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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The nervous system specific proteins glial fibrillary acidic protein (GFAp), S-100 and myelin basic protein (MBP) were determined in 535 human cerebrospinal fluid (CSF) samples.
Why it matters
This study found that levels of the protein GFAp were increased in the cerebrospinal fluid of some patients with Alzheimer-type dementia, and the authors suggest it could be used as a diagnostic tool for dementia. It does not report any treatment, cure, or prevention of Alzheimer's disease.
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Down syndrome (trisomy 21) is the most common genetic cause of intellectual disability.
Why it matters
This review discusses that seizures are common in Down syndrome, with peaks in infancy and after age 30 when dementia often begins, but the mechanisms are not well understood. It calls for more research into age-specific treatments for seizures in this population.
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In each case the framework recovered known disease genes and identified biologically coherent, disease-specific modules: in AD, 17 stable high-confidence genes and modules enriched in lipid and cholesterol metabolism and amyloid precursor protein processing; in PD, 17 stable genes and modules associated with mitophagy, ubiquitin-proteasome signaling, and mitochondrial dysfunction; in RA, 20 stable genes and modules enriched in antigen presentation and JAK-STAT cytokine signaling.
Why it matters
This describes a computational framework that recovered known disease genes and identified gene modules for Alzheimer's and other diseases. It is a gene prioritization method and does not test or demonstrate any treatment, cure or prevention.
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The onset and sustenance of Alzheimers and Parkinsons is solely dependent on the driving power of the immune cytokine interleukin-1 beta (IL-1β), arising from neuronal distress and release of sAPPα, which activates microglia for synthesis and release of IL-1β driving synthesis of βAPP, Aβ plaques and synthesis and activation of MAPKp38 for phosphorylation of tau for neurofibrillary tangle formation in Alzheimers and for a-synuclein for formation of Lewy bodies in Parkinsons.
Why it matters
In cellular models, ibuprofen decreased IL-1β and downstream proteins while increasing autophagy proteins, especially in APOE3 and APOE4 cells. These results suggest a potential mechanism for ibuprofen's reported risk reduction, but this is early cellular research.
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32/100
Defective mitochondrial quality control is increasingly implicated in tau-mediated neurodegeneration, but how distinct tau lesions in different cell types interact with PINK1-PRKN-mediated mitophagy remains unclear.
Why it matters
In 92 postmortem human brains, the amount of pS65-Ub and pS202-tau varied by disease, cell type and tau inclusion type across several primary tauopathies. This is autopsy research that describes patterns of pathology and does not test any treatment.
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Beyond their role in energy production, mitochondria also interact with other organelles through forming membrane contacts that serve as central hubs of cellular metabolism and signaling.
Why it matters
In tauopathy mice, raising levels of a protein called TBC1D15 restored autophagy and reduced tau pathology, neurodegeneration and cognitive impairment. This is early animal research, so it is not yet known whether targeting this mechanism would help people with tauopathies.
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For these neurodegenerative dementias, we observed that the chronological age did not align with their biological age, which was determined based on hippocampal transcript levels (i.e., transcriptional age).
Why it matters
Looking at gene activity in the hippocampus, a memory hub, of people with Alzheimer's disease, Down syndrome dementia and Parkinson's disease dementia, researchers found 45 genes changed in common across all three conditions. Two of these, EHMT2 and LMNB2, stood out as central 'hub' genes in a shared network. The authors suggest they could be universal biomarkers or targets across these dementias, but this is an early gene-expression finding rather than a test of any treatment.
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32/100
The locus of the gene PTK2B encoding the tyrosine kinase Pyk2 has been associated with the risk of late-onset Alzheimer’s disease, the predominant form of dementia.
Why it matters
In mouse and cell experiments, deleting the gene for the protein Pyk2 prevented amyloid-beta oligomer-induced hippocampal neuronal hyperactivity and synaptic loss, pointing to Pyk2 as a possible target in early Alzheimer's disease. These are laboratory findings, not yet evidence that targeting Pyk2 helps people.
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32/100
This method differentiated eight tauopathies, including Alzheimer's disease, Pick disease, progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), argyrophilic grain disease (AGD), frontotemporal dementia with parkinsonism associated with chromosome 17 with N279K mutation (FTDP-17 N279K), and globular glial tauopathies types II and III.
