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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One of the major consequences of diabetes mellitus that has gained attention due to its rising incidence is cognitive impairment.
Why it matters
In a rat model, empagliflozin combined with memantine improved cognitive performance and changed markers of neuroinflammation and oxidative stress. This is animal research, so it does not show that this drug combination treats or prevents Alzheimer's disease in humans.
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Existing models of frontotemporal dementia (FTD) may not fully recapitulate the pathophysiology of the disease.
Why it matters
Engineered MAPT knockin mouse lines exhibited robust tau pathology, synaptic loss, brain atrophy, and FTD-like behavioral abnormalities, establishing them as valuable models for investigating mechanisms underlying FTD and other tauopathies. These mice provide a relevant platform for in vivo drug screening, based on animal models.
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For diverse neurodegenerative disorders, microglial cells are activated.
Why it matters
This review summarizes how overactive microglia contribute to neuroinflammation and damage in Alzheimer's and other neurodegenerative diseases and discusses potential targets for microglial cell therapy. It identifies possible targets but does not show that any treatment works in patients.
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Tau pathology in the locus coeruleus (LC) is associated with several neurodegenerative conditions including Alzheimer's disease and frontotemporal dementia.
Why it matters
In aged P301S tauopathy mice, locus coeruleus neurons showed reduced excitatory inputs, decreased spontaneous discharge and decreased excitability, though tissue norepinephrine levels did not differ in prefrontal cortex or hippocampus. These are animal findings about brain changes, not a treatment, cure or prevention for Alzheimer's disease.
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In addition to the core clinical features of fluctuating cognition, visual hallucinations, and parkinsonism, individuals with dementia with Lewy bodies (DLB) frequently experience chronic and debilitating major depression.
Why it matters
In post-mortem brain tissue, this study found reduced dopaminergic innervation in the subgenual anterior cingulate cortex of dementia with Lewy bodies cases with depression compared to controls, but not in non-depressed cases. This links dopaminergic changes to depression in this disease but does not test any treatment, cure or prevention.
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In previous studies, we isolated a series of novel gentisides with nerve growth factor (NGF)-mimic activities from Gentiana rigescens Franch and conducted continuous structure–activity relationship (SAR) studies.
Why it matters
In a high-fat diet-induced Alzheimer's disease mouse model, the compound TBG096 improved memory dysfunction and increased mature and newborn neurons in the hippocampus and cortex. This is an animal study, so it does not establish that TBG096 treats Alzheimer's disease in people.
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39/100
Gene-proxy for Graves' disease was associated with an increased risk of major depressive disorder (P-value = 0.02), whereas gene-proxy for autoimmune thyroiditis was linked to a greater risk of bipolar disorder (P-value = 0.043).
Why it matters
This Mendelian randomization study found no evidence of a causal relationship between autoimmune thyroid disease and dementia. It did find links between Graves' disease and major depressive disorder and between autoimmune thyroiditis and bipolar disorder, but these are not dementia outcomes.
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Oculomics is an emerging field that leverages ophthalmic imaging data to identify biomarkers of systemic disease, facilitating early diagnosis and risk stratification.
Why it matters
This review describes how corneal imaging, including with artificial intelligence, might reveal biomarkers of systemic diseases such as dementia. It is a review of a diagnostic approach and does not test any treatment, cure or prevention.
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Salmonellosis in humans is a public health threat and cattle are important reservoirs for the pathogen.
Why it matters
This review discusses sources and control of Salmonella infection in cattle to prevent human salmonellosis. It contains no information on Alzheimer's disease.
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Missense mutations in the amyloid precursor protein (APP) and presenilin-1 (PSEN1) cause early-onset familial Alzheimer’s disease (FAD) and alter proteolytic production of secreted 38-to-43-residue amyloid β-peptides (Aβ) by the PSEN1-containing γ-secretase complex, ostensibly supporting the amyloid hypothesis of pathogenesis.
