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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CSF and plasma SNAP25 were positively correlated, but no correlation was observed for VAMP2 in these matrices.
Why it matters
The synaptic markers SNAP25 and VAMP2 were higher in Alzheimer's disease than in Parkinson's disease and other neurological disorders, and were not affected by alpha-synucleinopathy. This supports their use for detecting Alzheimer's-related synaptic dysfunction, but the study does not test any treatment.
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The SorLA protein, encoded by the Sortilin-related receptor 1 ( SORL1 ) gene, is a major player in Alzheimer’s disease (AD) pathophysiology.
Why it matters
This study found significantly decreased levels of soluble SorLA in cerebrospinal fluid from Alzheimer's patients carrying SORL1 variants that disrupt protein trafficking, compared with other groups. This supports sSorLA as a potential biomarker for disrupted SorLA trafficking, but it is a biomarker study and does not test any treatment, cure or prevention.
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The 4R-like pattern was more prevalent and more strongly expressed (84.3%, mean score, 2.0 ± 1.1) in patients with a consensus diagnosis of PSP/CBD (joint diagnostic group of clinically likely 4R tauopathies) than in all other groups (11.6%, 0.26 ± 0.75, P < 0.0001).
Why it matters
In patients with parkinsonism, a 4R-like binding pattern on [18F]florzolotau PET identified those with a consensus diagnosis of PSP/CBD with an area under the ROC curve of 0.87. The authors call it a promising biomarker for differential diagnosis, not a treatment or cure.
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TDP-43 protein is an RNA-binding protein linked to amyotrophic lateral sclerosis, frontotemporal dementia, and Alzheimer disease.
Why it matters
In biophysical experiments with a TDP-43 fragment and synthetic membranes, a higher negative lipid charge caused the protein to bind to the bilayer surface and promoted its aggregation. This is early laboratory work on how TDP-43 interacts with membranes, with no treatment, cure or prevention reported.
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Neurodegenerative diseases are characterized by protein aggregation and overlapping pathologies, challenging traditional classifications and highlighting shared underlying mechanisms.
Why it matters
This review describes how tau and alpha-synuclein co-aggregate and interact, and argues for integrated therapies targeting protein cross-seeding. It is a review of mechanisms and does not report any treatment that has been shown to work in patients.
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Radial diffusivity analyses detected impaired bilateral cerebello-frontal, cerebello-parietal, and cerebello-temporal connectivity in all study groups along the ALS-FTD spectrum.
Why it matters
This study found significant cerebro-cerebellar disconnection and intra-cerebellar pathology in frontotemporal dementia, with different patterns across subtypes. It suggests that cerebellar network dysfunction should be considered in FTD, but no treatment or prevention is offered.
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The brain metabolic decline in DS with age reflects Alzheimer's pathological processes and involves temporoparietal regions in a similar pattern to that found in other forms of AD.
Why it matters
In 105 adults with Down syndrome, brain metabolism declined with age in a more distributed pattern than in healthy controls, and those at the prodromal stage showed medial parietal hypometabolism that later extended to other regions at the dementia stage. All measured CSF biomarkers were closely associated with hypometabolism in affected regions, suggesting these imaging and biomarker changes track the progression of Alzheimer's disease in Down syndrome.
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Transactive response (TAR) DNA-binding protein 43 (TDP-43) is a critical RNA/DNA-binding protein involved in various cellular processes, including RNA splicing, transcription regulation, and RNA stability.
Why it matters
This review covers the history and structural understanding of TDP-43 and assesses therapeutic strategies targeting TDP-43 pathology, including direct and indirect approaches and modulating its phase separation. It proposes future research directions but reports no treatment that has been shown to cure or prevent disease.
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γ-Secretase modulators (GSMs) represent an emerging oral therapy for preventing and targeting Aβ-amyloidosis in Alzheimer disease.
Why it matters
In APP/PS1dE9 transgenic mice, 28 days of oral treatment with the gamma-secretase modulator AZ4126 reduced plaque formation and growth and also shrank established plaques, with changes in Aβ peptide levels. These are animal and cell results, so it is too early to say whether this approach treats or prevents Alzheimer's disease in people.
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Chitinase-3-like-1 (CHI3L1) is an evolutionarily conserved protein involved in key biological processes, including tissue remodeling, angiogenesis, and neuroinflammation.
Why it matters
This review describes CHI3L1 as a protein involved in neuroinflammation that is elevated in Alzheimer's and other brain disorders and may serve as a biomarker. It discusses therapeutic strategies targeting CHI3L1 but does not report an established treatment or cure.
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Aggregation of microtubule-associated tau protein is a distinct hallmark of several neurodegenerative disorders such as Alzheimer’s disease (AD), dementia with Lewy bodies (DLB), and progressive supranuclear palsy (PSP).
Why it matters
Tau oligomers amplified from the brains of people with Alzheimer's disease, dementia with Lewy bodies, and progressive supranuclear palsy differed in structure and stability and affected neuronal function differently. This suggests that therapies might one day be tailored to specific tau forms, but the work is laboratory-based and no treatment is established.
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The study population demonstrated limited PET-based amyloid-β and tau pathology, which did not associate with any of the investigated plasma biomarkers.
Why it matters
In older adults without dementia who had limited amyloid-β and tau pathology on PET, plasma VAMP2 and GFAP were associated with synaptic vesicle glycoprotein 2A PET, suggesting they may reflect synapse pathology. This is a cross-sectional biomarker study and does not test any treatment, cure or prevention.
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These findings suggest that subcortical VCIND modifies the relationship between FPN lateralization and cognitive functions, rather than altering the lateralization pattern itself.
