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.
-
. Here, to gain deeper insights into the aetiology of different brain diseases, we used specimens from 1,494 unique donors to generate a population-scale single-cell transcriptomic atlas of the human dorsolateral prefrontal cortex, comprising over 6.3 million individual nuclei.
Why it matters
This large single-cell atlas of the brain's prefrontal cortex compared gene activity across Alzheimer's and other brain disorders, finding that more severe Alzheimer's was tied to fewer neurons and more immune and vascular cells. It describes disease patterns rather than testing any treatment, so it does not show how to cure or prevent Alzheimer's.
-
In vivo biomarkers for detecting neuropathologies from repetitive head impacts (RHI), including chronic traumatic encephalopathy (CTE), are needed.
Why it matters
This longitudinal multicenter case-control study evaluated plasma p-tau217 as a biomarker in people with repetitive head impacts at risk for chronic traumatic encephalopathy, including a postmortem subsample. It is about detecting a different condition and does not show a way to treat, cure, or prevent Alzheimer's disease.
-
In both cohorts, CSF MTBR-tau243 was associated with tau-PET temporal meta-ROI burden (BioFINDER-2: β = 1.1, p = < 0.0001 and Knight-ADRC: β = 0.7, p = < 0.0001), and this association did not differ by sex (BioFINDER-2 β = 0.04, p = 0.6 and Knight-ADRC: β = 0.009, p = 0.9).
Why it matters
This study found that a fluid marker of tau aggregation matches tau PET brain scans in both men and women, and that the link between them did not differ by sex. This suggests that higher tau PET signal in females reflects a genuinely greater susceptibility to tau pathology rather than a measurement problem.
-
52/100
A total of 2,642 participants with a mean age of 64.3 years (95% CI 63.4-65.1, 44% male) were included.
Why it matters
This observational study found that higher Mediterranean diet adherence was linked to better white matter structural integrity, which together with cardiovascular health mediated the link to global cognition. It cannot show that the diet prevents or treats Alzheimer's disease.
-
Our aim is to examine the interplay between cerebral small vessel disease (CSVD) pathology, Alzheimer’s disease (AD) related amyloid-β (Aβ) clearance, and cognition in general population.
Why it matters
In people without dementia, greater cerebral small vessel disease burden was associated with poorer cognition, and plasma amyloid-β42/40 ratios partially mediated this link. This suggests small vessel disease may contribute to Alzheimer's-related amyloid problems, but the cross-sectional design cannot prove that treating vascular disease would prevent dementia.
-
This study investigated whether longitudinal changes in CSF AD biomarkers were associated with 18 F-MK6240 tau PET measures in early Braak stage subregions.
Why it matters
This retrospective analysis of cognitively unimpaired participants examined whether longitudinal changes in CSF Alzheimer biomarkers were associated with tau PET measures in early Braak stage subregions. It addresses the temporal relationship between biomarkers, not any treatment or cure.
-
After expert panel review, only 50/67 patients met consensus criteria for DLB, 26/151 controls had a reduced MoCA, and 120/151 controls had a normal MoCA.
Why it matters
This cross-sectional study found that a high proportion of subjects meeting clinical criteria for dementia with Lewy bodies had phosphorylated alpha-synuclein detected in skin biopsies. It supports a role for skin biopsy detection in diagnosis, not treatment, cure, or prevention.
-
These analyses suggest that CenTauR harmonization increases the comparability of tau‐PET data acquired with different tracers.
Why it matters
This study found that a cut-off of 18 CenTauRs best classified visual reads of flortaucipir tau PET scans. The results suggest that CenTauR harmonization improves the comparability of tau PET data collected with different tracers.
-
Pathological inclusions of the C-terminal domain (CTD) of TAR DNA binding protein-43 (TDP-43) are neurodegenerative hallmarks in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia, yet CTD's aggregation propensity complicates structural characterization of native TDP-43.
