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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Modern clinical studies have demonstrated its significant therapeutic effects in treating Alzheimer’s disease (AD) without notable adverse reactions.
Why it matters
In laboratory and mouse experiments, Xixin Decoction changed proteins involved in amyloid-beta transport across the blood-brain barrier, reduced amyloid accumulation and eased neuroinflammation. These are early laboratory and animal findings, not proof of benefit in people.
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Cerebral small vessel disease can manifest as vascular dementia, typically associated with vascular risk factors or cerebral amyloid angiopathy, and more rarely associated with hereditary conditions.
Why it matters
This single case describes a woman with late-onset dementia and a variant in the COL4A2 gene, along with widespread white matter changes on brain imaging. The authors state it is unclear whether the gene variant caused her dementia or was an unrelated finding, so no conclusions about cause or treatment can be drawn.
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We report that pan-neuronal expression of each ApoE allele induces lipid accumulation specifically in the brain, but not in the muscle.
Why it matters
This study in fruit flies found that different ApoE alleles cause lipid buildup in the brain, with ApoE4 acting independently of Dgat2, and that time-restricted feeding prevented this buildup. It is early animal work and does not test a treatment, cure, or prevention for Alzheimer's disease in people.
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is a rich source of valuable secondary metabolites, particularly terpene trilactones (TTLs) such as ginkgolides and bilobalides, which are obtained from the leaves and seeds of the plant.
Why it matters
This review describes research on producing terpene trilactones from Ginkgo biloba cell and organ cultures, noting that these compounds have anti-dementia effects among other properties. The work is laboratory-based and does not test any treatment in people with Alzheimer's disease.
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Tau phosphorylation and aggregation is the final common pathway for neuronal toxicity across multiple neurodegenerative diseases including Alzheimer disease, progressive supranuclear palsy, and corticobasal degeneration.
Why it matters
This study characterized the tau interactome in human fetal, adult and Alzheimer's disease brains and found isoform-dependent interaction with 14-3-3 family proteins, aiming to explain why fetal phosphorylated tau and aggregates appear non-toxic. It is laboratory work on mechanisms and does not test any treatment, cure or prevention.
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Lysosome dysfunction arises early and propels Alzheimer’s Disease (AD).
Why it matters
In human Down syndrome cells, a fragment of the amyloid precursor protein was found to inhibit a lysosomal pump and reduce lysosomal acidification. This is laboratory cell research identifying a possible mechanism, not a treatment, cure or prevention for Alzheimer's disease.
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Alzheimer's disease (AD) is the most common type of dementia worldwide, characterized by the deposition of neurofibrillary tangles and amyloid-β (Aβ) peptides in the brain.
Why it matters
In a non-genetic mouse model of Alzheimer's, a ribonucleotide-based supplement reduced oxidative stress, brain inflammation, and amyloid pathology. This is animal research only and does not show that this supplement treats, cures, or prevents Alzheimer's disease in people.
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Amyloid-β (Aβ) aggregated forms are highly associated with the onset of Alzheimer's disease (AD).
Why it matters
This study synthesized 17 benzofuran derivatives and tested whether they could disaggregate Aβ oligomers and plaques in the brains of 5XFAD Alzheimer transgenic mice. The findings are from animal research and do not establish a treatment for people.
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Further research is needed to elucidate factors underlying differences in SFU and BI prescribing patterns.
Why it matters
This abstract concerns prescribing patterns of sulfonylureas and basal insulin after metformin in older adults with diabetes. It contains no information about treating, curing, or preventing Alzheimer's disease.
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36/100
In the last decade, a number of important research advances in different fields have allowed Down syndrome (DS) research to flourish, creating a time of both unparalleled opportunity and considerable challenge.
Why it matters
This conference report describes ongoing efforts to understand the mechanisms behind intellectual disability and the early-onset Alzheimer disease component in Down syndrome. It announces no treatment or prevention result.
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A 2-dimensional high-throughput screening method is presented to select peptide sequences from large peptide libraries for precision formulation additives, having a high capacity to specifically host a drug of interest and provide tailored drug release properties.
Why it matters
Researchers screened large libraries of peptides to find molecules that can dissolve and release a drug, using an experimental tau aggregation inhibitor as the test drug. This is early formulation chemistry and does not show that any treatment works in patients.
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Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) levels in the cerebrospinal fluid (CSF) have been associated with Alzheimer disease (AD) status.
Why it matters
This genome-wide association study found that common variants in the MS4A gene region were associated with cerebrospinal fluid soluble TREM2 levels, linking this gene cluster to Alzheimer's disease risk. It identifies a possible biological mechanism and target but does not report any treatment, cure, or prevention.