Why it matters
In this randomized study of 60 patients with vascular cognitive impairment no dementia, cognitive training shifted brain network lateralization toward a more bilateral pattern, and these changes correlated with improved executive and memory functions. The findings suggest cognitive training reorganizes brain networks, though the changes disappeared by follow-up.
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Epidemiological studies show that individuals who carry the relatively uncommon APOE ε2 allele rarely develop Alzheimer disease, and if they do, they have a later age of onset, milder clinical course, and less severe neuropathological findings than people without this allele.
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45/100
This molecular genetics study found that several TREM2 gene variants previously thought to work only by altering the TREM2 protein itself, also disrupt how the TREM2 gene's RNA message is spliced together, sometimes producing dysfunctional protein versions.
Why it matters
Several TREM2 variants, including the common Alzheimer's risk variants R62H and T96K, disrupt how the gene's RNA is spliced, not just the protein itself. This is a molecular genetics finding about how these risk variants work, not a treatment or prevention result.
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Tauopathies are a diverse group of progressive and fatal neurodegenerative diseases characterized by aberrant tau inclusions in the central nervous system.
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Disordered lipid accumulation in the arterial wall is a hallmark of atherosclerosis.
Why it matters
In atherosclerosis-prone mice and cells, TREM2 promoted cholesterol uptake and foam cell formation, a process tied to artery disease. This concerns heart and blood vessel disease rather than Alzheimer's, so it does not directly inform Alzheimer's treatment, cure or prevention.
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TREM2 is a myeloid cell receptor that has been extensively described in the context of neuroinflammation and neurodegenerative diseases.
Why it matters
This review focuses on TREM2 in the tumor microenvironment, where TREM2-deficiency or blockade protected mice and improved response to anti-PD1 therapy. It does not report any findings about treating, curing, or preventing Alzheimer's disease, though it notes TREM2 has been studied in neuroinflammation.
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A non-coding variant (rs35349669) in INPP5D increases the risk for Alzheimer's disease (AD), and elevated INPP5D expression is associated with increased plaque deposition.
Why it matters
In a 5xFAD mouse model, reducing Inpp5d lessened amyloid pathology. This is animal research, so it is preliminary and does not yet show a treatment for people.
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Triggering receptor expressed on myeloid cells-2 (TREM2) is a key pro-tumorigenic marker of tumor-infiltrating macrophages, showing potent immunosuppressive activity in tumor microenvironment.
Why it matters
A platinum-based compound inhibited TREM2 on macrophages and slowed tumor growth in mouse colorectal cancer models. It does not test any treatment, cure, or prevention for Alzheimer's disease.
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Early life adversity impairs normal hippocampal function and connectivity in various mammalian species, including humans and rodents.
Why it matters
This study examines how early life stress affects synaptic pruning in the developing mouse hippocampus, not Alzheimer's disease. It provides no information on treating, curing or preventing Alzheimer's disease.
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Prevalent LB- and AD-related neurodegenerative pathologies affect a significant proportion of iNPH patients and contribute to cognitive decline (both) and motor impairment (only LB pathology) but do not significantly influence the surgical outcome at 6 months.
Why it matters
In people with idiopathic normal pressure hydrocephalus, about one in five showed Lewy body pathology markers and about one in four showed amyloid positivity, with some links to symptoms and surgery outcome. The study is about co-pathologies in this condition and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Triggering receptors expressed on myeloid cells 2 (TREM2) is considered a protective factor to protect host from bacterial infection, while how it elicits this role is unclear.
Why it matters
This study found that TREM2 deficiency increased macrophage pyroptosis and reduced bacterial killing in response to pyogenic bacteria. It is about bacterial infection, not Alzheimer's disease, and does not show a treatment or cure for Alzheimer's.
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The existence of individuals who remain cognitively intact despite presenting histopathological signs of Alzheimer's disease (AD), here referred to as "Nondemented with AD neuropathology" (NDAN), suggests that some mechanisms are triggered to resist cognitive impairment.
Why it matters
In people who remained cognitively intact despite having Alzheimer's brain pathology, TREM2-related microglial activity appeared to help clear damaged synapses and preserve synaptic integrity. This suggests a possible protective mechanism, but it is an observational study and not a treatment or prevention trial.
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The mechanism of sphingosine-1-phosphate (S1P)-mediated phagocytosis remains unknown.
Why it matters
This study found that sphingosine-1-phosphate acts as a TREM2 ligand and promoted microglial phagocytosis in stroke. It does not test any treatment, cure, or prevention for Alzheimer's disease.
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.
- Human stem cell-derived monocytes and microglia-like cells reveal impaired amyloid plaque clearance upon heterozygous or homozygous loss of TREM2
- C9orf72 poly(GR) aggregation induces TDP-43 proteinopathy
- Human immunodeficiency virus encephalitis is the pathological correlate of dementia in acquired immunodeficiency syndrome
- Prion-like spreading of pathological α-synuclein in brain
- A mutation in VPS35, encoding a subunit of the retromer complex, causes late-onset Parkinson disease
- Extensive astrocyte infection is prominent in human immunodeficiency virus-associated dementia
- Microstructural disruption of the right inferior fronto-occipital and inferior longitudinal fasciculus contributes to WMH-related cognitive impairment
- TREM2hi resident macrophages protect the septic heart by maintaining cardiomyocyte homeostasis
- Increased midlife triglycerides predict brain β-amyloid and tau pathology 20 years later
- Soluble TREM2 and biomarkers of central and peripheral inflammation in neurodegenerative disease