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.
-
The human ETS2 gene, a member of the ETS gene family, with sequence homology with the retroviral ets sequence of the avian erythroblastosis retrovirus E26 is located on chromosome 21.
Why it matters
This genetic analysis found no rearrangements or duplications of the ETS2 gene in DNA from Alzheimer's disease patients. It concludes that altered ETS2 gene dosage does not appear to be a genetic cause or component of Alzheimer's disease.
-
This study demonstrated that selectively targeting PDE4A rescued cognitive and neuropathological deficits in a validated mouse model of AlD.
Why it matters
In a mouse model of alcohol-induced cognitive impairment, knocking down PDE4A improved memory and reduced amyloid-beta deposition, phosphorylated tau and synaptic damage via the cAMP/PKA/CREB pathway. These are animal findings for alcohol-induced impairment, not evidence of treating, curing or preventing Alzheimer's disease in people.
-
Ginsenosides are the primary active constituents derived from the dried roots of ginseng, a staple in traditional Chinese medicine.
Why it matters
In cell and mouse models of Alzheimer's disease, this ginseng compound reduced oxidative stress and inflammation and improved learning and memory in the mice. These are early laboratory and animal findings, so it is not yet known whether it would help people.
-
Age-related upregulation in microRNA (miR)-204 and downregulation in long noncoding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) were observed to disrupt Ephrin-B1 (EFNB1)/EphB2 interactions, leading to reduced cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway activation.
Why it matters
In this animal study with mice, cognitive-exercise dual-task training was found to delay aging-related cognitive decline, possibly through effects on microRNA-204, lncRNA NEAT1 and related signaling pathways. These are animal findings and cannot be directly applied to treating or preventing Alzheimer's disease in people.
-
BackgroundEpigenetic mechanisms, particularly histone modifications at gene promoters, are crucial for controlling gene transcription.
Why it matters
In postmortem prefrontal cortex, people with mild cognitive impairment and Alzheimer's disease showed losses of activating histone marks at synaptic genes and gains of repressive marks at synaptic gene promoters. This describes epigenomic changes during disease progression, not a treatment or cure.
-
Hexanucleotide repeat expansion in the chromosome 9 open reading frame 72 ( C9orf72 ) gene has been identified as the most common genetic cause of both frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS).
Why it matters
This single case report describes a patient with behavioral variant frontotemporal dementia carrying a C9orf72 repeat expansion of 49 units, within the intermediate-length range. It adds clinical evidence to the debate about which repeat lengths are pathogenic, but it is one case and offers no treatment, cure, or prevention.
-
. The area under the receiver operating characteristic curve of plasma p -tau217 was 0.941.
Why it matters
This plasma p-tau217 test showed high agreement with amyloid PET, with 90% sensitivity and 90% specificity, and its measurements were not significantly affected by reduced kidney function. The authors conclude it may aid in the diagnostic workup of Alzheimer's disease and can give reliable results in people with kidney impairment.
-
In the colocalization of cis-eQTL and GWAS signals for Hispanics, we observed a high posterior probability (posterior prob = 0.9947) for the upstream gene variant rs755980338 on chromosome 11, which locally regulates EHD1 gene (GWAS p-value = 0.009, cis-eQTL p-value = 0.0041).
Why it matters
This genetic study found ancestry-specific colocalization signals linking variants regulating EHD1, TMEM68, and DEFA10P to Alzheimer's disease risk in Hispanic and non-Hispanic white brain samples. It suggests these genes may play an ancestry-specific role in Alzheimer's disease, with potential implications for precision medicine, but no treatment is tested.
-
MTX46943-mediated TREM2 activation leads to TREM2/DAP12 receptor complex formation and stabilizes surface location required for downstream signaling and microglia activation.
Why it matters
This study reports that the small molecule TREM2 agonist MTX46943 activates microglia and, with chronic systemic treatment, reduces brain amyloid pathology in vivo. The company is advancing MTX46943 into clinical studies for early Alzheimer's, so this remains a preclinical compound that has not yet been shown to treat or prevent the disease in patients.
