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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Recently, we showed that behavioural variant frontotemporal dementia and Alzheimer's disease cause atrophy within two major networks, an anterior 'Salience Network' (atrophied in behavioural variant frontotemporal dementia) and a posterior 'Default Mode Network' (atrophied in Alzheimer's disease).
Why it matters
This study explored whether combining measures of two brain networks — a front-of-brain "Salience Network" and a back-of-brain "Default Mode Network" — might help tell behavioural variant frontotemporal dementia apart from Alzheimer's disease. The authors report that their findings "suggest" the two diseases "lead to divergent network connectivity patterns", but this record gives no accuracy figures, so it should not be read as a validated diagnostic test. It does not address treatment, cure or prevention.
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We conducted a genome-wide association study among 2,323 individuals with sporadic amyotrophic lateral sclerosis (ALS) and 9,013 control subjects and evaluated all SNPs with P < 1.0 x 10(-4) in a second, independent cohort of 2,532 affected individuals and 5,940 controls.
Why it matters
This genome-wide association study identified 19p13.3 (UNC13A) and 9p21.2 as susceptibility loci for sporadic amyotrophic lateral sclerosis. The 9p21.2 locus is in a linkage region for familial ALS with frontotemporal dementia found previously in several large pedigrees.
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Mutations in the glucocerebrosidase gene (GBA) are associated with Gaucher's disease, the most common lysosomal storage disorder.
Why it matters
This study found that mutations in the GBA gene were more common in British Parkinson's disease patients than in controls, and all GBA mutation carriers examined had widespread alpha-synuclein pathology. It concerns Parkinson's disease genetics and pathology, not Alzheimer's disease treatment, cure, or prevention.
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Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disorder characterized pathologically by ubiquitinated TAR DNA binding protein (TDP-43) inclusions.
Why it matters
This study identified mutations in the TARDBP gene in people with amyotrophic lateral sclerosis (ALS), a motor neuron disorder, and found that mutant TDP-43 caused neural apoptosis in a chick embryo model. It does not test a treatment or cure for Alzheimer's disease.
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Little work has directly examined the course of hippocampal volume in children and adults with childhood maltreatment-related posttraumatic stress disorder (PTSD).
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Frontotemporal dementia (FTD) with ubiquitin-immunoreactive neuronal inclusions (both cytoplasmic and nuclear) of unknown nature has been linked to a chromosome 17q21 region (FTDU-17) containing MAPT (microtubule-associated protein tau).
Why it matters
This study found that mutations in the progranulin gene (PGRN) cause frontotemporal dementia linked to chromosome 17q21, with loss of the mutant allele and reduced PGRN expression. It provides genetic evidence that reduced PGRN-mediated neuronal survival leads to neurodegeneration, but no treatment was tested.
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Cerebral deposition of amyloid beta peptide (Abeta) is an early and critical feature of Alzheimer's disease.
Why it matters
This study cloned and characterized BACE, an enzyme with the characteristics of beta-secretase, which cleaves amyloid precursor protein to produce amyloid beta peptide. It suggests that future development of BACE inhibitors may be beneficial for treating Alzheimer's disease, but no treatment was tested in people.
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64/100
Thirteen families have been described with an autosomal dominantly inherited dementia named frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), historically termed Pick's disease.
Why it matters
This study identified missense and splice-site mutations in the tau gene in families with the inherited dementia FTDP-17. It concerns the genetic cause of that inherited dementia and does not test any treatment, cure or prevention for Alzheimer's disease.
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Biomarkers to determine underlying frontotemporal lobar degeneration (FTLD) tau or TAR DNA-binding protein (TDP) pathology during life are needed to advance clinical trials targeting specific FTD pathologies.
Why it matters
A new immunoassay measuring acetylated tau at lysine 174 in cerebrospinal fluid was higher in all dementia groups than in controls, with the largest increase in FTLD-TDP, and it distinguished FTLD-TDP from FTLD-Tau with high accuracy in the main cohort. Higher levels were also associated with faster cognitive decline in some groups, suggesting potential as a biomarker to tell these pathologies apart.
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Obicetrapib significantly slowed AD biomarker progression over 12 months in participants with ASCVD, with the greatest effects in ApoE4 carriers.
