Integrated Biomarkers for Depression in Alzheimer’s Disease: A Critical Review

2017 ◽  
Vol 14 (4) ◽  
pp. 441-452 ◽  
Author(s):  
Sofia Wenzler ◽  
Christian Knochel ◽  
Ceylan Balaban ◽  
Dominik Kraft ◽  
Juliane Kopf ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Affect Regulation ◽  
Current Evidence ◽  
Diagnostic Process ◽  
Neuropsychiatric Manifestation ◽  
The Brain ◽  
Control Functional

Depression is a common neuropsychiatric manifestation among Alzheimer’s disease (AD) patients. It may compromise everyday activities and lead to a faster cognitive decline as well as worse quality of life. The identification of promising biomarkers may therefore help to timely initiate and improve the treatment of preclinical and clinical states of AD, and to improve the long-term functional outcome. In this narrative review, we report studies that investigated biomarkers for AD-related depression. Genetic findings state AD-related depression as a rather complex, multifactorial trait with relevant environmental and inherited contributors. However, one specific set of genes, the brain derived neurotrophic factor (BDNF), specifically the Val66Met polymorphism, may play a crucial role in AD-related depression. Regarding neuroimaging markers, the most promising findings reveal structural impairments in the cortico-subcortical networks that are related to affect regulation and reward / aversion control. Functional imaging studies reveal abnormalities in predominantly frontal and temporal regions. Furthermore, CSF based biomarkers are seen as potentially promising for the diagnostic process showing abnormalities in metabolic pathways that contribute to AD-related depression. However, there is a need for standardization of methodological issues and for replication of current evidence with larger cohorts and prospective studies.

Natural product-based nanomedicine: Recent advances and issues for the treatment of Alzheimer's disease

2021 ◽  
Vol 20 ◽  
Author(s):  
Choy Ker Woon ◽  
Wong Kah Hui ◽  
Razif Abas ◽  
Muhammad Huzaimi Haron ◽  
Srijit Das ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Natural Products ◽  
Medicinal Plants ◽  
Drug Transport ◽  
The Elderly ◽  
Current Evidence ◽  
Alternative Approach ◽  
Progressive Neurodegeneration ◽  
The Brain

: Alzheimer's disease (AD) affects the elderly and is characterized by progressive neurodegeneration caused by different pathologies. The most significant challenges in treating AD include the inability of medications to reach the brain because of its poor solubility, low bioavailability, and the presence of the blood-brain barrier (BBB). Additionally, current evidence suggests the disruption of BBB plays an important role in the pathogenesis of AD. One of the critical challenges in treating AD is the ineffective treatments and its severe adverse effects. Nanotechnology offers an alternative approach to facilitate the treatment of AD by overcoming the challenges in drug transport across the BBB. Various nanoparticles (NP) loaded with natural products were reported to aid in drug delivery for the treatment of AD. The nano- sized entities of NP are great platforms for incorporating active materials from natural products into formulations that can be delivered effectively to the intended action site without compromising the material’s bioactivity. The review highlights the applications of medicinal plants, their derived components, and various nanomedicine-based approaches for the treatment of AD. The combination of medicinal plants and nanotechnology may lead to new theragnostic solutions for the treatment of AD in the future.

Short and Longer Term Effects of Musical Intervention in Severe Alzheimer's Disease

2012 ◽  
Vol 29 (5) ◽  
pp. 533-541 ◽  
Author(s):  
Sylvain Clément ◽  
Audrey Tonini ◽  
Fatiha Khatir ◽  
Loris Schiaratura ◽  
Séverine Samson
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Facial Expressions ◽  
Emotional State ◽  
Present Finding ◽  
Well Being ◽  
Music Intervention ◽  
Short Term

in this study, we examined short and longer term effects of musical and cooking interventions on emotional well-being of severe Alzheimer's disease (AD) patients. These two pleasurable activities (i.e., listening to music, tasting sweets) that were collectively performed (i.e., playing music together, collaborative preparation of a cake) were compared in two groups of matched patients with AD (N = 14). Each intervention lasted four weeks (two sessions per week) and their effects were regularly assessed up to four weeks after the end of the intervention. We repeatedly evaluated the emotional state of both groups before, during, and after the intervention periods by analyzing discourse content and facial expressions from short filmed interviews as well as caregivers' judgments of mood. The results reveal short-term benefits of both music and cooking interventions on emotional state on all these measures, but long-term benefits were only evident after the music intervention. The present finding suggests that non-pharmacological approaches offer promising methods to improve the quality of life of patients with dementia and that music stimulation is particularly effective to produce long lasting effects on patients' emotional well-being.