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Proteinopathies such as Alzheimer, Parkinson, and Huntington diseases, where aberrant proteins spread throughout the brain during disease progression, may share a molecular basis and mechanisms of propagation.
Why it matters
This study found increased reactivity of astrocytes and microglia in brain tissue from people who had Creutzfeldt-Jakob disease, a prion disease, not Alzheimer's disease. It does not test any treatment or prevention for Alzheimer's, so it offers no direct implications for treating or curing the disease.
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In this study, we investigated the effects of chronic administration of an inhibitor of the β-site amyloid precursor protein-cleaving enzyme 1 (BACE1) on Alzheimer-related pathology by multitracer PET imaging in transgenic APPPS1-21 (TG) mice.
Why it matters
This study used small-animal PET imaging to investigate the effects of chronic BACE1 inhibitor administration on Alzheimer-related pathology in transgenic mice. This is animal research, so it does not yet show whether BACE inhibition modifies disease in people.
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Arterial spin labeling (ASL) is a magnetic resonance (MR) imaging technique used to assess cerebral blood flow noninvasively by magnetically labeling inflowing blood.
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We found that these brain ApoE knock-out (bEKO) mice had synaptic loss and dysfunction similar to that of ApoE KO mice; however, the bEKO mice did not have the learning and memory impairment observed in ApoE KO mice.
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The role of inflammation in neurological disorders is increasingly recognised.
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Defining the multiple roles of the mechanistic (formerly 'mammalian') target of rapamycin (mTOR) signalling pathway in neurological diseases has been an exciting and rapidly evolving story of bench-to-bedside translational research that has spanned gene mutation discovery, functional experimental validation of mutations, pharmacological pathway manipulation, and clinical trials.
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SET is a multifunctional protein, but when present in the cytoplasm, acts as a powerful inhibitor of phosphatase 2A. We previously observed that in CA1 of Down syndrome (DS) patients, the level of SET is increased, and SET is translocated to the cytoplasm and associated with the hyperphosphorylation of tau at ser202/thr205.
Why it matters
In 3-month-old Ts65Dn mice modeling Down syndrome, SET protein levels were increased and SET moved to the cytoplasm, where it was associated with tau hyperphosphorylation at ser202/thr205 and with caspase-cleaved amyloid precursor protein. The authors propose these mice as a model for therapeutic approaches focused on SET overexpression and its cytoplasmic translocation to slow disease progression, but this is animal work and no treatment was tested in people.
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The discovery of C9orf72 mutations as the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) has awakened a surge of interest in deciphering how mutations in this mysterious gene cause disease and what can be done to stop it.
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Tau toxicity has been implicated in the emergence of synaptic dysfunction in Alzheimer's disease (AD), but the mechanism by which tau alters synapse physiology and leads to cognitive decline is unclear.
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Chemokine receptors are implicated in inflammation and immune responses.
Why it matters
In mice lacking CCR5, injections of lipopolysaccharide worsened memory, increased astrocyte activation, increased β-secretase and led to more amyloid-beta deposits in the brain. This is an animal study and does not show any treatment, cure or prevention for people.
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Chronic inflammation is characterized by longstanding microglial activation followed by sustained release of inflammatory mediators, which aid in enhanced nitrosative and oxidative stress.
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Chronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy that develops after repetitive head injury.
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The formation and deposition of tau protein aggregates is proposed to contribute to cognitive impairments in dementia by disrupting neuronal function in brain regions, including the hippocampus.
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.
- Potential Benefits of Quercetin through P2X7 Modulation against Neuroinflammation in Alzheimer's Disease
- A Genome-wide CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) Screen Identifies NEK7 as an Essential Component of NLRP3 Inflammasome Activation
- Generation of beta-amyloid in the secretory pathway in neuronal and nonneuronal cells
- Altered microRNA profiles in cerebrospinal fluid exosome in Parkinson disease and Alzheimer disease
- The pro-remyelination properties of microglia in the central nervous system
- Novel compound heterozygous mutation in TREM2 found in a Turkish frontotemporal dementia-like family
- Divergent CSF τ alterations in two common tauopathies: Alzheimer's disease and progressive supranuclear palsy
- MRI hyperintensities of the temporal lobe and external capsule in patients with CADASIL
- Therapeutic modulation of Notch signalling--are we there yet?
- Increased Medial Temporal Tau Positron Emission Tomography Uptake in the Absence of Amyloid-β Positivity