Why it matters
In a clinical trial of people with cardiovascular disease, obicetrapib slowed the rise in Alzheimer's blood biomarkers over 12 months, with the largest effects in ApoE4 carriers. The findings are described as the first demonstration of an oral intervention affecting these biomarkers, but the study did not measure whether this changes dementia outcomes.
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A total of 3828 titles and abstracts and 434 full-text articles were reviewed, yielding 12 articles meeting eligibility criteria.
Why it matters
This systematic review found that levels of neurofilament light chain in CSF and blood were higher in patients with behavioral variant frontotemporal dementia than in patients with psychiatric disorders. It suggests NfL may help supplement clinical diagnostic evaluations in telling these conditions apart, but it is about diagnosis, not treating, curing or preventing Alzheimer's disease.
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Cerebrospinal fluid (CSF) α-synuclein (α-syn) seed amplification assays (SAAs) can detect Lewy body pathology (LBP) with high accuracy but are invasive and costly.
Why it matters
This study evaluated a two-step approach combining smell-function testing with confirmatory CSF α-synuclein seed amplification to detect Lewy body pathology. Among 358 autopsied participants, the workflow predicted brain Lewy body pathology with 94% accuracy and reduced the need for confirmatory CSF testing by 43%, which the authors say may reduce invasive testing and lower healthcare costs.
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63/100
A total of 60 860 adults with type 2 diabetes and obesity were included, with 30 430 each in the GLP-1RA group (mean [SD] age, 57.9 [9.9] years; 50.2% female) and the other antidiabetic drug group (mean [SD] age, 58.0 [10.8] years; 51.4% female) after propensity score matching.
Why it matters
In this cohort of adults with type 2 diabetes and obesity, those taking the GLP-1 receptor agonists semaglutide or tirzepatide had a lower risk of dementia, stroke and death over 7 years. The authors call for further trials to confirm these potential neuroprotective and cerebrovascular benefits.
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Neurodegenerative diseases (NDs), such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and frontotemporal dementia (FTD), exhibit distinct yet overlapping pathological mechanisms.
Why it matters
This large plasma proteomics study identified proteins and pathways shared across and specific to Alzheimer's, Parkinson's and frontotemporal dementia, including potential regulatory proteins. These findings are about disease mechanisms and possible diagnostic or therapeutic targets, not about treating, curing or preventing Alzheimer's disease.
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Three progression clusters emerged in both cohorts: stable cognition, slow decline, and rapid decline-each including cases initially classified as CN or MCI.
Why it matters
Repeated plasma p-tau217 measurements identified stable, slow and rapid cognitive decline clusters, and higher baseline levels predicted faster decline in amyloid-beta-positive cases. The authors say plasma p-tau217 may help capture clinical heterogeneity and support stratification and monitoring in clinical trials, which is about tracking disease rather than treating it.
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63/100
Common variants within TMEM106B are associated with risk for frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP).
Why it matters
In a longitudinal study of genetic frontotemporal dementia, a common TMEM106B variant was linked to less brain atrophy, lower NfL levels, and better cognitive and behavioral measures in carriers of C9orf72 and GRN mutations, with limited effects in MAPT carriers. This suggests TMEM106B may modify disease course, but it is an observational finding, not a treatment.
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DOPA Decarboxylase (DDC) has been proposed as a cerebrospinal fluid (CSF) biomarker with increased concentrations in Lewy body disorders (LBDs) and highest levels in patients receiving dopaminergic treatment.
Why it matters
Plasma DDC was not altered between different Lewy body disorders and other disease groups or controls in absence of treatment, and levels increased with higher dosages of dopaminergic treatment. Plasma DDC is of limited use as a diagnostic biomarker for Lewy body disorders but could be valuable for treatment monitoring.
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Adults with Down syndrome demonstrate striatum-first amyloid accumulation with [ 11 C]PiB PET imaging, which has not been replicated with [ 18 F]florbetapir (FBP).
Why it matters
Using longitudinal PET data, this study found that the striatum shows early amyloid accumulation with PiB, and PiB showed greater striatal-to-cortical binding than florbetapir. It is an imaging biomarker study and reports no treatment, cure, or prevention.