-
Acute and chronic treatment of JRMS reduced TDP-25 aggregation in a dose-dependent manner by ∼75% in cells.
Why it matters
A small molecule called JRMS reduced clumps of TDP-25 protein in cells and in mice, including a roughly 30% reduction in aggregates after two weeks of treatment in mice. The authors call JRMS a preclinical candidate and say they are still working toward a product profile before it can be tested in clinical trials.
-
We demonstrate that irisin promotes the expression of brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), glial cell line-derived neurotrophic factor (GDNF), α5 subunits of integrin receptors and LDH5α, and stimulates transient activation of ERK 1/2 in astrocytes.
Why it matters
In an Alzheimer's mouse model, irisin reduced astrocyte activation and improved memory, alongside increased levels of growth factors in the hippocampus. This is animal and cell work, so its relevance to treating people is unknown.
-
We found that induction of adult human brain-like 4R Tau isoform expression enables endogenous formation of late-stage Tauopathy hallmarks in iPSC-derived neurons engineered to contain synergistic Tau mutations.
Why it matters
iPSC-derived neurons engineered to express adult brain-like 4R tau with synergistic tau mutations developed seeding-competent, hyperphosphorylated, fibrillar tau in tangle-like structures, and the model was used to test chemical modulators and a human tau PET tracer. This is a laboratory model for research and drug development, not a treatment, cure or prevention.
-
33/100
Barnes Maze Acquisition was performed on males (N = 4-5/genotype) after habituation and several days training.
Why it matters
Mice carrying Erbb4 mutations showed gene dosage-dependent problems with spatial learning, gait, body weight, and bone density that resemble features of frontotemporal dementia and ALS. These are early findings in small numbers of animals, and more testing is underway, so no treatment or prevention is established.
-
The basal nucleus showed significant neuronal loss in PPA versus controls (p <0.05).
Why it matters
This brain tissue study found that different amygdala nuclei are unequally damaged in primary progressive aphasia due to FTLD-tauopathies, with the basal nucleus showing the most neuronal loss and tau pathology. It describes patterns of damage only and does not test any treatment, so it offers no direct path to treating or preventing Alzheimer's disease.
-
PPA/3R had a mean age of 63.5 years (SD = 3.9), PPA/4R were 72.5 years (SD = 5.8), and controls were 63.4 years (SD = 6.8).
Why it matters
This imaging study found that in primary progressive aphasia, cases with 3R tauopathy had more widespread left amygdala shrinkage than cases with 4R tauopathy. It maps patterns of atrophy only and does not test any treatment or prevention.
-
PPA/3R had a mean age of 63.5 years (SD = 3.9), PPA/4R were 72.5 years (SD = 5.8), and controls were 63.4 years (SD = 6.8).
Why it matters
This imaging study found that in primary progressive aphasia, cases with 3R tauopathy had more widespread left amygdala shrinkage than cases with 4R tauopathy. It maps patterns of atrophy only and does not test any treatment or prevention.
-
Amnestic mild cognitive impairment (aMCI) represents a critical prodromal stage of Alzheimer's disease (AD), yet effective therapeutic interventions to prevent or delay this conversion remain an unmet clinical need.
Why it matters
This perspective proposes that acupuncture may modulate gut microbiota and restore homeostasis of the microbiota-gut-brain axis, potentially slowing progression from amnestic mild cognitive impairment to Alzheimer's. It calls for future investigations to clarify mechanisms and generate robust clinical evidence, so no treatment benefit has been demonstrated.
-
Cerebral small vessel disease (CSVD) is a major contributor to stroke and dementia.
Why it matters
In 61 patients with cerebral small vessel disease and 32 controls, patients showed increased iron-related susceptibility values in several deep brain nuclei, and higher iron deposition in the putamen and substantia nigra was associated with cognitive impairment. This identifies potential imaging markers of small vessel disease, but it is a small observational study and does not test any treatment.
-
33/100
Astrocytes are a source of IL-15 in AD, particularly near localized Aβ pathology, and neurons are poised to respond.
Why it matters
In brain tissue from people with Alzheimer's disease and in mice, astrocytes near amyloid plaques produced more of the immune signal IL-15, and neurons appeared able to respond to it. This identifies a possible inflammatory pathway but does not yet show that targeting it helps patients.