Why it matters
This laboratory method used salt conditions to distinguish eight different tauopathies, including Alzheimer's disease, based on how tau aggregates. It is a diagnostic and research tool, not a treatment, and its clinical usefulness has not yet been established.
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Cystatin C (CST3) colocalizes with amyloid-β (Aβ) around vessels in cerebral amyloid angiopathy (CAA).
Why it matters
Examining brain tissue from 12 Alzheimer disease and 5 control subjects plus AD model mice, this study found that aggregated cystatin C binds to amyloid-β and accumulates around vessels, and that cathepsin B was significantly decreased in AD and inversely correlated with CAA severity. These findings suggest a possible contribution to CAA pathogenesis but no treatment, cure or prevention is tested.
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Acupuncture ameliorated cognitive impairment in VD rats, reduced hippocampal neuronal damage and apoptosis, downregulated pro-apoptotic proteins (cleaved-caspase 3 and Bax), and upregulated anti-apoptotic Bcl-2.
Why it matters
In rats with vascular dementia, acupuncture improved cognitive impairment and reduced neuroinflammation and neuronal apoptosis, possibly through effects on peripheral immunity. This is animal research, so it does not establish that acupuncture treats dementia in people.
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Imbalanced medical datasets significantly impair the performance of diagnostic models by biasing predictions towards majority classes.
Why it matters
This study built a method for generating fake medical images, including Alzheimer MRI scans, to balance imbalanced datasets, and it produced more realistic images than an older method on the Alzheimer MRI data. Downstream classification improved measurably when the augmented datasets were used, but this is a technical image-generation tool, not a treatment, cure or prevention for Alzheimer's disease.
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Semantic dementia (SD) is a type of dementia characterized by a loss of semantic memory, typically presenting with left-predominant temporal lobe atrophy and a frontotemporal lobar degeneration with TDP-43 (FTLD-TDP) type C pathology.
Why it matters
This single case report describes an 81-year-old woman with atypical semantic dementia whose imaging suggested a primary tauopathy, possibly argyrophilic grain disease. It is one patient's case and cannot establish any treatment, cure or prevention for Alzheimer's disease.
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2′-FL improved cognitive performance in 5xFAD mice, reduced Aβ plaque deposition and pro-inflammatory cytokine levels in vivo , and mitigated oxidative stress and synaptic dysfunction in cellular models.
Why it matters
In a mouse model of Alzheimer's disease, oral 2'-Fucosyllactose improved cognitive test performance and reduced amyloid plaque load in the hippocampus and cortex, but it did not significantly affect tau hyperphosphorylation. These findings are from animal and cell experiments, so it is not yet known whether this compound would help people.
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Familial frontotemporal dementia (FTD) is a genetically heterogeneous disease with various clinical manifestations, making it difficult to diagnose.
Why it matters
This review describes fluid biomarkers in blood and cerebrospinal fluid that may change years before symptoms in familial frontotemporal dementia. Such biomarkers could aid diagnosis and possibly serve as outcome endpoints in future clinical trials, but no treatment, cure or prevention is reported.
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We recently confirmed and extended these findings using recombinant TauOs generated from full-length human tau in the presence of arachidonic acid (Balducci et al., 2025; Figure 1).
Why it matters
In mice, tau oligomers impaired recognition memory in normal mice but not in mice lacking the cellular prion protein, supporting a role for this protein in tau oligomer toxicity. This is animal and laboratory work, and the authors say it still needs validation using tau oligomers purified from patients' brains.
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Mild cognitive impairment (MCI) is the in-between stage between healthy cognitive aging and neurodegenerative diseases such as Alzheimer's disease (AD).
Why it matters
This review discusses extracellular vesicles and carbon nanotubes as nanocarrier systems that can cross the blood-brain barrier and deliver therapeutic cargo, with current applications being preclinical. It outlines potential approaches to delay mild cognitive impairment progression, but no treatment or cure is established.
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As the term limbic-predominant age-related transactive response DNA-binding protein 43 (TDP-43) encephalopathy (LATE) was coined in 2019, more than 200 articles addressing the subject were published.
