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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Alzheimer´s disease (AD) is dominated by a complex cellular pathology which involves most brain cell types with glial cells increasingly recognized as playing fundamental roles in neurodegeneration.
Why it matters
In this laboratory study, astrocytes derived from Alzheimer's patients with the APOE4/4 genotype showed a reactive, senescent, and pro-inflammatory state that compromised their support of neurons. These findings are from cell models and human tissue and do not yet show a treatment for people.
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Analysis of the genotyping data revealed that the TMEM106B locus consists of four major haplotypes: HA/Ha (covering the coding region), and HB/Hb (covering the upstream regulatory region).
Why it matters
This genetic study found that the TMEM106B locus has four haplotype combinations, with one combination increasing risk of neurodegeneration and another being protective, and that cognitively healthy centenarians were more enriched with the protective combination. It links the protective combination to lower TMEM106B C-terminal peptide abundance, but these are association findings and no treatment is tested.
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Overall PiB-PET uptake increased during the first two years (before ARIA-E) and decreased during the last two years (including ARIA-E episodes) (0.03±0.05 vs. -0.04±0.04 SUVR/year, p-value=0.01, Figure 2).
Why it matters
In one DIAN-TU-001 participant treated with gantenerumab, PiB-PET uptake decreased during the years including ARIA-E episodes, and the ARIA-E region showed lower amyloid area fraction at autopsy. These are preliminary single-case imaging-neuropathology findings about ARIA-E and local amyloid removal, not evidence of a cure or prevention.
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Living in more deprived neighborhoods was associated with an accelerated disease course in bvFTD, highlighting an important socioeconomic disparity in disease prognosis.
Why it matters
Among 311 people with behavioral-variant frontotemporal degeneration, those in the most deprived neighborhoods had shorter survival and faster decline in cognition, executive function, and language. This shows a socioeconomic disparity in disease course but does not test any treatment or cure.
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180 patients (46 %) developed delirium and 70% of these had dementia.
Why it matters
In this multicentre cross-sectional study of hip fracture patients, cerebrospinal fluid neurogranin concentrations did not differ significantly between those with and without delirium. The authors conclude that synaptic dysfunction involving neurogranin may not be a key process in delirium, and the study concerns delirium rather than Alzheimer's disease treatment.
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Eleven studies involving 1,536 PLWH were included.
Why it matters
This meta-analysis of eleven studies with 1,536 people living with HIV looked at CXCL10, an inflammatory signaling molecule, in spinal fluid. People with HIV-associated neurocognitive disorders had significantly higher CXCL10 levels than those without. The authors call it a promising but not definitive marker for this HIV-related condition; the record does not address Alzheimer's itself.
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Dopamine transporter (DAT) imaging and electroencephalography (EEG) are recommended biomarkers for diagnosing dementia with Lewy bodies (DLB).
Why it matters
This retrospective analysis of 120 patients found that dopamine transporter imaging and EEG biomarkers independently explained clinical symptoms in dementia with Lewy bodies. These findings relate to diagnosis and understanding of symptoms, not to treating, curing or preventing the disease.
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We previously reported that T96K is a gain-of-function mutation in TREM2 based on its ability to increase ligand-dependent activation.
Why it matters
This study found that the TREM2 T96K mutation increases Alzheimer's disease risk and impairs microglial function, including reduced clustering around amyloid-beta plaques and impaired uptake of amyloid-beta, in a sex-dependent manner in mice and cell cultures. It identifies a genetic risk mechanism and does not test any treatment, cure or prevention.
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Sortilin (SORT1) is a lipoprotein receptor that shows genome-wide association with hypercholesterolaemia, explained by its ability to control hepatic output of lipoproteins.
Why it matters
In mouse and cell models, sortilin was shown to help neurons take up polyunsaturated fatty acids carried by apolipoprotein E, providing an alternative fuel when glucose is limited. This pathway worked with apoE3 but not with the Alzheimer risk factor apoE4, which disrupted sortilin's activity.