Why it matters
This study found that six additional PSEN1 familial Alzheimer mutations cause deficiencies in multiple processing steps of APP by γ-secretase and lead to stalled enzyme-substrate or intermediate complexes. The results support the stalled complex hypothesis of familial Alzheimer's pathogenesis, but they are laboratory findings and do not demonstrate a treatment or cure.
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It primarily affects cerebral regions responsible for cognition, memory, and language processing, significantly impeding the functional independence of patients.
Why it matters
The available text only describes that Alzheimer's disease affects brain regions for cognition, memory, and language and impairs independence. It provides no findings on treating, curing, or preventing the disease.
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Lewy bodies and neurofibrillary tangles, composed of α-synuclein (α-syn) and tau, respectively, often are found together in the same brain and correlate with worsening cognition.
Why it matters
This study found that in Lewy body disease, phosphorylated alpha-synuclein rarely colocalized with phosphorylated tau or PAD-tau, though overlap of p-alpha-syn with PAD-tau was associated with LBD. It provides pathological insights but no treatment or cure.
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The rising global prevalence of Alzheimer's disease (AD) and mild cognitive impairment (MCI) underscores the urgent need to elucidate their underlying pathogenic mechanisms.
Why it matters
This small study of 10 Alzheimer's patients, 9 MCI patients, and 10 normal controls found distinct exosomal miRNA profiles across disease stages, with two miRNAs showing superior diagnostic performance. The findings identify potential circulating biomarkers for diagnosis, but the sample is small and no treatment was tested.
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Chronic psychological stress is a well-known risk factor for neurodegenerative diseases including Alzheimer disease (AD), yet the underlying mechanisms remain unclear.
Why it matters
In cell and animal models, the stress hormone corticosterone raised Psen2 and deleting Psen2 prevented corticosterone-induced death of adult hippocampal neural stem cells, but the Psen2 N141I mutation did not worsen this death or behavioral deficits. The authors conclude that the Psen2 N141I mutation alone may not be sufficient to link chronic stress to Alzheimer's disease.
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The human brain is one of the most metabolically active tissues in the body, due in large part to the activity of trillions of synaptic connections.
Why it matters
This review discusses autophagy and mitophagy at the synapse and their links to neurodegenerative diseases including Alzheimer's. It summarizes research in cells and animal models and discusses diagnostic and therapeutic potential, but does not demonstrate any treatment, cure or prevention.
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• APOE4 carriers exhibit cerebrovascular dysfunction. • Endothelial progenitor cells (EPC) represent cell populations involved in facilitating vascular repair. • In APOE4 carriers, EPC colony count is associated with cerebral small vessel disease. • EPC colony count may indicate activation of mechanisms which protect cerebrovascular function in APOE4 carriers prior to the development of cognitive decline.
Why it matters
In APOE4 carriers without dementia, having more endothelial progenitor cell colonies was associated with less cerebral small vessel disease. This is an association in a small group of older adults, so it does not show that boosting these cells would prevent or treat Alzheimer's disease.
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Our results suggest that increased neighborhood deprivation contributes to shorter survival in bvFTD.
Why it matters
In 147 people with behavioral-variant frontotemporal degeneration, living in the most deprived neighborhoods was linked to shorter survival compared with the least deprived neighborhoods. Intermediate deprivation was not significantly linked to survival.
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Treatment strategies that are efficient against established Alzheimer's disease (AD) are needed.
Why it matters
In a mouse model of Alzheimer's disease, giving the chaperone protein rh Bri2 BRICHOS R221E intravenously reduced amyloid plaque burden and markers of brain inflammation, and it normalized the activity of certain plaque-related genes. This is early animal research, so it is not yet known whether the same treatment would be safe or effective in people with advanced Alzheimer's disease.
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Alzheimer's disease (AD) is the most prevalent dementia, affecting a large number of populations.
Why it matters
In rats given amyloid-β 42 fibrils into the hippocampus, oral Bacopa monnieri extract for 4 weeks improved cognitive changes and affected mitochondrial dysfunction and GSK-3β/Wnt/β-catenin signaling. This is animal work, so it does not show that Bacopa monnieri treats, cures or prevents Alzheimer's disease in people.
