-1488.

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Alzheimer's disease (AD) is a neurodegenerative disorder with a complex etiology and pathogenesis. Mutations in presenilin 1 gene (PSEN1), located on chromosome 14, more rarely in amyloid-? protein precursor (APP) on chromosome 21, and presenilin 2 genes (PSEN2) on chromosome 1, underlie the pathogenesis of most cases of familial early onset of AD (EOAD). The genetics of late-onset AD (LOAD) have been more enigmatic and the only confirmed risk factor for LOAD remains the apolipoprotein E4 allele (ApoE4) on chromosome 19. In this review, we discuss the genetics of AD with a focus on the role of

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Jehangir, Muhammad, Rahman Ali, Wang Xiao Hui, and Yifeng Wang. "An Updated Review of Amyloid Beta Oligomer Toxicity Inhibition and Detection for Alzheimer's Disease Diagnosis." Cognizance Journal of Multidisciplinary Studies 4, no. 7 (2024): 164–86. http://dx.doi.org/10.47760/cognizance.2024.v04i07.015.

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Amyloid beta oligomers (AβOs), which are soluble oligomeric state assemblies of amyloid β-protein (Aβ), have been identified as the main pathogenetic factors in the molecular pathology of Alzheimer's disease (AD). Through their disquieting affect on oxidative stress and synaptic disruptions, AβOs exhibit neurotoxicity and synaptotoxicity, and are crucial in the pathological progression of AD. That being said, a number of recent studies have been made impressive strides in characterizing the traits and pathogenicity of Aβos. Reducing the levels of harmful beta-amyloid (Aβ) species by employing

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Guo, Zhen. "The Gut-brain axis: the role of gut microbiome in Alzheimer's disease." Highlights in Science, Engineering and Technology 74 (December 29, 2023): 110–15. http://dx.doi.org/10.54097/3pk3th41.

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Alzheimer's disease is one of the most severe and wide-spread neurodegenerative diseases in the world. WHO estimates that more than 47 million people (8.1% of women and 5.4% of men over the age of 65) are currently living with dementia. Despite the long history and wide impact in humans of AD, the disease remains in mist. Until now, we cannot determine which factors cause AD and how to find a cure. There is several hypotheses about the pathogenesis of AD, of which cholinergic hypothesis and Nucleic acid oxidation hypothesis are two of the most insightful ones. Besides, increasing evidence sugg

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Kalaria, Raj N. "Vascular Factors in Alzheimer's Disease." International Psychogeriatrics 15, S1 (2003): 47–52. http://dx.doi.org/10.1017/s1041610203008950.

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Vascular involvement in Alzheimer disease (AD) is not necessarily coincident. Current evidence suggests the neuropathology of Alzheimer type of dementia comprises more than amyloid plaques and neurofibrillary tangles. At least a third of recognized AD cases may exhibit cerebrovascular pathology, which also constitutes distinct small vessel disease. Cerebral amyloid angiopathy, microvascular degeneration affecting the cerebral endothelium and smooth muscle cells, basal lamina alterations, hyalinosis, and fibrosis are frequently evident in AD. These changes may be accompanied by perivascular den

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SR, SHARUNYA, VIJAYALAKSHMI DESAI, MEENAKSHI SINGH, and KUSUMA M. "Survey on Early Detection of Alzhiemer’s Disease Using Capsule Neural Network." International Journal of Artificial Intelligence 7, no. 1 (2020): 7–12. http://dx.doi.org/10.36079/lamintang.ijai-0701.65.

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Alzheimer's disease (AD) is an disorder which is irreversible of the brain related to memory loss, mostly found in the old and aged population. Alzheimer's dementia results from the degeneration or loss of brain cells. The brain-imaging technologies most often used to diagnose AD is Magnetic resonance imaging (MRI). MRI or structural magnetic resonance is a very popular and actual technique used to diagnose AD. An MRI uses magnets and powerful radio waves to create a complete view of your brain. To actually detect the presence of Alzheimer’s, the MRI should me studied carefullyImplementation o

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Guariglia, Carla Cristina, and Ricardo Nitrini. "Topographical disorientation in Alzheimer's disease." Arquivos de Neuro-Psiquiatria 67, no. 4 (2009): 967–72. http://dx.doi.org/10.1590/s0004-282x2009000600001.

