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 the most common cause of dementia and a great socioeconomic burden in the aging society.
Why it matters
This review describes evidence that oxidative stress and amyloid beta changes begin decades before clinical dementia, and discusses possible therapies targeting oxidant/antioxidant imbalance and blood-based biomarkers for early diagnosis. These are prospects for future research, not established treatments or cures for Alzheimer's disease.
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Brain aging is central to late-onset Alzheimer's disease (LOAD), although the mechanisms by which it occurs at protein or cellular levels are not fully understood.
Why it matters
This review describes how aging affects the handling of amyloid-β and tau proteins, and how microglia carry out non-autonomous clearance of protein aggregates. It frames microglia as central players in Alzheimer's disease biology but offers no treatment or cure.
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Astrocytes are glial cells that are distributed throughout the central nervous system in an arrangement optimal for chemical and physical interaction with neuronal synapses and brain blood supply vessels.
Why it matters
This review describes how astrocytes normally support brain function and how amyloid beta is associated with astrocyte dysfunction in Alzheimer's disease. It does not report a specific treatment, cure, or prevention for Alzheimer's disease.
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A novel amyloid β (Aβ) synthetic peptide vaccine (UB-311) has been evaluated in a first-in-human trial with patients of mild-to-moderate Alzheimer's disease.
Why it matters
This report describes the design, preclinical testing, and phase-I trial of UB-311, an amyloid beta peptide vaccine for mild-to-moderate Alzheimer's disease, which is advancing into a phase-II trial. It is early-stage vaccine development and does not establish that UB-311 treats, cures, or prevents Alzheimer's disease.
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Memory loss in Alzheimer's disease (AD) is attributed to pervasive weakening and loss of synapses.
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Triggering receptor expressed on myeloid cells 2 (TREM2) and apolipoprotein E (APOE) are genetically linked to Alzheimer's disease.
Why it matters
In engineered reporter cells, this lab study found that human ApoE acted as an "agonist to human TREM2 with EC 50 in the low nM range" (it switched the receptor on at low concentrations) and acted on mouse TREM2 "with reduced potency." It links two genes tied to Alzheimer's risk in a single signalling step. It is a cell-based experiment, not a study in patients or a treatment trial.
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Chronic psychosocial stress is increasingly recognized as a risk factor for late-onset Alzheimer's disease (LOAD) and associated cognitive deficits.
Why it matters
This paper proposes that chronic psychosocial stress may raise the risk of late-onset Alzheimer's disease by priming microglia and triggering inflammation. It is a review of existing evidence, not a trial, so it does not show that reducing stress prevents or treats the disease.
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Rey's Auditory Verbal Learning Test (RAVLT) is a powerful neuropsychological tool for testing episodic memory, which is widely used for the cognitive assessment in dementia and pre-dementia conditions.
Why it matters
A machine learning model estimated scores on a verbal learning and memory test from MRI scans of the brain, with moderate accuracy, in a group that included people with Alzheimer's disease, mild cognitive impairment, and healthy subjects. This is a research finding about predicting test scores from scans, not a treatment or cure.
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Physical exercise may have some effect on cognition in patients with Alzheimer disease (AD).
Why it matters
This study found that 16 weeks of moderate- to high-intensity physical exercise did not change cerebrospinal fluid amyloid beta or tau concentrations in patients with Alzheimer's disease. It plainly shows no effect of exercise on these biomarkers and does not demonstrate that exercise treats or prevents the disease.
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Stroke is a brain disease that occurs when blood flow stops, resulting in reduced oxygen supply to neurons.
Why it matters
This review describes molecular links between stroke and vascular dementia and Alzheimer's disease, noting that ischemic stroke is a major risk factor for both. It summarizes research findings rather than testing a treatment.
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The study of brain networks by resting-state functional magnetic resonance imaging (rs-fMRI) is a promising method for identifying patients with dementia from healthy controls (HC).
Why it matters
Combining graph measures from resting-state fMRI with machine learning classified healthy controls, mild cognitive impairment, and Alzheimer's disease with reported accuracies of 88.4% for three groups and 72.0% for identifying MCI. The authors state this approach may assist in diagnosis, not treatment, cure, or prevention.
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We aimed to identify new candidate genes potentially involved in early-onset Alzheimer's disease (EOAD).
Why it matters
This study identified rare TYROBP genetic variants in some patients with early-onset Alzheimer's disease. It points to a possible genetic contributor but does not test any treatment, cure, or prevention.
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Observations Genotype-phenotype correlations of AD are presented to provide a comprehensive appreciation of the spectrum of disease causation.
Why it matters
This review covers the genomics of Alzheimer's disease and discusses DNA amyloid beta 42 vaccination as a potential therapy. It is a review of existing knowledge and does not report that any vaccine or genetic treatment works in patients.
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These findings lay groundwork to enable AD clinical trials with characterization and disease-specific tracking of DS adults.
Why it matters
In 12 non-demented adults with Down syndrome, imaging showed distinctive patterns of glucose metabolism and brain volume that could separate Down syndrome and Alzheimer's disease effects. This lays groundwork for clinical trials but does not itself treat, cure or prevent Alzheimer's disease.
