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.
-
Quinoa is an ancient Andean crop with a significant interest due to its nutritional and health benefits.
Why it matters
This laboratory study analyzed chemicals in quinoa grains and found that certain compounds were associated with inhibition of an enzyme called AChE. This is early, preliminary work and does not show that quinoa or its compounds can treat, cure, or prevent Alzheimer's disease in people.
-
Reimbursement decisions for new Alzheimer's disease (AD) treatments are informed by economic evaluations.
Why it matters
This paper describes a new open-source model framework for health-economic evaluation of early Alzheimer's disease treatment, using lecanemab as an example. It does not test any treatment, cure, or prevention, but provides a tool for cross-validating economic models.
-
We demonstrated a moderate positive correlation between PDGFRβ and both total Tau and phosphorylated Tau 181 in cognitively normal individuals.
Why it matters
In 36 cognitively normal volunteers, higher CSF PDGFRβ, a marker of pericyte injury, correlated with higher total tau and phosphorylated tau 181 but not with amyloid measures. This is a small cross-sectional biomarker study and does not test any treatment, cure or prevention.
-
We enrolled 69 individuals diagnosed with Lewy body dementia (LBD), comprising both dementia with Lewy bodies (DLB) (n = 36) and Parkinson's disease dementia (PDD) (n = 33).
Why it matters
Among 69 people with Lewy body dementias, those with likely Alzheimer's-type copathology based on spinal fluid markers were compared for neuropsychiatric symptoms. This describes how pathology relates to symptoms and does not test any treatment.
-
Using a large and diverse community‐based cohort, we demonstrate that ethno‐racial differences in AD‐specific plasma biomarkers are, in part, due to modifiable health and comorbidity factors.
Why it matters
This study assessed ethno-racial differences in plasma amyloid, tau and neurodegeneration biomarkers of Alzheimer's disease and whether structural and social determinants of health and comorbidities mediate these differences. It found that plasma Aβ42 was significantly lower in Mexican Americans compared to non-Hispanic Whites, and that Mexican Americans had greater BMIs and history of diabetes, both associated with lower plasma Aβ42 levels.
-
The blood-brain barrier (BBB) is a unique and selective feature of the central nervous system's vasculature.
-
Alzheimer's disease (AD) is one of the most common neurodegenerative disorders associated with age or inherited mutations.
-
Blood cadmium, lead, neurofilament light (NfL) chain, total tau (TTau), and amyloid beta (Aβ) 40 and Aβ42 concentrations were measured in 1516 participants in the Beaver Dam Offspring Study.
Why it matters
In 1516 participants, higher blood cadmium and lead levels in women were associated with changes in blood markers of neurodegeneration over 10 years. This links exposure to markers but does not show that avoiding these metals prevents Alzheimer's disease.
-
43/100
Alzheimer's disease (AD) is a brain disorder that progressively undermines memory and thinking skills by affecting the hippocampus and entorhinal cortex.
-
This study provides genetic evidence supporting the potential therapeutic benefits of targeting the three druggable genes for AD treatment, which will be useful for prioritising AD drug development.
-
The accumulated evidence on increased levels of inflammatory markers in the cerebrospinal fluid (CSF) of AD patients, along with reports describing CNS alterations caused by senescent immune cells in neuro-degenerative diseases, set out a conceptual framework in which the neuroinflammation hypothesis is being challenged from different angles towards developing new therapies against AD.
-
Amyloid-β (Aβ) deposition in the brain parenchyma is one of the pathological hallmarks of Alzheimer disease (AD).
Why it matters
This laboratory work identified ADAMTS4 as an enzyme involved in producing the APP669-711 fragment used in a plasma biomarker, and knockout of ADAMTS4 reduced its production in cells and mouse plasma. It is about how a biomarker is generated, not a treatment or cure.
-
These results suggest that both current physical activity and levels of amyloid can be important predictors of spatial navigation skills.
Why it matters
In this small study of cognitively normal adults, higher amyloid levels were linked to worse performance on a spatial navigation task, and greater physical activity was linked to better learning, but physical activity did not change the relationship between amyloid and learning. Spatial navigation performance did not predict later tau or amyloid levels, so it is unclear whether this task can be used to track Alzheimer's disease progression.