scholarly journals Impact of Alzheimer’s disease on the family caregiver’s long-term quality of life: results from an ALSOVA follow-up study

2015 ◽  
Vol 25 (3) ◽  
pp. 687-697 ◽  
Author(s):  
Tarja H. Välimäki ◽  
Janne A. Martikainen ◽  
Kristiina Hongisto ◽  
Saku Väätäinen ◽  
Harri Sintonen ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Follow Up Study ◽  
The Family

scholarly journals Influencia del estrés en la Enfermedad de Alzheimer. // Stress influence in Alzheimer’s disease

Ciencia Unemi ◽  
2018 ◽  
Vol 10 (25) ◽  
pp. 123
Author(s):  
Maria Alejandra Vallejo-Johnson ◽  
Patricia Marcial-Velastegui
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neuronal Damage ◽  
The Body ◽  
Daily Routine ◽  
Stressful Situation ◽  
The Individual ◽  
Stress Influences ◽  
The Brain

Existen diversos estudios que proponen las causas de la Enfermedad de Alzheimer (EA), las cuales pueden ser: biológicas, genéticas, cronológicas y ambientales, dentro de ésta última se encuentra el estrés como una influencia para el inicio de dicha patología. Según las distintas teorías del estrés, el sujeto, al encontrarse frente a una situación estresante, sufre diversos cambios en su cuerpo para sobrellevar dicho acontecimiento. El cerebro es el encargado de poner al cuerpo en alerta y en marcha para actuar frente a dicho cambio. El estrés prolongado conlleva a alteraciones en las vías cerebrales, específicamente un daño neuronal del hipocampo, el cual es el encargado de los recuerdos y memoria. Éste al verse afectado, repercute en la memoria del sujeto y por lo tanto empieza a fallar; el sujeto se ve en la incapacidad para recordar y realizar distintas actividades rutinarias. Mediante la investigación documental y encuestas a profesionales de la salud, se obtuvo información tanto del estrés como de la Enfermedad de Alzheimer para luego concluir en la influencia del mismo en el origen de la enfermedad. Se concluye que el estrés perenne repercute en la muerte de neuronas del hipocampo lo que conlleva a la EA. AbstractThere are different studies that propose that the causes of Alzheimer might be biological, genetic, chronological and environmental. Within the environmental aspects, the stress influences the beginning of this pathology. There are several studies that propose the causes of Alzheimer's disease (AD), which can be: biological, genetic, chronological and environmental, within the latter is the stress that influences the beginning of this pathology. According to different theories of stress, the individual, while facing a stressful situation, experiences many changes in the body in order to deal with this situation. The brain is in charge of alerting the body to protect itself against that change. The long-term stress alters the brain pathways, producing specifically a neuronal damage in the hippocampus that is responsible for memories and memory. This affects memory and therefore individual begins to fail, and then, the person cannot remember how to do the daily routine. Through bibliographical research and surveys applied to healthcare professionals, information was obtained on both stress and Alzheimer's disease to establish the influence of that condition on the disease. The study concludes that long-term stress affects the death of neurons in the hippocampus, which leads to AD.

