Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Download bibliography of all 5,209 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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Alzheimer's disease (AD) is a multifactorial age-related brain disease.
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Alzheimer's disease is the most common form of dementia.
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Alzheimer´s disease (AD) and related forms of dementia are increasingly affecting the aging population throughout the world, at an alarming rate.
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Alzheimer's disease (AD) is the most common form of dementia characterized neuropathologically by senile plaques and neurofibrillary tangles (NFTs).
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Moreover, they exhibit decreased astrocyte and microglial activation markers GFAP and CD68, suggesting that a suppressed neuroinflammatory response may be implicated in human brain resilience to Alzheimer's pathology.
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Emerging evidence indicates that moderate intensity aerobic exercise is positively correlated with cognitive function and memory.
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Prolonged stress predisposes susceptible individuals to a number of physiological disorders including cardiovascular disease, obesity and gastrointestinal disorders, as well as psychiatric and neurodegenerative disorders.
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Aggregation of tau into fibrillar structures within the CNS is a pathological hallmark of a clinically heterogeneous set of neurodegenerative diseases termed tauopathies.
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Since its discovery some hundred years ago, Alzheimer's disease (AD), a neurodegenerative disease and an eminent cause of most dementia, continues to pose problems for affected families and society, especially in developed countries.
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Diverse pathogens are detected in Alzheimer's disease (AD) brains.
Why it matters
This bioinformatics survey found that Alzheimer's risk genes relate to interactomes of many pathogens and that upregulated Alzheimer's hippocampal genes match those upregulated by multiple microbes. It is a data analysis only and reports no treatment, cure or prevention.
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Available drugs for the global Alzheimer disease (AD) epidemic only treat the symptoms without modifying disease progression.
Why it matters
This review examines the status of clinical trials for passive immunotherapy against amyloid-β42, noting that available drugs for Alzheimer's disease only treat symptoms without modifying disease progression. It reviews the trial landscape rather than reporting a successful disease-modifying treatment.
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Like many humans, non-human primates deposit copious misfolded Aβ protein in the brain as they age.
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Biomarkers of the molecular pathology underpinning dementia syndromes are increasingly recognized as crucial for diagnosis and development of disease-modifying treatments.
Why it matters
Amyloid PET is already used in diagnosing Alzheimer disease, and tau PET is expected to help with diagnosis, monitoring and treatment of dementias. Using tau PET to study how tau relates to amyloid and other markers may improve understanding of the process that leads to dementia.
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Alzheimer's disease (AD) is the most common cause of dementia, and its prevalence will increase significantly in the coming decades.
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We will consider also emerging data dealing with potential therapeutic approaches for ameliorating the cognitive and memory deficits associated with these disorders.
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The search for new therapeutic approaches to Alzheimer disease (AD) is a major goal in medicine and society, also due to the impressive economic and social costs of this disease.
Why it matters
In 24-month-old Tg2576 Alzheimer's model mice, REAC RGN-N treatment increased astroglial reaction around amyloid plaques, reduced some microglia-associated neuroinflammation markers, and increased locomotion. This is animal research and does not establish any treatment, cure, or prevention for Alzheimer's disease in people.
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In normal brain, neurons in the cortex and hippocampus produce insulin, which modulates glucose metabolism and cognitive functions.
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Alzheimer disease (AD) primarily affects older adults.
Why it matters
This single case report describes improvement in one patient with advanced Alzheimer's disease in hospice after five brain CT scans over three months. A single case report cannot show that CT scans treat Alzheimer's disease, and no conclusion about curing or preventing the disease can be drawn.
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In the sample studied, music therapy improved some cognitive, psychological, and behavioural alterations in patients with Alzheimer disease.
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Both (18)F-FDG and (11)C-PiB imaging appear to be of limited use for predicting the progression from MCI to dementia due to AD in short-term follow-up, irrespective of the strategy of analysis.