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Topographical disorientation (TD) has not been as extensively studied as other frequent manifestations of Alzheimer's disease (AD). OBJECTIVE: To verify the occurrence of TD and to identify the neuropsychological dysfunctions associated with TD in AD. METHOD: Thirty patients with probable AD, their caregivers and 30 subjects without dementia (controls) were interviewed with a questionnaire and evaluated with tests related to topographical orientation. RESULTS: AD patients, even those with mild dementia, differ from controls in the questionnaire on topographical orientation and in most neuropsy

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Kihara, Takeshi, and Shun Shimohama. "Alzheimer's disease and acetylcholine receptors." Acta Neurobiologiae Experimentalis 64, no. 1 (2004): 99–105. http://dx.doi.org/10.55782/ane-2004-1495.

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Cholinergic abnormalities, alongside senile plaques, neurofibrillary tangles, and extensive neuronal loss, are the major characteristics in Alzheimer's disease (AD). Both nicotinic and muscarinic acetylcholine receptors are decreased in AD, and it has been shown that the reduction in the number of acetylcholine receptors precedes other pathologic changes. Anti-cholinergic drugs induce amnesia, which can be reversed by withdrawal of the medication. Inhibition of the down-regulation of acetylcholine is, therefore, a strategy for the treatment of AD because it could augment acetylcholine levels w

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Salloway, Stephen. "Introduction: The Prevalence of Alzheimer's Disease — A Growing Crisis." CNS Spectrums 13, S3 (2008): 3. http://dx.doi.org/10.1017/s109285290001717x.

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In 1906, the German physician Alois Alzheimer provided the first description of the “serious and peculiar disease” of mental deterioration that would later on take his name. Alzheimer described the classic pathology of neuritic plaques and neurofibrillary tangles in an affected patient. Since that time, understanding of Alzheimer's disease (AD) has progressed substantially, although the ability to influence disease progression has not progressed as rapidly. It is likely that over the next decade these advances will lead to earlier diagnosis and development of disease-modifying treatments for A

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Asem, Surindro Singh, та Chanu Takhellambam Machathoibi. "Alzheimer's disease and Aβ pathways". World Journal of Advanced Research and Reviews 12, № 3 (2021): 542–44. https://doi.org/10.5281/zenodo.5813925.

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Alzheimer's disease (AD) is a neurodegenerative disease which is one of the major health issues globally. It is the 6<sup>th</sup> cause of death in the United States. Approximately, 60–70% of cases of dementia are caused by AD. The disease advances with age worsening the symptoms that include problems with declining memory, language, mood swings, loss of motivation, self-neglect, and other behavioral issues. AD patients need a long-term health care and hospital services as the disease worsens with the advancing of their age. However, proper medications and treatment is still un

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Grundman, Michael, and Patrick Delaney. "Antioxidant strategies for Alzheimer's disease." Proceedings of the Nutrition Society 61, no. 2 (2002): 191–202. http://dx.doi.org/10.1079/pns2002146.

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Oxidative damage is present within the brains of patients with Alzheimer's disease (AD), and is observed within every class of biomolecule, including nucleic acids, proteins, lipids and carbohydrates. Oxidative injury may develop secondary to excessive oxidative stress resulting from β-amyloid-induced free radicals, mitochondrial abnormalities, inadequate energy supply, inflammation or altered antioxidant defences. Treatment with antioxidants is a promising approach for slowing disease progression to the extent that oxidative damage may be responsible for the cognitive and functional decline o

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Kummer, Markus P., and Michael T. Heneka. "PPARs in Alzheimer's Disease." PPAR Research 2008 (2008): 1–8. http://dx.doi.org/10.1155/2008/403896.

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Peroxisome proliferator-activated receptors (PPARs) are well studied for their peripheral physiological and pathological impact, but they also play an important role for the pathogenesis of various disorders of the central nervous system (CNS) like multiple sclerosis, amyotrophic lateral sclerosis, Alzheimer's, and Parkinson's disease. The observation that PPARs are able to suppress the inflammatory response in peripheral macrophages and in several models of human autoimmune diseases lead to the idea that PPARs might be beneficial for CNS disorders possessing an inflammatory component. The neu

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Staehelin, Hannes B. "Micronutrients and Alzheimer's disease." Proceedings of the Nutrition Society 64, no. 4 (2005): 565–70. http://dx.doi.org/10.1079/pns2005459.

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The current high life expectancy is overshadowed by neurodegenerative illnesses that lead to dementia and dependence. Alzheimer's disease (AD) is the most common of these conditions, and is considered to be a proteinopathy, with amyloid-β42 as a key factor, leading via a cascade of events to neurodegeneration. Major factors involved are oxidative stress, perturbed Ca homeostasis and impaired energy metabolism. Protection against oxidative stress by micronutrients (including secondary bioactive substances) has been shown in transgenic Alzheimer model systems to delay AD. Epidemiological evidenc

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