The contribution of astrocytes to Alzheimer's disease

2014 ◽  
Vol 42 (5) ◽  
pp. 1316-1320 ◽  
Author(s):  
Amy M. Birch
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Current Evidence ◽  
Amyloid Β Peptide ◽  
Substantial Evidence ◽  
Supporting Cells ◽  
Pathological Conditions ◽  
The Brain

Astrocytes were historically classified as supporting cells; however, it is becoming increasingly clear that they actively contribute to neuronal functioning under normal and pathological conditions. As interest in the contribution of neuroinflammation to Alzheimer's disease (AD) progression has grown, manipulating glial cells has become an attractive target for future therapies. Astrocytes have largely been under-represented in studies that assess the role of glia in these processes, despite substantial evidence of astrogliosis in AD. The actual role of astrocytes in AD remains elusive, as they seem to adopt different functions dependent on disease progression and the extent of accompanying parenchymal inflammation. Astrocytes may contribute to the clearance of amyloid β-peptide (Aβ) and restrict the spread of inflammation in the brain. Conversely, they may contribute to neurodegeneration in AD by releasing neurotoxins and neglecting crucial metabolic roles. The present review summarizes current evidence on the multi-faceted functions of astrocytes in AD, highlighting the significant scope available for future therapeutic targets.

scholarly journals Can Porphyromonas gingivalis Contribute to Alzheimer’s Disease Already at the Stage of Gingivitis?

2021 ◽  
pp. 1-5
Author(s):  
Ingar Olsen
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Porphyromonas Gingivalis ◽  
Blood Stream ◽  
Brain Inflammation ◽  
Periodontal Pathogens ◽  
M1 Phase ◽  
Supragingival Plaque ◽  
The Brain

Alzheimer’s disease (AD) has been associated with periodontitis, which starts as gingivitis. Similar to periodontitis, gingivitis bacteria, bacterial products, and inflammatory mediators can travel to the brain via the blood stream and promote brain inflammation. Periodontal pathogens such as Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, both associated with AD, have been found in dental plaque of children already at the age of 3. It is suggested that these bacteria during long-term exposure may drive microglia (brain resident macrophage cells) into a pro-inflammatory M1 phase where they contribute to AD rather than protect against it. This notion comes from studies in mice showing that microglia actually can “remember” previous inflammatory challenge and become “trained” or “tolerant” to toxins like lipopolysaccharide. If gingivitis has an impact on AD, which should be verified, AD prophylaxis should start already at this pre-periodontitis stage with removal of supragingival plaque.

scholarly journals Biomarkers to Evaluate Androgen Deprivation Therapy for Prostate Cancer and Risk of Alzheimer’s Disease and Neurodegeneration: Old Drugs, New Concerns

2021 ◽  
Vol 11 ◽  
Author(s):  
Vérane Achard ◽  
Kelly Ceyzériat ◽  
Benjamin B. Tournier ◽  
Giovanni B. Frisoni ◽  
Valentina Garibotto ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cancer Patients ◽  
Androgen Deprivation Therapy ◽  
Androgen Deprivation ◽  
Cortical Activation ◽  
Current Evidence ◽  
The Impact

Androgen deprivation therapy (ADT) is a standard treatment for prostate cancer patients, routinely used in the palliative or in the curative setting in association with radiotherapy. Among the systemic long-term side effects of ADT, growing data suggest a potentially increased risk of dementia/Alzheimer’s disease in prostate cancer patients treated with hormonal manipulation. While pre-clinical data suggest that androgen ablation may have neurotoxic effects due to Aβ accumulation and increased tau phosphorylation in small animal brains, clinical studies have measured the impact of ADT on long-term cognitive function, with conflicting results, and studies on biological changes after ADT are still lacking. The aim of this review is to report on the current evidence on the association between the ADT use and the risk of cognitive impairment in prostate cancer patients. We will focus on the contribution of Alzheimer’s disease biomarkers, namely through imaging, to investigate potential ADT-induced brain modifications. The evidence from these preliminary studies shows brain changes in gray matter volume, cortical activation and metabolism associated with ADT, however with a large variability in biomarker selection, ADT duration and cognitive outcome. Importantly, no study investigated yet biomarkers of Alzheimer’s disease pathology, namely amyloid and tau. These preliminary data emphasize the need for larger targeted investigations.

scholarly journals Recovery of Dementia Syndrome following Treatment of Brain Inflammation