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44/100
Delirium is a neuropsychiatric syndrome that is pathophysiologically related to both mental (dementia, depression) and physical illness.
Why it matters
This study examined whether certain brain-related miRNAs are linked to postoperative delirium in cardiac surgery patients. After multivariate analysis, only miR-183-5p was independently associated with delirium risk, alongside other predictors such as depression, peripheral vascular disease, female gender, smoking and increased postoperative pCO2.
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Tauopathies encompass a large majority of dementia diagnoses and are characterized by toxic neuronal or glial inclusions of the microtubule-associated protein tau.
Why it matters
This review describes how immune responses, including microglial activation and T cell responses, accompany tau aggregation and may drive tauopathy progression. It notes that tauopathies currently lack an effective therapy or cure and discusses potential ways the immune system could be harnessed to treat them.
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Postoperative delirium (POD) is a common and severe neuropsychiatric complication affecting older adults after surgery.
Why it matters
This review discusses biomarkers linked to dementia pathology, neuronal injury, glial activation, and systemic inflammation that may help predict or diagnose postoperative delirium in older adults. It notes that findings vary and that larger, more standardized studies are needed, so no biomarker is established for clinical use.
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Atherosclerosis is a progressive, multifactorial disease driven by the interplay of lipid dysregulation, chronic inflammation, oxidative stress, and maladaptive vascular remodeling.
Why it matters
This review is about targeted drug delivery and nanomedicine for atherosclerosis and cardiovascular risk, not about Alzheimer's disease. It provides no information relevant to treating, curing, or preventing Alzheimer's disease.
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WMH burden positively correlated to Neurofilament-Light (NfL) and pTau181.
Why it matters
In this cross-sectional study, white matter hyperintensity burden correlated with neurofilament-light and pTau181, and several blood markers moderated the relationship between executive function or processing speed and white matter hyperintensities. The authors link inflammatory mechanisms represented by GFAP to tau pathology and white matter hyperintensities, but the study does not test any treatment, cure, or prevention.
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These findings establish IF as a potent modulator of synaptic resilience in VaD, acting through coordinated preservation of synaptic structure, inhibition of inflammatory synapse loss, and metabolic reprogramming.
Why it matters
This study reports that intermittent fasting preserved synaptic structure, reduced inflammatory synapse loss and reprogrammed metabolism in a vascular dementia model, suggesting it as a possible non-pharmacological strategy. The findings come from a model rather than patient trials, so no treatment, cure or prevention in people is established.
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Forty bvFTD patients and 40 HC (56.25% female, mean age of 63.55 years) were involved.
Why it matters
This study found that behavioral variant frontotemporal dementia exhibits peripheral metabolic and inflammatory dysregulation associated with frontotemporal lobar degeneration and clinical symptoms, and that the interaction of these dysregulations has a greater impact. It does not test any treatment, so it does not show a cure or prevention.
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44/100
The most common clinical symptoms in FTLD-TDP-PSP were memory loss (100%) followed by parkinsonism (80%), early falls (60%), and behavioral variant FTD (60%).
Why it matters
This study describes a small subset of patients with frontotemporal lobar degeneration with TDP-43 pathology who presented with symptoms resembling progressive supranuclear palsy, with memory loss in all five patients and parkinsonism in most. It is a small case series about diagnosis and does not test any treatment, cure or prevention.
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Early isolated functional disruptions in salience/visual networks were present in asymptomatic carriers, along with anterior cingulate gray matter reductions.
Why it matters
In people carrying MAPT mutations, functional connectivity changes appeared in asymptomatic carriers before structural damage, and later stages showed additional structural damage. The authors suggest connectivity measures could serve as biomarkers, but this is about tracking disease, not treating or preventing it.
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Surprisingly, levels of strain A and B aSyn species were higher in plasma from individuals with PD compared to DLB in 2 independent cohorts.
