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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Five weeks of daily IN dosing of Long Evans rats with 15 μL of a 1% (0.3 mg), but not 0.1% (0.03 mg), solution of DFO rescued cognitive impairment caused by ICV STZ administration as assessed with the Morris Water Maze (MWM) test of spatial memory and learning.
Why it matters
In a rat model of Alzheimer's disease, five weeks of daily intranasal deferoxamine at one dose rescued cognitive impairment and modulated neuroinflammation and neuronal survival pathways. This is early animal research and does not establish benefit in people.
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The MoCA score and the SCWT duration of the real group improved significantly compared with that of the sham group.
Why it matters
This randomized controlled trial found that intermittent theta burst stimulation over the right DLPFC improved global cognition and response inhibition in patients with mild cognitive impairment at risk of dysphagia compared with sham. Some swallowing measures improved only in certain subgroups, and changes in functional connectivity between right and left DLPFC may underlie the effects.
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Our data suggest that FXN ameliorates AD pathology, by simultaneously targeting two key pathological features: Aβ deposits and neuroinflammation.
Why it matters
In 5XFAD mice and mouse astrocytes, fluvoxamine maleate promoted autophagy-mediated clearance of amyloid beta and inhibited the NLRP3 inflammasome, improving Alzheimer-like pathology. This is animal and cell research, so it does not yet show that fluvoxamine treats Alzheimer's disease in people.
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Regression analyses showed that with the inclusion of socioenvironmental factors, the model was significant (p < .001), and sociodemographic (ethnic/race) group differences were not significant (p = .118).
Why it matters
This study found that combined socioenvironmental risk factors and higher chronic pain severity were linked to thinner bilateral temporal lobes. It does not test any treatment, cure, or prevention for Alzheimer's disease.
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Creatine transporter deficiency (CTD) is a rare X-linked disorder of creatine transport caused by pathogenic variants in SLC6A8 (Xq28).
Why it matters
This study found elevated Aβ40, Aβ42 and total tau in cerebrospinal fluid in individuals with creatine transporter deficiency, a rare disorder of creatine transport. It describes biomarker abnormalities in a different condition and does not test any treatment, cure or prevention of Alzheimer's disease.
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Preeclampsia is a multisystemic, pregnancy-specific disorder united by new-onset hypertension but with considerable variation in clinical manifestation, onset, and severity.
Why it matters
This study used single-cell transcriptomics to examine molecular changes in the placenta in early- and late-onset preeclampsia. It does not test any treatment, cure, or prevention for Alzheimer's disease.
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The expression of the triggering receptor on myeloid cell-2 (TREM2) knockdown in microglia from the lateral habenula (LHb) reportedly induces depression-like behaviors in mice.
Why it matters
In mice, activating Nrf2 increased the microglial arginase 1+ phenotype by initiating TREM2 transcription and reduced depression-like behavior. This is animal research about depression, not Alzheimer's disease, and does not show a treatment or cure for Alzheimer's.
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The Hong Kong Grocery Shopping Dialog Task (HK-GSDT) is a short and easy-to-administer cognitive test developed for quickly screening neurocognitive disorders (NCDs).
Why it matters
A new short verbal test about grocery shopping was able to distinguish between normal cognition, mild neurocognitive disorder, and major neurocognitive disorder about as well as existing tests. This is a screening tool and does not treat, cure, or prevent Alzheimer's disease.
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A total of 321 people with cirrhosis (60 years, 78% men, 75% non-Hispanic White, 24% non-Hispanic African American, 4% Hispanic) were included. 45% had prior HE and 56% MHE.
Why it matters
This study found that the Area Deprivation Index was not associated with gut microbiome composition or cognitive impairment in people with cirrhosis, and that cirrhosis-related variables may be more influential. It does not test a dementia treatment or prevention, so it cannot show how to cure or prevent dementia.
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Although epilepsy as a comorbidity in neurodegenerative disorders is increasingly recognized, its incidence is still underestimated and the features of epilepsy in the different neurodegenerative conditions are still poorly defined.
Why it matters
This review covers how epilepsy occurs alongside neurodegenerative disorders including Alzheimer disease and Down syndrome, and notes that its frequency is underestimated and its features poorly defined. It is about diagnosis and management of seizures as a comorbidity, not about treating, curing or preventing Alzheimer's disease itself.
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We aimed to determine whether genetically determined CRP was associated with hundreds of human phenotypes to guide anti-inflammatory interventions.
Why it matters
This Mendelian randomization study examined whether genetically determined C-reactive protein, a marker of chronic low-grade inflammation, was linked to hundreds of health outcomes including diseases in UK Biobank and FinnGen data. It explores possible targets for anti-inflammatory interventions but does not test any treatment or prevention for Alzheimer's disease.
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Stevens-Johnson Syndrome (SJS) is a rare life-threatening condition characterized by severe mucocutaneous epidermal necrolysis and detachment of the epidermis.
Why it matters
This review describes Stevens-Johnson Syndrome risk associated with lamotrigine and the role of HLA genetic testing before prescribing. It contains no information on Alzheimer's disease.
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Alcohol use disorder (AUD) pathology features pro-inflammatory gene induction and microglial activation.
Why it matters
In primary organotypic brain slice culture, ethanol caused a unique immune gene signature and microvesicles promoted microglia-mediated pro-inflammatory responses. This is a laboratory study of alcohol-related inflammation, so it does not show any effect on treating, curing or preventing Alzheimer's disease.
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Alzheimer's disease (AD) is characterized by the accumulation in the brain of extracellular amyloid β (Aβ) plaques as well as intraneuronal inclusions (neurofibrillary tangles) consisting of total tau and phosphorylated tau.
