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.
-
Patient inclusion started in January 2023, and study enrollment of patients is expected to finish in the second quarter of 2027, whereas the main results are expected to be published in the first quarter of 2028.
Why it matters
This is a protocol for an ongoing study that will examine white matter hyperintensity shape and brain clearance markers using 7T MRI. No results are available yet, so it provides no information on treating, curing, or preventing Alzheimer's disease.
-
of 0.928 and bias of 6.0% (n =396, Deming regression, Figure 1).
Why it matters
This study describes the analytical validation of a plasma p-tau217 test on one platform, showing acceptable performance for measuring p-tau217 in human plasma and establishing negative, indeterminate and positive cutoffs. The results support the assay as an aid in diagnosis, though this is a technical validation rather than a test of treatment or prevention.
-
Adults with DS are often supported by family caregiver(s), who face challenges including lack of awareness of the increased risk of developing AD, difficulty in obtaining a timely diagnosis, limited resources for psychosocial support, and lack of access to clinical trials.
Why it matters
This work adapted an amyloid PET result disclosure protocol for adults with Down syndrome and their caregivers, the first such adaptation to the authors' knowledge. It is a first step toward equity in AD diagnosis and treatment for this population, with pilot testing planned next.
-
40/100
We replicated three distinct spatiotemporal subtypes of tau PET accumulation and their associations with individual differences and AD severity in an independent sporadic AD cohort.
Why it matters
Three tau PET subtypes were identified, and the MTL-sparing group was younger, more impaired, and had greater amyloid PET levels than other groups. The findings describe differences in network patterns and amyloid across tau subtypes, which may help explain varied disease presentations.
-
40/100
We replicated three distinct spatiotemporal subtypes of tau PET accumulation and their associations with individual differences and AD severity in an independent sporadic AD cohort.
Why it matters
Three tau PET subtypes were identified, and the MTL-sparing group was younger, more impaired, and had greater amyloid PET levels than other groups. The findings describe differences in network patterns and amyloid across tau subtypes, which may help explain varied disease presentations.
-
Average age of participants was 66 (21-88) years. 25 were biologically female and 15 were amyloid positive.
Why it matters
Off-target extra-cerebral signal was more pronounced and widespread in 18F-MK-6240 than 18F-AV-1451 tau-PET, potentially affecting cerebellar reference quantification. This is a technical comparison of tracer signal, not a treatment, cure, or prevention.
-
Compared to controls, MAO-B immunoreactive area fraction was significantly increased in the frontal cortex and white matter of AD, CBD, and especially PiD and FTLD-TDP, but not PSP.
Why it matters
In brain tissue from people who died with Alzheimer's disease and related dementias, MAO-B was increased in cortical astrocytes and was negatively associated with cortical thickness even after adjusting for amyloid, pTau or pTDP43 burden. This is tissue-based biomarker research, and the authors state that PET-MRI studies are still needed to test whether MAO-B predicts future neurodegeneration.
-
Using a unique dataset of the same participants scanned close in time on different scanner and protocols, we found that (1) MMD measurements were useful to test the need/improvement due to harmonization; (2) ComBat was not substantially better at creating compatible distributions between scanner vendors than Deming regression, and both were sometimes inadequate.
Why it matters
This methods study compared two ways of harmonizing white matter hyperintensity measurements taken on different scanners and found that Deming regression made the distributions more similar than ComBat in cognitively unimpaired participants. It addresses how to compare imaging data across sites in dementia research, but it does not test any treatment, cure, or prevention.
-
The diagnostic precision of Parkinsonian disorders is not accurate enough.
Why it matters
This study found that diagnostic accuracy for Parkinsonian disorders was highest for multiple system atrophy and lowest for dementia with Lewy bodies, with many cases mislabeled in life. The researchers developed a probabilistic model and likelihood ratios to help refine and improve diagnostic accuracy.
-
Two distinct subtypes emerged. Subtype 1 (n = 63) features localized supra-normal gray matter volume deviations in dorsolateral prefrontal regions, elevated free water indicating microstructural disruption, executive dysfunction, and transcriptional enrichment in metabolic dysfunction and neurodegenerative pathways.