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These findings suggest a benefit of MI plus omega 3 in positive blood amyloid subjects.
Why it matters
In this subgroup analysis of the MAPT trial, a multidomain intervention plus omega 3 was linked to better cognitive scores at some time points in people with positive plasma amyloid status, but these differences were not significant after correction for multiple comparisons. It does not establish a treatment, cure or prevention for Alzheimer's disease.
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Debate surrounds the role of chronic pain as a risk factor for cognitive decline and dementia.
Why it matters
This study examined whether chronic pain is associated with CSF markers of neurodegeneration, microglial activation and inflammation, and with cognitive function. It investigates chronic pain as a possible risk factor but does not test any treatment or show that treating pain prevents dementia.
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Based on the title and abstracts, 830 papers were screened from which 250 primary research papers met the eligibility criteria (original research articles with patients or with a strict diabetes model without comorbidities, that included direct data about microglia in the brain or retina), and 17 additional research papers were included through forward and backward citations, resulting in a total of 267 primary research articles included in the scoping systematic review.
Why it matters
Drawing on 267 studies in cells, animals and patients, this review describes how diabetes changes microglia, the immune cells of the brain and retina. Diabetes pushes microglia toward an activated state, with more inflammatory signals and oxidative stress, through pathways such as NF-κB and the NLRP3 inflammasome. The authors offer it as a starting point for research on how metabolism affects these brain immune cells rather than as a treatment finding.
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Limited evidence suggests that the APOEε4 allele may confer risk for CTE, but previous studies were small with limited scope.
Why it matters
This study of brain donors found that among those older than 65, the APOEε4 allele was associated with chronic traumatic encephalopathy stage and p-tau burden, but there was no significant association for CTE status. It concerns CTE risk and pathology, not the treatment, cure, or prevention of Alzheimer's disease.
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We evaluated 22 persons with nfvPPA (mean age: 67.3 years; 13 female patients) and confirmed underlying 4-repeat tauopathy, 15 persons with semantic variant primary progressive aphasia (svPPA; mean age: 66.5 years; 8 female patients), and 10 healthy controls (HCs; 70 years; 5 female patients).
Why it matters
In 22 people with nonfluent/agrammatic variant primary progressive aphasia confirmed at autopsy, automated speech timing measures differed from healthy controls and from another aphasia variant. This is a cross-sectional diagnostic study and reports no treatment or cure.
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This study examined plasma phosphorylated tau 181 (P-tau181) and 217 (P-tau217) in 1,329 individuals aged 30-98 years from the population-based Mayo Clinic Study of Aging.
Why it matters
Examines how well the blood tests plasma phosphorylated tau 181 and 217 perform in the community.
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The ordered assembly of tau protein into filaments characterizes several neurodegenerative diseases, which are called tauopathies.
Why it matters
This laboratory study used cryo-electron microscopy to show that tau filaments have distinct structures in different tauopathies, including Alzheimer's disease, and proposes classifying tauopathies by their filament folds. It is structural biology that may complement clinical diagnosis and neuropathology, 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.
- In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging
- Single-cell atlas reveals pathological amplification of aging programs and proteostasis collapse in microglia of Alzheimer′s disease mice
- KLOTHO KL-VS heterozygosity is associated with diminished age-related neuroinflammation, neurodegeneration, and synaptic dysfunction in older cognitively unimpaired adults
- Tumor necrosis factor-alpha, microglia and astrocytes in AIDS dementia complex
- Transcranial magnetic stimulation of the precuneus enhances memory and neural activity in prodromal Alzheimer's disease
- The Role of TDP-43 in SARS-CoV-2-Related Neurodegenerative Changes
- In vivo oxidative stress in brain of Alzheimer disease transgenic mice: Requirement for methionine 35 in amyloid beta-peptide of APP
- Chronic low-dose-rate ionising radiation affects the hippocampal phosphoproteome in the ApoE-/- Alzheimer's mouse model
- Structural maturation of neural pathways in children and adolescents: in vivo study
- The Triggering Receptor Expressed on Myeloid Cells 2 Binds Apolipoprotein E