Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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BACE1 is the β-secretase enzyme that initiates production of the β-amyloid peptide involved in Alzheimer disease.
Why it matters
BACE1-deficient mice showed axon guidance defects in the hippocampus as well as the olfactory bulb, suggesting that blocking BACE1 therapeutically may not be free of side effects. This is animal work and reports no treatment, cure or prevention for people.
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The amyloid β (Aβ) peptide, which is abundantly found in the brains of patients suffering from Alzheimer disease, is central in the pathogenesis of this disease.
Why it matters
This laboratory work shows that the enzyme meprin β can cut the amyloid precursor protein in a way similar to β-secretase, producing shortened amyloid β peptides. It is early, cell-based research and does not by itself show any treatment, cure, or prevention for Alzheimer's disease.
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The activation of the immune system in neurodegeneration has detrimental as well as beneficial effects.
Why it matters
This study examines the immune response after acute peripheral nerve injury in a Wallerian degeneration model. It concerns peripheral nerve injury, not Alzheimer's disease treatment or prevention.
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Anatomical lesions in Alzheimer disease-affected brains mainly consist of senile plaques, inflammation stigmata, and oxidative stress.
Why it matters
This study examined how nuclear factor-κB regulates beta-amyloid precursor protein and the beta- and gamma-secretases at physiological versus supraphysiological amyloid-beta concentrations. It is experimental cell work on disease mechanisms and does not provide a treatment or prevention for patients.
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Parkinson's disease (PD) is a multisystem neurodegenerative disorder.
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Accumulating evidence suggests that some dietary patterns, specifically high fat diet (HFD), increase the risk of developing sporadic Alzheimer disease (AD).
Why it matters
In amyloid precursor protein transgenic mice, exercise was more effective than diet control in preventing high fat diet-induced amyloid-beta deposition and memory deficit. This is animal work and does not establish the same effect in people.
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Oxidative stress is a key pathologic factor in neurodegenerative diseases such as Alzheimer and Parkinson diseases (AD, PD).
Why it matters
This review argues that overactivated phagocyte NADPH oxidase contributes to chronic neuroinflammation and neurodegeneration, and that blocking it might be a therapeutic target. It is based on preclinical evidence, so no NADPH oxidase treatment has been shown to work in people with Alzheimer's disease.
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Biochemical and genetic evidence establishes a central role of the amyloid precursor protein (APP) in Alzheimer disease (AD) pathogenesis.
Why it matters
This review summarizes evidence that amyloid precursor protein and its processing products are central to Alzheimer's disease pathogenesis and that APP mutations and duplications cause some early-onset familial cases. It is a review of existing knowledge and does not report a new treatment, cure or prevention.
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Various experimental models are used to study brain development and degeneration.
Why it matters
This describes a laboratory microfluidic platform using asymmetric micro-channels to build oriented neuronal networks, including a cortico-striatal network with functional synapses. It is a cell-culture method with no direct testing in Alzheimer disease and no treatment implications.
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It has long been assumed that β-amyloid (Aβ) had to assemble into fibrillar amyloid plaques to exert its neurotoxic effects in Alzheimer disease.
Why it matters
In double-transgenic APP-tau mice, brain oligomeric amyloid-beta but not total plaque burden correlated with neuronal loss and astrocyte inflammatory response. This is animal evidence about which form of amyloid-beta relates to damage and does not test a treatment in people.
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Apolipoprotein (apo) E4 is the major genetic risk factor for Alzheimer disease (AD) and likely contributes to neuropathology through various pathways.
Why it matters
In cells and neurons, apolipoprotein E4 showed impaired intracellular trafficking compared with apolipoprotein E3, and small-molecule structure correctors rescued the detrimental effects. These are laboratory findings, so it is not yet known whether such correctors would help people with Alzheimer's disease.
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A 7-min window, corresponding to minutes 1-8 (frames 5-15), produced the highest voxelwise correlation between (18)F-FDG and pPIB (R = 0.78 ± 0.05).
Why it matters
This study found that early 11C-PIB PET frames provided information comparable to 18F-FDG PET for measuring brain perfusion or metabolism in people with Alzheimer's disease or frontotemporal lobar degeneration. It is about improving dementia diagnosis with imaging, not about treating, curing, or preventing Alzheimer's disease.
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45/100
Individuals with Down syndrome (DS) will inevitably develop Alzheimer disease (AD) neuropathology sometime after middle age, which may be attributable to genes triplicated in individuals with DS.
Why it matters
This study found that the RCAN1 protein is elevated in the cortex of Down syndrome and Alzheimer's disease patients and that overexpressing RCAN1-1 in primary neurons activates caspase-9 and caspase-3 and causes neuronal apoptosis. It proposes a mechanism by which RCAN1 contributes to stress- and amyloid beta-induced neuronal death, but it is laboratory work and identifies no treatment.
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Cerebral atrophy, detected as ventricular enlargement or sulcal widening on MRI, is recognized as a risk factor for vascular dementia or Alzheimer disease.
Why it matters
This prospective population-based study of 810 middle-aged people examined whether retinal microvascular signs predict ventricular enlargement or sulcal widening on MRI over about 10 years. It is observational, so it cannot show that treating retinal changes would prevent cerebral atrophy or dementia.
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Recent studies have suggested that children undergoing surgery under anesthesia could be at an increased risk for the development of learning disabilities, but whether anesthetics contribute to this learning disability is unclear.