Why it matters
This study identified two brain structural subtypes in Parkinson's disease with mild cognitive impairment, one with executive dysfunction and metabolic and neurodegenerative pathway changes, and another with preserved microstructure and enhanced cognitive network connectivity. It is about Parkinson's disease cognitive impairment, not Alzheimer's disease treatment or cure, and it suggests these subtypes may support precision medicine approaches.
-
Emerging evidence implicating glymphatic dysfunction contributes to the pathogenesis of frontotemporal dementia (FTD).
Why it matters
In 37 patients with behavioral frontotemporal dementia and 40 healthy controls, glymphatic-associated metabolites were mainly enriched in the synaptic vesicle cycle pathway, and plasma NPTX2 correlated with anterior glymphatic indices. This shows an association between the glymphatic system and synaptic function but does not test any treatment, cure or prevention.
-
Alzheimer's disease (AD), the most prevalent form of dementia, leads to progressive cognitive decline due to pathological hallmarks including amyloid plaques, neurofibrillary tangles, synaptic loss, neuroinflammation, and neuronal cell death, highlighting the urgent need for multitarget therapeutic strategies.
Why it matters
Several synthesized benzoxazole compounds showed dual inhibition of p38α MAPK and acetylcholinesterase in laboratory assays, with molecular docking describing their binding. These are in vitro findings, and the authors state that further in vivo testing is needed.
-
could serve as potential biomarkers for NAFLD-associated mild cognitive impairment; 3) bacterial metabolic functions involved in sugar degradation and the breakdown of tryptophan and glutamate were downregulated and linked to CXCL13 plasma levels and neuroinflammation; 4) correlations between SCFA concentrations disappeared with liver disease and cognitive impairment.
Why it matters
This study identified gut microbiome features and bacterial metabolic pathways as potential biomarkers for mild cognitive impairment associated with non-alcoholic fatty liver disease. It is a biomarker study and does not test any treatment, cure or prevention.
-
Phenoconverters had higher FW in the NBM and posterior SN.
Why it matters
This study found that free water in the nucleus basalis of Meynert predicted conversion to dementia with Lewy bodies in people with isolated REM sleep behavior disorder, and correlated with lower cognition scores. It concerns a potential biomarker for early stratification, not a treatment or cure.
-
Alzheimer's disease (AD) is one of the leading causes of dementia in the elderly, and no effective treatment is currently available.
Why it matters
In mice and patient serum samples, the miR-96-5p/CTSB pathway was linked to neuroinflammation and cognitive impairment, and targeting it rescued memory impairment in mice. The serum marker combination showed diagnostic potential, but this is not yet a proven treatment or cure for Alzheimer's disease in people.
-
While cerebrovascular dysfunction and reactive astrocytosis are extensively characterized hallmarks of Alzheimer's disease (AD) and related dementias, the dynamic relationship between reactive astrocytes and cerebral vessels remains poorly understood.
Why it matters
In an amyloid mouse model, calcium signaling in reactive astrocytes was disrupted and their communication with small blood vessels was impaired. This is a mouse study of brain signaling, so it does not yet show a treatment or prevention for Alzheimer's disease in people.
-
40/100
TMEM106B is a lysosome/late endosome protein that is a potent genetic modifier of multiple neurodegenerative diseases as well as general aging.
Why it matters
In mouse models of C9-ALS/FTD and tauopathy, endogenous TMEM106B protein correlated with known TDP-43 and tau pathology, and similar analysis was done on postmortem human brain tissue from C9-ALS/FTD, Alzheimer's disease and AD/LATE. This is animal and autopsy research describing pathology and does not test a treatment.
-
Neuroinflammation is a key feature of Alzheimer’s disease (AD), and stem cell therapies have emerged as promising candidates due to their immunomodulatory properties.
Why it matters
In APPswe/PS1dE9 mice, injected Neuro-Cells improved learning, object exploration and anxiety-like behavior, normalized several immune and plasticity markers, and reduced GFAP-positive cell density, while also reducing IL-6 production in cultured human monocytes. This is animal and cell research only, so it does not show any benefit for people with Alzheimer's disease.