Why it matters
Using HMC3 cells, this study examined how TREM2 alters phagocytic, apoptotic and inflammatory responses to amyloid beta 42. These are cell-based laboratory findings and do not demonstrate a treatment, cure or prevention for Alzheimer's disease.
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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by dementia, memory impairment, cognitive dysfunction, and speech impairment.
Why it matters
This laboratory study designed and tested new benzoic acid derivatives that inhibit acetylcholinesterase and carbonic anhydrase in vitro, with some compounds showing low KI values. These are early in-vitro and in-silico findings and do not establish any treatment, cure, or prevention for Alzheimer's disease in people.
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Cerebral amyloid angiopathy (CAA) is typified by the cerebrovascular deposition of amyloid.
Why it matters
In a mouse model of cerebral amyloid angiopathy, A1 reactive astrocytes and a loss of TREM2 were associated with an early stage of pathology. This is an animal study of a related condition and does not test a treatment, so it does not show how to treat, cure or prevent Alzheimer's.
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Type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD) share several common pathophysiological features.
Why it matters
In mice fed a long-term high-fat diet, overexpressing TREM2 in the hippocampus improved cognitive impairment and changed microglial polarization. This is animal research, so it is early and does not yet show a treatment for people.
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A population of >6 million people worldwide at high risk of Alzheimer’s disease (AD) are those with Down Syndrome (DS, caused by trisomy 21 (T21)), 70% of whom develop dementia during lifetime, caused by an extra copy of β-amyloid-(Aβ)-precursor-protein gene.
Why it matters
In this laboratory study, cerebral organoids grown from hair samples of people with Down syndrome developed Alzheimer-like pathology, and the BACE2 gene was identified as a suppressor of this pathology. This is early in-vitro work and does not show any treatment or prevention in people.
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Alzheimer´s disease (AD) is a progressive neurodegenerative disorder of complex etiology, while Down syndrome (DS) is considered a genetically determined form of AD.
Why it matters
In post-mortem brain tissue, cholesterol trafficking proteins STARD1 and NPC1 were increased in people with Alzheimer's disease and Down syndrome, and STARD1 distinguished these groups from controls better than Aβ42. The authors suggest STARD1 could be a potential pre-clinical marker, but this is tissue analysis only and no treatment was tested.
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Pomegranate juice (PGJ) is rich in unique bioactive compounds that can be used in the management of various diseases/disorders such as cancer, heart disease, Alzheimer disease, hypertension, and diabetes.
Why it matters
In this randomized trial of 28 people with impaired fasting glucose, fresh pomegranate juice lowered melatonin, increased insulin, and improved insulin resistance. The study did not test any effect on Alzheimer's disease, so it provides no evidence about treating, curing, or preventing the disease.
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Aging is associated with an exaggerated response to peripheral inflammatory challenges together with behavioral and cognitive deficits.
Why it matters
In adult and aged mice given a single peripheral LPS injection, the inflammatory response differed by age and sex, with aged females showing a distinct response. This is animal research only and reports no Alzheimer's treatment, cure or prevention.
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Stroke is the second most common cause of death and permanent disability.
Why it matters
This review discusses TREM2 as a possible target for immunomodulation after ischemic stroke, where microglia can adopt damaging or reparative phenotypes. It concerns stroke, not Alzheimer's disease, and reports no treatment, cure or prevention for Alzheimer's disease.
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Traumatic brain injury (TBI) refers to any insult to the brain resulting in primary (direct) and secondary (indirect) damage to the brain parenchyma.
Why it matters
This is a review of molecular mechanisms such as excitotoxicity, neuroinflammation, oxidative damage and cell death that occur after traumatic brain injury. It discusses how these processes damage brain tissue and their possible link to long-term conditions, but it reports no new treatment or cure for Alzheimer's disease.
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Triggering receptor expressed in myeloid cells (TREM)2 is a genetic high-risk factor for sporadic Alzheimer's disease (AD) and is considered a potential target for AD diagnosis and therapy, although its role in the different stages of AD remains controversial.
Why it matters
In APP/PS1 mice, microglial Trem2 caused synaptic impairment early in the disease process but prevented amyloidosis later, so its role differed by stage. This is animal research only and reports no treatment, cure or prevention for people.
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Features for rule-based systems, including significant words and patterns related to SBI, were generated using pointwise mutual information.
Why it matters
This work developed a natural language processing method to identify silent brain infarcts from neuroimaging reports, using features generated by pointwise mutual information and compared against a manually created gold standard. It is about detecting a related brain condition from reports and 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.
- GSK189254, a novel H3 receptor antagonist that binds to histamine H3 receptors in Alzheimer's disease brain and improves cognitive performance in preclinical models
- Minocycline for sporadic and hereditary cerebral amyloid angiopathy (BATMAN): study protocol for a placebo-controlled randomized double-blind trial
- Reduced Slow-Wave Sleep Is Associated with High Cerebrospinal Fluid Aβ42 Levels in Cognitively Normal Elderly
- Transethnic meta-analysis of rare coding variants in PLCG2, ABI3, and TREM2 supports their general contribution to Alzheimer's disease
- Neuropathological and genetic correlates of survival and dementia onset in synucleinopathies: a retrospective analysis
- Decreased cyclin dependent kinase in brain of patients with Down syndrome
- Presenilin 1 and alpha-1-antichymotrypsin polymorphisms in Down syndrome: no effect on the presence of dementia
- Staging of argyrophilic grains: an age-associated tauopathy
- Lysosomal dysfunction in Down syndrome and Alzheimer mouse models is caused by v-ATPase inhibition by Tyr682-phosphorylated APP βCTF
- Genome-wide association study of neuropathological features in Lewy body disease