Why it matters
In a small group of 28 people with mild cognitive impairment, visual reading of amyloid PET scans varied a lot between raters but predicted progression to Alzheimer's dementia better than fully automated analysis. This is a small imaging comparison about prediction, not about treating, curing or preventing the disease.
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TAR DNA binding protein 43 kDa (TDP-43), for instance, has been shown to cause frontotemporal dementia as well as some cases of familial ALS, and is associated with frontotemporal dysfunction in ALS.
Why it matters
This review describes ALS and other motor neuron diseases, noting that TDP-43 has been shown to cause frontotemporal dementia as well as some cases of familial ALS. It is a clinical review and does not test any treatment, cure or prevention for Alzheimer's disease.
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38/100
Imaging of brain β-amyloid plaques with (18)F-labeled tracers for PET will likely be available in clinical practice to assist the diagnosis of Alzheimer disease (AD).
Why it matters
Imaging of brain β-amyloid plaques with 18F-labeled tracers for PET will likely become available in clinical practice to assist in diagnosing Alzheimer's disease. Physicians reading these scans will need to understand the complex relationship between amyloid and cognitive decline and how to recognize tracer binding patterns.
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A key challenge to adults with Down syndrome (DS) as they age is an increased risk for cognitive decline, dementia, and Alzheimer disease (AD).
Why it matters
This review notes that by age 40 virtually all people with Down syndrome have enough senile plaques and neurofibrillary tangles for a neuropathological diagnosis of Alzheimer disease, yet clinical dementia signs increase later. It discusses possible contributors to dementia onset but reports no treatment, cure or prevention.
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Prior research has shown that arsenic exposure induces changes that coincide with most of the developmental, biochemical, pathologic, and clinical features of Alzheimer disease (AD) and associated disorders.
Why it matters
This paper proposes the Arsenic Exposure Hypothesis for Alzheimer's disease, suggesting arsenic toxicity induces tau hyperphosphorylation and overtranscription of amyloid precursor protein. It is a hypothesis based on prior literature, not a clinical trial, so it does not show that reducing arsenic exposure treats, cures or prevents Alzheimer's disease.
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In this study, we aimed to compare cerebrospinal fluid (CSF) levels of total tau (t-tau), phosphorylated tau (p-tau(181)) and positron emission tomography with (18)F-fluorodeoxyglucose (FDG-PET) in the differential diagnosis of Alzheimer's disease (AD) under clinical conditions.
Why it matters
In 75 memory clinic patients, spinal fluid phosphorylated tau and FDG-PET performed similarly in separating Alzheimer's dementia from controls. This is a diagnostic comparison and does not address treating or curing the disease.
From across this topic
10 of the 5,172 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Defining the Lowest Threshold for Amyloid-PET to Predict Future Cognitive Decline and Amyloid Accumulation
- Signs and Artifacts in Amyloid PET
- Pathologic accumulation of α-synuclein and Aβ in Parkinson disease patients with dementia
- P3‐429: Response to cholinesterase inhibitor medication at first renewal in a Canadian provincial drug coverage initiative: the British Columbia Alzheimer's Drug Therapy Initiative (BC ADTI) experience
- Aducanumab Use in Symptomatic Alzheimer Disease Evidence in Focus [RETIRED]: A Report of the AAN Guidelines Subcommittee
- Tracking early decline in cognitive function in older individuals at risk for Alzheimer disease dementia: the Alzheimer's Disease Cooperative Study Cognitive Function Instrument
- Magnetic resonance imaging evidence for presymptomatic change in thalamus and caudate in familial Alzheimer's disease
- Random Forest Algorithm for the Classification of Neuroimaging Data in Alzheimer's Disease: A Systematic Review
- Obesity and Alzheimer's disease, does the obesity paradox really exist? A magnetic resonance imaging study
- Cardiovascular risk factors and incident Alzheimer disease: a systematic review of the literature