-
High-fat diet (HFD) poses various health risks, such as obesity, insulin resistance (IR), fatty liver, gut microbiota dysbiosis, cognitive impairment, inflammation, and oxidative stress.
Why it matters
This review is about how a high-fat diet may raise the risk of insulin resistance through gut bacteria changes, and it does not study Alzheimer's disease directly. It mentions cognitive impairment only as one of several health risks linked to a high-fat diet, so it provides no evidence on treating, curing, or preventing Alzheimer's.
-
Loss-of-function mutations affecting the lysosomal protein progranulin are a leading cause of frontotemporal dementia.
Why it matters
In mice lacking progranulin, acid sphingomyelinase activity was reduced, and restoring progranulin with gene therapy corrected this deficit. In brain tissue from patients with progranulin mutations, a different enzyme, neutral sphingomyelinase, was reduced instead, so it is not yet clear how these findings could be used to treat frontotemporal dementia.
-
Transactive response DNA-binding protein of 43 kDa (TDP-43) and tau proteins play critical roles in neurodegenerative diseases, particularly frontotemporal lobar degeneration (FTLD) and Alzheimer's disease (AD).
Why it matters
This review reports that when tau and TDP-43 pathologies occur together, the literature links this to more severe and poorer clinical outcomes than either pathology alone. It argues for considering mixed pathologies in diagnosis and treatment, but presents no therapy that changes these outcomes.
-
Nucleocytoplasmic transport defects are observed in Alzheimer's disease (AD) and frontotemporal dementia (FTD).
Why it matters
In human iPSC-derived cortical neurons, this study found that mislocalisation of nucleic acids, mitochondrial dysfunction and cGAS-STING activation can be ameliorated through VCP D2 ATPase inhibition. This is a cell model, so it is early and preliminary and does not yet show a treatment for people.
-
White matter hyperintensities (WMHs) and cerebral β-amyloid (Aβ) have been characterized as clinically significant biomarkers associated with greater cognitive decline and incidence of Alzheimer's Disease (AD) dementia.
Why it matters
In people with mild cognitive impairment, amyloid burden was linked to poorer memory, executive function and language, while white matter hyperintensities in certain regions predicted progression to dementia. This is observational and does not test any treatment, but it may help explain how vascular and amyloid changes together affect thinking.
-
Adults with DS may have unique neuro- and cardio- protective factors that deserve future investigation.
Why it matters
In 96 adults with Down syndrome, elevated lipoprotein(a) levels were not associated with an earlier age of Alzheimer's disease onset. This retrospective study found no evidence of increased risk and does not test any treatment, cure or prevention.
-
Metabolic syndrome (MetS) is characterized by central obesity, insulin resistance, hypertension, dyslipidemia, and chronic inflammation, significantly increasing the risk of cardiovascular disease and type 2 diabetes.
Why it matters
This review is about exercise and diet in metabolic syndrome, not Alzheimer's disease. It reports that low and moderate intensity exercise improved insulin sensitivity and reduced oxidative stress and inflammation, while high-intensity interval training temporarily increased oxidative stress and inflammation.
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.
- Lipid and immune abnormalities causing age-dependent neurodegeneration and Parkinson's disease
- Presynaptic accumulation of APP-CTFβ may contribute to synaptic dysfunction in Alzheimer’s disease
- Aβ mediates F-actin disassembly in dendritic spines leading to cognitive deficits in Alzheimer's disease
- Neuroinflammation and protein pathology in Parkinson's disease dementia
- MK-8719, a Novel and Selective O-GlcNAcase Inhibitor That Reduces the Formation of Pathological Tau and Ameliorates Neurodegeneration in a Mouse Model of Tauopathy
- There's Something Wrong with my MAM; the ER-Mitochondria Axis and Neurodegenerative Diseases
- Soluble aβ promotes wild-type tau pathology in vivo
- Quantitative detection of α-Synuclein and Tau oligomers and other aggregates by digital single particle counting
- Sleep Drives Metabolite Clearance from the Adult Brain
- Abnormal phosphorylation of the microtubule-associated protein tau (tau) in Alzheimer cytoskeletal pathology.