Prognosis of Alzheimer’s Disease: The Rotterdam Study

Ruitenberg, Annemieke; Kalmijn, Sandra; Ridder, Maria A. J. de; Redekop, William K.; Harskamp, F. van; Hofman, Albert; Launer, Lenore J.; Breteler, Monique M.B.

doi:10.1159/000054786

Cited by 30 publications

(23 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This is because consumption of foods or artificial supplements rich in essential fatty acids may decrease the risk of developing Alzheimer's disease (Ruitenberg et al, 2001;Barberger-Gateau et al, 2002;Morris et al, 2003a, b). …”

Section: Alzheimer's Diseasementioning

confidence: 99%

Neuroprotective and disease-modifying effects of the ketogenic diet

Gąsior¹,

Rogawski²,

Hartman³

2006

Behavioural Pharmacology

396

324

View full text Add to dashboard Cite

The ketogenic diet has been in clinical use for over 80 years, primarily for the symptomatic treatment of epilepsy. A recent clinical study has raised the possibility that exposure to the ketogenic diet may confer long-lasting therapeutic benefits for patients with epilepsy. Moreover, there is evidence from uncontrolled clinical trials and studies in animal models that the ketogenic diet can provide symptomatic and disease-modifying activity in a broad range of neurodegenerative disorders including Alzheimer's disease and Parkinson's disease, and may also be protective in traumatic brain injury and stroke. These observations are supported by studies in animal models and isolated cells that show that ketone bodies, especially β-hydroxybutyrate, confer neuroprotection against diverse types of cellular injury. This review summarizes the experimental, epidemiological and clinical evidence indicating that the ketogenic diet could have beneficial effects in a broad range of brain disorders characterized by the death of neurons. Although the mechanisms are not yet well defined, it is plausible that neuroprotection results from enhanced neuronal energy reserves, which improve the ability of neurons to resist metabolic challenges, and possibly through other actions including antioxidant and anti-inflammatory effects. As the underlying mechanisms become better understood, it will be possible to develop alternative strategies that produce similar or even improved therapeutic effects without the need for exposure to an unpalatable and unhealthy, high-fat diet.

show abstract

Section: Alzheimer's Diseasementioning

confidence: 99%

Neuroprotective and disease-modifying effects of the ketogenic diet

Gąsior¹,

Rogawski²,

Hartman³

2006

Behavioural Pharmacology

396

324

View full text Add to dashboard Cite

show abstract

“…They may also be involved in several neurodegenerative diseases, and modulation of inflammation may contribute to current and future treatments (Gao et al 2011;Heneka et al 2014Heneka et al , 2015In'T Veld et al 2001;Rees et al 2011;Ruitenberg et al 2001). At present, only few drugs are available that reach therapeutically effective levels within the brain and can be tolerated well for prolonged treatment periods.…”

Section: Introductionmentioning

confidence: 99%

Switching from astrocytic neuroprotection to neurodegeneration by cytokine stimulation

et al. 2016

View full text Add to dashboard Cite

were involved in this neurodegeneration. The neurotoxicity-mediating effect of IMA was faithfully reproduced by human astrocytes. Moreover, glia-dependent toxicity was also observed, when IMA cultures were stimulated with CM, and the culture medium was transferred to neurons. Such neurotoxicity was prevented when astrocytes were treated by p38 kinase inhibitors or dexamethasone, whereas such compounds had no effect when added to neurons. Conversely, treatment of neurons with five different drugs, including resveratrol and CEP1347, prevented toxicity of astrocyte supernatants. Thus, the sequential IMA-LUHMES neuroinflammation model is suitable for separate profiling of both glial-directed and directly neuroprotective strategies. Moreover, direct evaluation in co-cultures of the same cells allows for testing of therapeutic effectiveness in more complex settings, in which astrocytes affect pharmacological properties of neurons.Keywords LUHMES · Astrocyte · p38 kinase · Neuroinflammation · Neuropharmacology Abstract Astrocytes, the largest cell population in the human brain, are powerful inflammatory effectors. Several studies have examined the interaction of activated astrocytes with neurons, but little is known yet about human neurotoxicity under such situations and about strategies of neuronal rescue. To address this question, immortalized murine astrocytes (IMA) were combined with human LUHMES neurons and stimulated with an inflammatory (TNF, IL-1) cytokine mix (CM). Neurotoxicity was studied both in co-cultures and in monocultures after transfer of conditioned medium from activated IMA. Interventions with >20 drugs were used to profile the model system. Control IMA supported neurons and protected them from neurotoxicants. Inflammatory activation reduced this protection, and prolonged exposure of co-cultures to CM triggered neurotoxicity. Neither the added cytokines nor the release of NO from astrocytes Liudmila Efremova and Petra Chovancova have contributed equally to this study.

show abstract

“…Cognitive deficits severe enough to interfere with instrumental and basic activities of daily living are a main clinical finding in Alzheimer disease (AD), and once detected at the patient evaluation it might be an indication not only of the possibility of dementia, but also of its severity 1 , though with disease progression tools to evaluate cognition and functionality have limited positive and negative values 2 .…”

Section: Introductionmentioning

confidence: 99%

Correlation and adaptation among functional and cognitive instruments for staging and monitoring Alzheimer?s disease in advanced stages

Wajman¹,

Schultz²,

Marin³

et al. 2014

Rev. psiquiatr. clín.

View full text Add to dashboard Cite

Background: Although Alzheimer's disease (AD) is the most prevalent form of dementia, little is known about cognitive and functional aspects in its advanced stages. Objective: This study aimed the adaptation and correlation among specific instruments for AD in advanced stages with regard to cognition objectively weighted, besides the comparison between static and ecological aspects of functional capacity. Methods: 95 moderate, moderatly severe and severe AD patients (33 men and 62 women) underwent the scales CDR (Clinical for Dementia Rating), FAST (Functional Assessment Scale), MMSE (Mini-Mental State Exame), MMSEsev (Severe Mini-Mental State Examination), SIB-8 (Severe Impairment Battery) and TSI (Test for Severe Impairment), for the comparison with a golden-standard ecological scale the PADL (Performance Activities of Daily Living). Results: The evidence suggests an increasing and statistically significant linear correlation between the ecological functional scale and cognitive tests according to the stratification of AD stages once weighted by static functional scale. Discussion: The results indicate that for patients in advanced stages of AD, appropriate cognitive tests and performance-based functional scales are useful in more accurate assessment of disease staging and monitoring its progression.

show abstract

Prognosis of Alzheimer’s Disease: The Rotterdam Study

Cited by 30 publications

References 31 publications

Neuroprotective and disease-modifying effects of the ketogenic diet

Neuroprotective and disease-modifying effects of the ketogenic diet

Switching from astrocytic neuroprotection to neurodegeneration by cytokine stimulation

Correlation and adaptation among functional and cognitive instruments for staging and monitoring Alzheimer?s disease in advanced stages

Contact Info

Product

Resources

About