Why it matters
This review describes LATE-NC as marked by TDP-43 deposition in limbic structures and often associated with cognitive decline resembling Alzheimer's disease, though with slower progression in isolated cases. It notes that clinical criteria for in-vivo diagnosis have been established and that biomarker development in CSF and blood remains in its early stages.
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Since the term limbic-predominant age-related TDP-43 encephalopathy (LATE) was coined in 2019, more than 200 articles addressing the subject were published.
Why it matters
This review describes LATE-NC as a cause of age-related cognitive decline that often coexists with other neuropathologies like Alzheimer's disease changes and Lewy body dementia. It notes that clinical criteria for in-vivo diagnosis have been established and that biomarker development in CSF and blood remains in its early stages.
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OCTA is a handy, noninvasive tool that enables the visualization of diminished retinal microvascular density in cases of early CSVD.
Why it matters
In this small case-control study of 40 patients with cerebral small vessel disease and 20 controls, patients had significantly lower retinal capillary plexus density and macular thickness, and these impairments were associated with higher Fazekas and SVD scores. The authors suggest OCTA could serve as a screening tool for early small vessel disease, but it is a small observational study and not a treatment.
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These dysregulations are associated with malfunctions in multiple signaling pathways or disrupted mechanical cellular responses.
Why it matters
This review describes how vascular smooth muscle cell dysfunction contributes to cerebral small vessel disease through changes such as hypertrophy, degeneration, and phenotypic switching. It notes that emerging treatments targeting cyclic nucleotide pathways show promise in animal or preclinical work, but the molecular mechanisms remain incompletely understood and clinical translation is still needed.
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MDVs are small vesicles that bud from mitochondria and play an important role in removing damaged mitochondrial components.
Why it matters
This perspective article describes mitochondria-derived vesicles as involved in removing damaged mitochondrial components and notes that their release can trigger inflammatory responses contributing to neuronal damage. The author states there is only indirect evidence and no work reporting direct contributions, so no treatment is established.
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Idiopathic rapid eye movement (REM) sleep behavior disorder (iRBD) is characterized by the loss of atonia during REM sleep, causing dream-enacting behavior.
Why it matters
In 62 people with idiopathic REM sleep behavior disorder, certain alpha brain wave patterns were linked to lower scores on a cognitive test. This suggests these brain wave measures might one day help identify cognitive decline in this group, but the study only shows an association and does not test any treatment.
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A 52-year-old male with early-stage Alzheimer's disease and long-standing anxiety received 30 repetitive transcranial magnetic stimulation sessions over 8 months and 20-month Mediterranean diet intervention.
Why it matters
This is a single case report of one man with early Alzheimer's disease who received repetitive transcranial magnetic stimulation and a Mediterranean diet, and his cognitive and anxiety scores improved. As a single case with no control group, it cannot show that these treatments cure, treat or prevent Alzheimer's disease.
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Recently, an increasing number of genes have been associated with global developmental delay (GDD) and intellectual disability (ID).
Why it matters
This single case report links a newly found SNX13 gene change to developmental delay in one child, not to Alzheimer's disease. It provides no evidence about treating, curing or preventing 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.
- The physiological phosphorylation of tau is critically changed in fetal brains of individuals with Down syndrome
- Hippocampal specialization of food-storing birds
- Increase of TREM2 during Aging of an Alzheimer's Disease Mouse Model Is Paralleled by Microglial Activation and Amyloidosis
- A mutation at codon 279 (N279K) in exon 10 of the Tau gene causes a tauopathy with dementia and supranuclear palsy
- Hippocampal hypocellularity in the Ts65Dn mouse originates early in development
- Deciphering distinct genetic risk factors for FTLD-TDP pathological subtypes via whole-genome sequencing
- MRI volumes of amygdala and hippocampus in non-mentally retarded autistic adolescents and adults
- Deconstructing the intercellular interactome in vascular dementia with focal ischemia for therapeutic applications
- Evaluating the Patterns of Aging-Related Tau Astrogliopathy Unravels Novel Insights Into Brain Aging and Neurodegenerative Diseases
- Statins promote the degradation of extracellular amyloid {beta}-peptide by microglia via stimulation of exosome-associated insulin-degrading enzyme (IDE) secretion