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The lack of significant results for moderation effects of the targeted epigenetic markers in our pilot study were likely due to the small sample size.
Why it matters
In a preliminary analysis of 32 Mexican American participants, researchers tested whether DNA methylation moderates the effect of neighborhood disadvantage on neurodegenerative biomarkers. The small sample size means these findings are early and cannot yet inform treatment, cure, or prevention.
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Donepezil and silymarin improved lipid profile associated with increased NAA/Cr, and decreased mI/Cr, in AD patients.
Why it matters
In this small trial of 36 patients with mild Alzheimer's disease, silymarin increased levels of LRP1 and Aβ1-42 and improved lipid profile compared with other groups. The study was small and short, and it did not report clear cognitive benefits, so it does not show that silymarin treats Alzheimer's disease.
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This study examines cortical organoids generated from a panel of isogenic trisomic and disomic iPSC lines (subclones) as a model of early fetal brain development in Down syndrome (DS).
Why it matters
In a large organoid study using isogenic cell lines, differences in non-chromosome-21 gene expression seen in a smaller experiment fell away, and cell-type differences did not correlate with trisomy 21. The results suggest that variation between cell lines may obscure subtle neurodevelopmental phenotypes, and this is an early laboratory model with no treatment tested.
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In the 2-month-old mice, sonobiopsy significantly increased the normalized levels of plasma p-tau species compared with the conventional blood-based liquid biopsy (p-tau-181-to-mouse tau [m-tau] ratio: 1.7-fold increase, P = .006; p-tau-231-to-m-tau ratio: 1.4-fold increase, P = .048).
Why it matters
In a mouse model of tauopathy, focused ultrasound briefly raised blood levels of p-tau, suggesting a possible way to detect brain proteins through blood. This is early animal work and does not show any treatment, cure, or prevention for Alzheimer's disease.
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Since the role of estrogen in postmenauposal-associated dementia is still debatable, this issue urges the search for other medications.
Why it matters
In a rat model resembling postmenopausal dementia, dimethyl fumarate improved learning and short- and long-term memory deficits and was associated with more intact neurons and less hippocampal CA1 neurodegeneration and astrocyte activation. It also suppressed hippocampal levels of APO-E1, BACE1, Aβ42, and hyperphosphorylated Tau and increased p-AKT, CREB, and BDNF, but these are animal findings and do not establish a treatment for human Alzheimer's disease.
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There is an urgent need for objective markers of Alzheimer’s disease (AD)-related cognitive impairment in people with Down syndrome (DS) to improve diagnosis, monitor disease progression and assess response to disease-modifying therapies.
Why it matters
This study compared levels of several synaptic proteins in cerebrospinal fluid from adults with Down syndrome across the Alzheimer's continuum. It evaluates VAMP-2 as a possible marker of cognitive impairment, not a treatment, cure or prevention.
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.
- Deficiency of Neuronal p38α MAPK Attenuates Amyloid Pathology in Alzheimer Disease Mouse and Cell Models through Facilitating Lysosomal Degradation of BACE1
- A Systematic Review on Dementia and Translocator Protein (TSPO): When Nuclear Medicine Highlights an Underlying Expression
- Glycated tau protein in Alzheimer disease: a mechanism for induction of oxidant stress
- Purification and cloning of amyloid precursor protein β-secretase from human brain
- Neurodegenerative Disease Tauopathies
- Brain morphology links systemic inflammation to cognitive function in midlife adults
- Oxidative damage linked to neurodegeneration by selective alpha-synuclein nitration in synucleinopathy lesions
- Internalized antibodies to the Abeta domain of APP reduce neuronal Abeta and protect against synaptic alterations
- Gut Microbiota Modulation Through Mediterranean Diet Foods: Implications for Human Health
- Heritability of leukoaraiosis in hypertensive sibships