2020 ◽  
Vol 10 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Jong-hoon Lee ◽  
Su-hee Choi ◽  
Chul Joong Lee ◽  
Sang-suk Oh
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Cell ◽  
Brain Inflammation ◽  
Japanese Study ◽  
Long Period ◽  
Dementia Syndrome ◽  
Leprosy Patients ◽  
The Brain

Aim/Background: This research aims to prevent progression from mild cognitive impairment (MCI) to Alzheimer’s disease. A Japanese study of leprosy patients revealed that the incidence of dementia in leprosy patients was lower than that in patients taking dapsone who had never been treated. But a similar study the following year refuted the finding of less dementia in leprosy patients taking dapsone. According to conflicting reports, Mycobacterium leprae was a factor in reducing the incidence of Alzheimer’s disease. Thus, we formed a hypothesis that if dapsone is administered to patients without leprosy but with MCI and the prophylactic effect of dementia syndrome is observed over a long period of time, we can determine whether dapsone can prevent the progression of MCI to dementia syndrome. If dementia does not occur after treating inflammation in brain cells while dementia develops after a certain long-term period (usually within 2–3 years), brain cell inflammation can be demonstrated as the cause of dementia. Methods: This is a prospective cohort research. We report on an elderly patient diagnosed with MCI from February 2008 to January 2019. The patient took dapsone 100 mg once a day from 2010 to 2015 for the treatment of MCI. Since 2016, the production of dapsone has ceased in Korea. In June 2018, the patient was diagnosed with Alzheimer’s disease. The patient took Aricept for the treatment of Alzheimer’s disease but complained of serious side effects. And dapsone was re-administered to the patient from November 2018. Results: The patient recovered to MCI and improved her daily life owing to the treatment with dapsone. The drug controls the inflammatory response in the brain, irrespective of whether proteins are deposited in neurons. Conclusions:This finding means that dementia syndrome is an inflammatory disease. This research suggests that diagnostic criteria for Alzheimer’s disease should be based on the presence or absence of inflammation in neurons. Because inflammation in neurons can occur in middle age due to various causes, we can treat inflammation in neurons and prevent and treat dementia syndrome, including Alzheimer’s disease.

scholarly journals ABCA7 and Pathogenic Pathways of Alzheimer’s Disease

2018 ◽  
Vol 8 (2) ◽  
pp. 27 ◽  
Author(s):  
◽  
◽  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Association Studies ◽  
Amyloid Β ◽  
Current Evidence ◽  
Genome Wide Association Studies ◽  
In Vivo Models ◽  
Peripheral Tissues ◽  
Increased Risk ◽  
The Brain

The ATP-binding cassette (ABC) reporter family functions to regulate the homeostasis of phospholipids and cholesterol in the central nervous system, as well as peripheral tissues. ABCA7 belongs to the A subfamily of ABC transporters, which shares 54% sequence identity with ABCA1. While ABCA7 is expressed in a variety of tissues/organs, including the brain, recent genome-wide association studies (GWAS) have identified ABCA7 gene variants as susceptibility loci for late-onset Alzheimer’s disease (AD). More important, subsequent genome sequencing analyses have revealed that premature termination codon mutations in ABCA7 are associated with the increased risk for AD. Alzheimer’s disease is a progressive neurodegenerative disease and the most common cause of dementia, where the accumulation and deposition of amyloid-β (Aβ) peptides cleaved from amyloid precursor protein (APP) in the brain trigger the pathogenic cascade of the disease. In consistence with human genetic studies, increasing evidence has demonstrated that ABCA7 deficiency exacerbates Aβ pathology using in vitro and in vivo models. While ABCA7 has been shown to mediate phagocytic activity in macrophages, ABCA7 is also involved in the microglial Aβ clearance pathway. Furthermore, ABCA7 deficiency results in accelerated Aβ production, likely by facilitating endocytosis and/or processing of APP. Taken together, current evidence suggests that ABCA7 loss-of-function contributes to AD-related phenotypes through multiple pathways. A better understanding of the function of ABCA7 beyond lipid metabolism in both physiological and pathological conditions becomes increasingly important to explore AD pathogenesis.

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