Why it matters
In this animal study, sevoflurane anesthesia caused neurotoxicity that differed between newborn normal mice and Alzheimer's disease transgenic mice, with effects measured on caspase activation, apoptosis, beta-amyloid levels, and neuroinflammation. These are findings in mice and do not establish how sevoflurane affects the risk of Alzheimer's disease in people.
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Oxidative stress induced by inhibition of glutathione (GSH) biosynthesis with D,L-buthionine-S,R-sulfoximine (BSO) causes human microglia, human astrocytes, THP-1 cells, and U373 cells to secrete materials toxic to human neuroblastoma SH-SY5Y cells and stimulates them to release TNF-alpha, IL-6, and nitrite ions.
Why it matters
This laboratory study found that depleting glutathione in human glial cells caused them to release substances toxic to nerve cells and to activate inflammatory pathways, effects that were reduced by glutathione or clotrimazole. This is early cell-based research and does not yet show whether these findings would treat or prevent Alzheimer's disease in people.
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Progressive supranuclear palsy-parkinsonism (PSP-P) is a primary tauopathy characterised by neurofibrillary degeneration, which is frequently mistaken for Parkinson's disease (PD), multiple system atrophy (MSA), and vascular parkinsonism (VP) at presentation.
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The discordant topography between atrophy and hypometabolism reported in AD is already present at the aMCI stage.
Why it matters
In patients with amnestic mild cognitive impairment, those who later converted to Alzheimer's disease showed different patterns of brain shrinkage and reduced metabolism than those who did not. Posterior cingulate-precuneus hypometabolism appeared early, while left temporal hypometabolism marked conversion, but this does not test any treatment.
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45/100
TDP-43 is an RNA/DNA-binding protein implicated in transcriptional repression and mRNA processing.
Why it matters
This laboratory study in cells found that silencing TDP-43 lowers histone deacetylase 6, a finding relevant to frontotemporal dementia and ALS rather than Alzheimer's disease. It is early, cell-based work and reports nothing about treating, curing or preventing Alzheimer's disease.
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Ectopic cell cycle events (CCEs) mark vulnerable neuronal populations in human Alzheimer disease (AD) and are observed early in disease progression.
Why it matters
In the R1.40 transgenic mouse model of Alzheimer's disease, two different nonsteroidal anti-inflammatory drugs prevented but did not reverse neuronal cell cycle reentry. This is mouse work, and it found prevention but not reversal, so it does not show a treatment that helps people with existing disease.
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45/100
As they mix together, they become purple.2 According to a few previous reports, PUBS often occurred in elderly women who are bedridden, chronically catheterized, and constipated.3 In addition, PUBS was found in alkaline urine and with higher bacterial counts.3,4 Because of lack of significant patient numbers, the clinical background, underlining diseases, urinanalysis, and incidence of PUBS have not been well documented.
Why it matters
This study found that chronic kidney disease was the only significant risk factor for purple urine bag syndrome in a case-control study. It does not address treating, curing, or preventing Alzheimer's disease.
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Mutations in the presenilin genes are the main cause of familial Alzheimer's disease.
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Two different macrophage populations contribute to CNS neuroinflammation: CNS-resident microglia and CNS-infiltrating peripheral macrophages.
Why it matters
This study compares gene expression in activated microglia and macrophages to find markers that tell the two cell populations apart. It is a laboratory comparison and does not test any Alzheimer's treatment or prevention.
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A fundamental feature of Alzheimer disease (AD) is the accumulation of beta-amyloid (Abeta), a peptide generated from the amyloid precursor protein (APP).
Why it matters
In this laboratory study, beta-amyloid impaired the movement and function of AMPA receptors at synapses by reducing the synaptic distribution of CaMKII. These findings describe a mechanism of synaptic dysfunction in cells and do not establish any treatment or prevention for Alzheimer's disease.
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About one fourth of Lewy body disease (LBD) patients show cortical beta-amyloid load, basically a hallmark of Alzheimer disease (AD).
Why it matters
This study used brain scans to compare Lewy body disease patients with and without beta-amyloid buildup. It does not test any treatment, cure, or prevention for Alzheimer's disease.
From across this topic
10 of the 4,748 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.
- 0076 Effect of a Tryptophan Enriched Diet on Mood, Cognition, Sleep and Their Associated Neurotransmitters/Hormones in a Mouse Model of Down Syndrome
- The impact of a multi-domain intervention on cerebral glucose metabolism: analysis from the randomized ancillary FDG PET MAPT trial
- Microbial translocation is associated with increased monocyte activation and dementia in AIDS patients
- Mechanistic View of hnRNPA2 Low-Complexity Domain Structure, Interactions, and Phase Separation Altered by Mutation and Arginine Methylation
- The apolipoprotein E epsilon2 allele and the pathological features in cerebral amyloid angiopathy-related hemorrhage
- TIA1 Mutations in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia Promote Phase Separation and Alter Stress Granule Dynamics
- Identifying natural inhibitors against FUS protein in dementia through machine learning, molecular docking, and dynamics simulation
- Parallel compensatory and pathological events associated with tau pathology in middle aged individuals with Down syndrome
- Predictors of non-invasive ventilation tolerance in amyotrophic lateral sclerosis
- Mutations of tau protein in frontotemporal dementia promote aggregation of paired helical filaments by enhancing local beta-structure