-
It is now widely accepted that the development of neurodegenerative diseases depends on and affects many pathological processes, both in the brain and the periphery.
Why it matters
In two APP transgenic mouse models, only the 3xTg-AD mice showed splenomegaly, spleen amyloidosis and increased neutrophils, while Tg-SwDI mice did not. The authors caution that findings in any transgenic mouse strain should be interpreted with caution, and this offers no direct treatment for Alzheimer's disease.
-
Prion diseases are fatal neurological disorders characterized by the accumulation of abnormal proteins in the central nervous system, leading to rapid neurodegeneration.
Why it matters
This case report describes a man in his 70s who developed rapidly progressive dementia after a platelet-rich plasma injection and was confirmed to have sporadic Creutzfeldt-Jakob disease. It is a single case of a different prion disease and provides no treatment, cure or prevention for Alzheimer's disease.
-
White matter hyperintensity (WMH) is the core imaging hallmark of cerebral small vessel disease (CSVD).
Why it matters
This review describes how radiomics, a method of extracting many features from imaging, may help identify and stage white matter hyperintensity lesions and reveal their pathological mechanisms. It is a review of research progress and does not report a treatment, cure, or prevention.
-
Spatial transcriptomics (ST) data provide spatially informed gene expression profiles.
Why it matters
By combining spatial and single-cell gene expression data, this study identified genes linked to Alzheimer's-related brain changes that other methods missed. This is a methodological advance for research and does not directly provide a treatment or cure.
-
Our case series highlighted the relevance of neurological comorbidities in BP patients; although the pathogenesis is still to be elucidated, the neuroinflammation present in neurodegenerative diseases could explain the neurocutaneous link and the chronological relationship between these entities.
Why it matters
Looking back at 257 patients with bullous pemphigoid, an autoimmune blistering skin disease, researchers found 102 also had a neurological disease, most often senile dementia, Alzheimer's disease or vascular dementia. These patients showed more signs of immune activity, such as higher eosinophil counts and anti-BP180 IgG antibodies. The cause of the skin-brain link is still unknown; the authors suggest brain inflammation in neurodegenerative disease could help explain it.
-
Die Frühphasen- & R1-Bilder korrelierten signifikant in allen Gruppen (Gesunde: r=0,68-0,84; AD: r=0,81-0,9; PSP-RS: r=0,81-0,86; FTD: r=0,76-0,82).
Why it matters
Early-phase and R1 images from [18F]PI-2620 tau-PET correlated significantly in all groups, and disease-specific hypoperfusion patterns were seen in AD, bvFTD, and lvPPA but not in PSP or nfvPPA. The authors conclude that further study, including comparison with [18F]FDG, is needed to determine the biomarker value of this imaging.
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.
- Reduction of Nuak1 Decreases Tau and Reverses Phenotypes in a Tauopathy Mouse Model
- Pittsburgh compound B imaging and cerebrospinal fluid amyloid-β in a multicentre European memory clinic study
- Conditional BDNF Delivery from Astrocytes Rescues Memory Deficits, Spine Density, and Synaptic Properties in the 5xFAD Mouse Model of Alzheimer Disease
- Impact of hippocampal α‐synuclein oligomers on cognitive trajectory in patients with dementia with Lewy bodies
- Voluntary Exercise Promotes Glymphatic Clearance of Amyloid Beta and Reduces the Activation of Astrocytes and Microglia in Aged Mice
- Attenuation of frontal asymmetry in pediatric posttraumatic stress disorder
- MarkVCID2 Consortium for Clinical Validation of Biomarkers of Cerebral Small Vessel Disease: Validation Framework and Baseline Characteristics
- Glymphatic activity is linked to the synaptic vesicle cycle pathway in frontotemporal dementia: A metabolomics study
- Age-dependent neurofibrillary tangle formation, neuron loss, and memory impairment in a mouse model of human tauopathy (P301L)
- Prediction of continuous amyloid positron emission tomography with fluid measures of phosphorylated tau and β-amyloid