Why it matters
This study found that levels of strain A and B α-synuclein species were higher in plasma from people with Parkinson's disease compared to dementia with Lewy bodies, and that lower levels of strain A predicted a faster rate of cognitive decline in Parkinson's disease. It is about a potential biomarker, not a treatment, cure or prevention.
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A total of 197 participants were included in the study.
Why it matters
In 197 older adults, lower choroidal vascular volume was linked to more white matter hyperintensities, and both irregular white matter hyperintensity shape and reduced choroidal volume were linked to poorer memory. The authors suggest ischemia as a possible shared mechanism, but this is an observational study and does not test any treatment.
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Although apolipoprotein E (ApoE) ε4 is a well-established risk factor for Alzheimer disease, its role in the development of post-stroke cognitive impairment (PSCI) remains uncertain.
Why it matters
In this prospective cohort, the ApoE ε4 allele was not associated with the risk of post-stroke cognitive impairment at 3 or 12 months after stroke. Other factors such as age, body mass index, education level, and initial stroke severity were associated with risk at 3 months.
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Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD) are two neurodegenerative disorders that share common genes and pathomechanisms and are referred to as the ALS-FTD spectrum.
Why it matters
This review describes molecular mechanisms of protein aggregation in ALS-FTD, focusing on TDP-43, and the cell's protective responses such as molecular chaperones and post-translational modifications. It suggests these pathways could offer insights for future targeted interventions, but reports no treatment that has been shown to work.
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Biallelic loss-of-function variants in TYROBP and TREM2 cause autosomal recessive presenile dementia with bone cysts known as Nasu-Hakola disease (NHD, alternatively polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy, PLOSL).
Why it matters
This study found that carrying a monoallelic TYROBP deletion was associated with an increased risk and earlier onset of Alzheimer's disease and dementia in Finnish biobank participants. The authors also report the first case of a monoallelic carrier with NHD-type bone cysts and show that the deletion leads to decreased DAP12 protein and altered inflammatory and unfolded protein responses in microglia-like cells.
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The global aging population has led to a significant rise in dementia and cognitive decline, with Alzheimer's disease as the primary cause.
Why it matters
In this cross-sectional study of 510 participants, lower MMSE scores were associated with reduced gray matter volume in several brain regions, and the MCI group showed reductions in the left hippocampus, left parahippocampal gyrus, left anterior cingulate cortex, and right ventromedial prefrontal cortex compared with normal cognition. This links a common screening test to brain structure but does not test any treatment, cure, or prevention.
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44/100
Vascular dementia (VaD) is a heterogeneous group of brain disorders caused by cerebrovascular pathologies and the second most common cause of dementia, accounting for over 20% of cases and posing an important global health concern.
Why it matters
This review describes oxidative stress and neuroinflammation as central mechanisms in vascular dementia and notes that antioxidants and anti-inflammatory agents have emerged as potential therapeutic targets. It concerns vascular dementia rather than Alzheimer's disease and reports no established 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.
- Cellular players that shape evolving pathology and neurodegeneration following traumatic brain injury
- Autoimmune thyroiditis associated with mild "subclinical" hypothyroidism in adults with Down syndrome: a comparison of patients with and without manifestations of Alzheimer disease
- The mTOR Inhibitor Rapamycin Mitigates Perforant Pathway Neurodegeneration and Synapse Loss in a Mouse Model of Early-Stage Alzheimer-Type Tauopathy
- Arterial Spin Labeling Perfusion of the Brain: Emerging Clinical Applications
- Comparison of Common and Disease-Specific Post-translational Modifications of Pathological Tau Associated With a Wide Range of Tauopathies
- Pulse wave velocity is associated with β-amyloid deposition in the brains of very elderly adults
- Experimental cerebral hypoperfusion induces white matter injury and microglial activation in the rat brain
- Big tau and brain-derived tau reveal peripheral and central nervous system involvement in neuropathies
- Clinicopathological characterization of Pick's disease versus frontotemporal lobar degeneration with ubiquitin/TDP-43-positive inclusions
- Protein expression of BACE1, BACE2 and APP in Down syndrome brains