Why it matters
Using NMR spectroscopy and modeling, this study proposes structural models of how the conserved region of the TDP-43 C-terminal domain multimerizes, and suggests these structures could be pharmacologically targetable to prevent conversion into pathogenic aggregates. This is early structural laboratory work with no treatment tested in people.
-
Cerebral small vessel disease (cSVD) is a leading cause of stroke and dementia with no specific treatment, of which molecular mechanisms remain poorly understood.
Why it matters
This study identified 49 proteins linked to MRI markers of small vessel disease, most prominently in cerebrospinal fluid, and many also linked to stroke and dementia. These findings point to possible biomarkers and drug targets, but no treatment was tested.
-
52/100
Motor neuron hyperexcitability is a broadly observed yet poorly understood feature of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
Why it matters
In stem cell-derived neurons and postmortem ALS/FTD tissue, TDP-43 dysfunction caused mis-splicing of KCNQ2, producing a nonfunctional protein that led to neuronal hyperexcitability. The effect was rescued in cells by splice-modulating antisense oligonucleotides, an early laboratory result not yet a treatment for patients.
-
52/100
Diabetes was not associated with brain atrophy cross-sectionally or longitudinally.
Why it matters
Diabetes alone was not linked to brain atrophy, but diabetes and white matter hyperintensities together were linked to more atrophy, independent of Alzheimer's pathology. This suggests that diabetes-related cognitive problems may be driven mainly by cerebrovascular disease, but the study does not test any treatment.
-
Consensus was achieved on 28 statements.
Why it matters
This consensus statement is about screening for and eradicating Helicobacter pylori to prevent gastric cancer, and does not address Alzheimer's disease. It reports only that consensus was reached on 28 statements.
-
Both visual read methods exhibited strong concordance with semiquantitative SUVRs.
Why it matters
A visual read algorithm called BF-VR detected tau in the entorhinal cortex more accurately than the established FTP-VR method, though it was less accurate in the temporal meta-region, and it showed excellent reliability. This is a method for reading tau-PET scans, not a treatment, cure, or prevention.
-
Lewy body diseases are common neurodegenerative diseases, including Parkinson's disease (PD) and dementia with Lewy bodies, which lead to both motor and non-motor symptoms.
Why it matters
This postmortem study found widespread non-inclusion alpha-synuclein accumulation in Lewy body-negative LRRK2-mutant cases, suggesting these cases have a deficiency in forming inclusions rather than a lack of aggregation. It concerns Lewy body disease and Parkinson's disease, not Alzheimer's disease, and tests no treatment, cure or prevention.
-
Our meta-analyses confirmed significantly lower CSF TAU levels in DLB and CSF SYUA levels in PDD, when compared to Alzheimer's disease.
Why it matters
Screening 11,006 articles, this review found 193 studies of proteins that differ in people with Lewy body dementia. Meta-analyses confirmed six such proteins in dementia with Lewy bodies (TAU, SYUA, NFL, CHI3L1, GFAP, CLAT), and found lower spinal fluid TAU in that condition than in Alzheimer's, though no blood-based protein was replicated. The authors see promising diagnostic markers that could help tell Lewy body dementia apart and guide future drug target research.
-
Cytosolic aggregation of the RNA binding protein TDP-43 (transactive response DNA-binding protein 43) is a hallmark of amyotrophic lateral sclerosis and frontotemporal dementia.
Why it matters
In cell experiments, this study found that SUMO2/3 conjugation of TDP-43 helps stabilize the protein against irreversible aggregation during oxidative stress. This is an early laboratory finding about a possible protective mechanism, not a treatment tested in people.
-
Parkinson disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy are synucleinopathies, characterized by neuronal loss, gliosis and the abnormal deposition of α-synuclein in vulnerable areas of the nervous system.
Why it matters
This review describes isolated REM sleep behavior disorder as an early stage of synuclein-related disease such as Parkinson's disease and dementia with Lewy bodies, with alpha-synuclein pathology likely starting in the lower brainstem. It discusses mechanisms and future therapy directions, but no treatment or cure is established.