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Alzheimer's disease (AD) is a progressive, neurodegenerative disease and the most common form of dementia in elderly people.
Why it matters
This review describes genetic findings in Alzheimer's disease, including mutations in APP, PSEN1, and PSEN2 that cause early-onset AD, the apolipoprotein E-ε4 allele as a risk factor for late-onset AD, and over 20 genetic loci associated with late-onset AD. It is an overview of genetic research and states that understanding these mechanisms may lead to novel treatment, but no treatment, cure, or prevention is tested.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most common form of dementia.
Why it matters
This review discusses DNA damage and altered DNA repair capacity in relation to Alzheimer's disease, alongside the known genetic causes of familial and sporadic forms. It describes mechanisms and reports no treatment, cure or prevention.
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45/100
We report the case of a 73-year-old male patient with Alzheimer's disease who underwent 10-daily transcranial direct current stimulation (tDCS) sessions. tDCS was applied over the left dorsolateral prefrontal cortex as an adjuvant to the traditional treatment that the patient was receiving, which consisted of anticholinergic medication and cognitive training.
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We developed a biochemical/bioinformatics pipeline to optimize the handling of complex interactions between variables in validating biochemical markers of disease.
Why it matters
This study used data from the Alzheimer's Disease Neuroimaging Initiative and an independent test cohort to build machine learning models incorporating CSF complement 3 and factor H levels. Introduction of these levels reproducibly improved the distinction between mild cognitive impairment and mild Alzheimer's disease stages, suggesting they may reflect stage-associated biomarker changes.
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Cognitive impairment in patients with Alzheimer's disease (AD) is associated with reduction in hippocampal volume in magnetic resonance imaging (MRI).
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Diabetes is a risk factor for Alzheimer disease (AD).
Why it matters
This review describes how disruptions in lipid and glucose metabolism affect the production and clearance of amyloid-beta and tau phosphorylation, and can lead to nerve cell damage. It argues that understanding how fat and sugar metabolism interact is needed to explain the disease and to develop future treatments.
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Alzheimer's disease (AD), the most common neurodegenerative disorder associated with dementia, is typified by the pathological accumulation of amyloid Aβ peptides and neurofibrillary tangles (NFT) within the brain.
Why it matters
This paper proposes that oxidative stress, inflammation and altered cholesterol metabolism contribute to Alzheimer's disease progression, with lipid peroxidation and cholesterol oxidation forming products such as 4-hydroxynonenal and oxysterols. It presents a proposed mechanism rather than evidence that targeting cholesterol oxidation treats or prevents the disease.
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Amyloid-β plaques and neurofibrillary tangles are the main neuropathological hallmarks in Alzheimer's disease (AD), the most common cause of dementia in the elderly.
Why it matters
This review summarizes research on neuroinflammation and its connections to Alzheimer's disease, including blood-brain barrier dysfunction and microglial and astrocyte responses. As a review of existing knowledge, it offers no new treatment, cure or prevention.
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Alzheimer disease (AD) is a primary cause of cognitive dysfunction in the elderly population worldwide.
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Mild cognitive impairment (MCI) is considered to be an early stage in the progression of Alzheimer's disease (AD) providing an opportunity to investigate brain pathogenesis prior to the onset of dementia.
Why it matters
In postmortem brain tissue, people in early stages of Alzheimer's disease had significantly fewer synapses in the posterior cingulate gyrus than people with no cognitive impairment, and those with mild cognitive impairment had synapse numbers in between. This is a tissue study describing brain changes, not a test of any treatment, cure, or prevention.
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Since the original publication describing the illness in 1907, the genetic understanding of Alzheimer's disease (AD) has advanced such that it is now clear that it is a genetically heterogeneous condition, the subtypes of which may not uniformly respond to a given intervention.
Why it matters
This review argues that Alzheimer disease is genetically heterogeneous, so subtypes may not respond the same way to a given treatment. It recommends that trials account for genetic differences but reports no treatment or prevention result itself.
From across this topic
9 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 9. The same 9 appear here every time.
- CHMP2B p.Ala30Ser Variant in Biomarker-Confirmed Early-Onset Alzheimer Disease: A Potential Endolysosomal Disease Modifier
- Effects of multiple genetic loci on age at onset in late-onset Alzheimer disease: a genome-wide association study
- Association Between Decline in Cognitive Processing Speed and CSF Amyloid‐β 42/40 in Cognitively Healthy Older Adults Aged 70, Followed over 5 to 7 Years: Data from the Gothenburg H70 Birth Cohort Study
- Exploring the Role of microRNAs as Blood Biomarkers in Alzheimer’s Disease and Frontotemporal Dementia
- Role for glyoxalase I in Alzheimer's disease
- The Addenbrooke's Cognitive Examination Revised (ACE-R): a brief cognitive test battery for dementia screening
- RAGE and amyloid-β peptide neurotoxicity in Alzheimer's disease
- Posterior Cortical Atrophy Due to Alzheimer Disease in a Person With Down Syndrome: A Case Report
- Neuropharmacology of Alzheimer Disease