-
Fifty-two papers were finally retained after screening.
-
Alzheimer's disease (AD) was used to describe pre-senile dementia to differentiate it from senile dementia, which develops in the adult age group of more than 65 years.
-
Incorporating AD blood tests into screening for AD clinical trials may reduce the time and financial cost of enrollment.
Why it matters
A modeling study found that adding an Alzheimer's blood test at any point in screening for clinical trials reduced the time and financial cost of enrollment compared with using amyloid PET alone. This is about making trials faster and cheaper to run, not about treating, curing or preventing Alzheimer's disease.
-
Our comprehensive search yielded 5 eligible studies.
Why it matters
This review of five randomized trials found all of them were at high risk of bias, and the overall quality of evidence for the cognitive measures was rated very low. Because of this, the evidence is not strong enough to show that Bacopa monnieri helps treat dementia due to Alzheimer's disease.
-
Alzheimer's disease (AD) is a progressive neurodegenerative disease and is closely associated with the accumulation of β-amyloid (Aβ) and neurofibrillary tangles (NFTs).
Why it matters
This review describes how pathogenic proteins such as extracellular Aβ plaques and hyperphosphorylated tau induce the transformation of ramified microglia, and how Alzheimer's patients show widespread microglial activation with elevated pro-inflammatory cytokines. It discusses microglia-based therapies as an implication but reports no treatment tested in patients.
-
Alzheimer's disease (AD) constitutes the most prominent form of dementia among elderly individuals worldwide.
-
PBM treatment significantly improved the typical AD pathologies of memory loss, amyloid plaques, tau hyperphosphorylation, neuronal degeneration, spine damage, and synaptic loss.
-
Alzheimer's disease (AD) incidence is increasing worldwide at an alarming rate.
-
43/100
Alzheimer disease (AD) is a neurodegenerative disorder characterized pathologically by the presence of neurofibrillary tangles and amyloid beta (Aβ) plaques in the brain.
Why it matters
This review covers the history of Alzheimer's disease neuropathology research, including microscopy, staining, diagnostic criteria, and co-pathologies, and notes there is still no cure. It discusses future phenotyping approaches and does not report any treatment, cure, or prevention.
-
Subtle changes in objective spatial navigation ability have been observed in the preclinical stage of Alzheimer disease (AD) cross-sectionally and have been found to predict clinical progression.
Why it matters
This longitudinal study found limited change over time in people's self-reported spatial navigation ability in the preclinical stage of Alzheimer's disease. It is about a self-reported symptom measure, not about treating, curing or preventing the disease.
-
Alzheimer's disease (AD) is a major cause of dementia in older adults and is fast becoming a major societal and economic burden due to an increase in life expectancy.
-
43/100
Here, we found a close association of the metabolic reconfiguration of microglia with increased hippocampal glucose uptake on [ 18 F]fluorodeoxyglucose (FDG) PET.
Why it matters
In a 5xFAD mouse model, the study linked microglial metabolic reconfiguration with increased hippocampal glucose uptake on FDG PET. This is animal research and does not yet provide a treatment for Alzheimer's 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.
- Electromagnetic signatures of the preclinical and prodromal stages of Alzheimer's disease
- Discriminative Accuracy of [18F]flortaucipir Positron Emission Tomography for Alzheimer Disease vs Other Neurodegenerative Disorders
- TREM2 and the neuroimmunology of Alzheimer's disease
- Metal dyshomeostasis and oxidative stress in Alzheimer's disease
- Independent validation of the PrecivityAD2 blood test to identify presence or absence of brain amyloid pathology in individuals with cognitive impairment
- Two Randomized Phase 3 Studies of Aducanumab in Early Alzheimer's Disease
- The Alzheimer's Association appropriate use recommendations for blood biomarkers in Alzheimer's disease
- Role of synucleins in Alzheimer's disease
- Associations Between Changes in Levels of Phosphorylated Tau and Severity of Cognitive Impairment in Early Alzheimer Disease
- Exploring the neuromagnetic signatures of cognitive decline from mild cognitive impairment to Alzheimer's disease dementia