-
Polyphenols, naturally occurring phytonutrients found in plant-based foods, have attracted significant attention for their potential therapeutic effects in neurological diseases and neuroinflammation.
Why it matters
This review summarizes evidence that polyphenols from plant foods have antioxidant, anti-inflammatory, and anti-amyloid properties that may help in Alzheimer's and other brain diseases. It reports potential from epidemiological and clinical studies but does not establish that polyphenols prevent or treat Alzheimer's disease.
-
Among 2935 patients (50.4% women; mean age=72.2 years; 19.8% subjective cognitive impairment, 39.8% mild cognitive impairment, and 40.4% dementia), larger WMH volume within projection fibres (B=0.24, SE=0.10, p=0.013) was associated with greater apathy.
Why it matters
In memory clinic patients, greater white matter hyperintensity volume in specific fibre tracts was linked to more apathy and hyperactivity, but not to affective or psychosis symptoms. This suggests that damage to particular brain pathways from small vessel disease may contribute to these behavioural symptoms, though the study does not test any treatment.
-
These findings emphasize the necessity of tailoring mAb trials for DS, considering age-related AD characteristics.
Why it matters
Among 409 adults with Down syndrome, amyloid PET positivity increased with age, and there was a significant lag between amyloid positivity and clinical symptom onset. This cross-sectional study is intended to guide monoclonal antibody trial designs and does not itself test any treatment, cure, or prevention for Alzheimer's disease.
-
Triggering receptor expressed on myeloid cells 2 (TREM2) is a transmembrane protein that is predominantly expressed by microglia in the brain.
Why it matters
In this work, soluble TREM2 released by microglia bound to a neuronal receptor called transgelin-2 and reduced tau phosphorylation and cognitive deficits. These findings point to a possible mechanism for lowering tau damage, but they come from experimental models and do not yet establish a treatment for patients.
-
Accumulation of mononuclear phagocytes [monocytes, macrophages, and dendritic cells (DCs)] in the vessel wall is a hallmark of atherosclerosis.
Why it matters
This study classified immune cells in the blood vessel walls of mice and humans with atherosclerosis, not Alzheimer's disease. It provides no information about treating, curing or preventing Alzheimer's.
-
Microglia are central players in brain innate immunity and have been the subject of extensive research in Alzheimer's disease (AD).
Why it matters
This review summarizes what is known about how microglia, and the TREM2 receptor in particular, respond to amyloid plaques, tau and demyelination in mice and humans. It is a summary of research directions and does not report a treatment, cure or prevention for Alzheimer's.
-
52/100
BACKGROUNDSoluble triggering receptor expressed on myeloid cells 2 (sTREM2) plays an important role in the clearance of pathological amyloid-β (Aβ) in Alzheimer's disease (AD).
Why it matters
This study found that soluble TREM2 levels in cerebrospinal fluid and plasma were associated with conversion from mild cognitive impairment to Alzheimer's disease. It suggests a possible predictor but does not provide a treatment or cure.
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.
- Efficacy of rivastigmine in dementia with Lewy bodies: a randomised, double-blind, placebo-controlled international study
- Propagation of tau misfolding from the outside to the inside of a cell
- Lysosomal proteinase antigens are prominently localized within senile plaques of Alzheimer's disease: evidence for a neuronal origin
- Exercise and metformin counteract altered mitochondrial function in the insulin-resistant brain
- Silent cerebral ischaemia: hidden fingerprints of invasive medical procedures
- Multiple isoforms of human microtubule-associated protein tau: sequences and localization in neurofibrillary tangles of Alzheimer's disease
- Retarded axonal transport of R406W mutant tau in transgenic mice with a neurodegenerative tauopathy
- Identification of a unique TGF-β–dependent molecular and functional signature in microglia
- The hemo-neural hypothesis: on the role of blood flow in information processing
- Familial amyotrophic lateral sclerosis and parkinsonism-dementia complex of the Kii Peninsula of Japan: clinical and neuropathological study and tau analysis