Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Download bibliography of all 4,766 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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41/100
While neuropathological and genetic studies have established the crucial involvement of TDP-43 proteinopathy in the pathogenesis of amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and related neurodegenerative disorders, multiple studies have described the presence of TDP-43 inclusions in muscular disorders, including inclusion body myositis but also other related rimmed vacuole myopathies.
Why it matters
This review highlights newly discovered pathogenic TDP-43 variants within the prion-like domain that are linked to muscle rather than neuronal pathology, and discusses how these findings challenge accepted views about TDP-43 aggregation and neurotoxicity. It is a review of genetic discoveries and does not test any treatment, cure or prevention.
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Alzheimer's disease (AD) is a common and increasing societal problem due to the extending human lifespan.
Why it matters
This laboratory study examined DNA methylation and RNA expression in blood cells with and without loss of chromosome Y from male Alzheimer patients, finding changes in genes involved in leukocyte differentiation. It reports no treatment, cure, or prevention findings.
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41/100
IRMA can be used to learn and disregard center-specific information in features extracted from brain $$^{18}$$ 18 F-FDG PET scans, while retaining disease-specific information.
Why it matters
This proof-of-concept study shows a machine learning method can harmonize brain PET scan data across different centers, which may help combine data in multi-center studies. It is a technical imaging method and does not test any treatment, cure or prevention.
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These findings indicate that CMHF may possess anti‐Alzheimer efficacy.
Why it matters
The n-hexane fraction of Crateva magna leaf extract showed AChE and BACE1 inhibitory activity in the laboratory and no cytotoxicity against several cell lines. The authors suggest it may possess anti-Alzheimer efficacy, but this is an in-vitro study and no testing in animals or people was reported.
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LAPs contained five monosaccharides. LAPs improved cognitive function and increased the number of Nissl bodies, lactate secretion, the IL-10 content, the relative fluorescence intensity of the IBA1 and AXL proteins, and the protein expression levels of AXL, Mertk, Glut1, HK2, PI3K, p-Akt/Akt, p-mTOR/mTOR and HIF-1α of immune-tolerant AD mice.
Why it matters
In a mouse model of Alzheimer's disease, polysaccharides from longan fruit improved cognitive performance and reduced pathological damage, apparently by promoting microglial phagocytosis through glycolysis and the PI3K/Akt/mTOR/HIF-1α pathway. These are animal and cell findings that have not been tested in people.
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We identified 13 meaningful resting-state networks, and the dFNC among them derived four states exhibiting different connection patterns.
Why it matters
This study found that functional network connectivity alterations in post-stroke dementia with subcortical lesions are state-dependent, showing both impairment and compensation in large-scale brain networks. It offers a perspective on the neural mechanisms of post-stroke dementia but does not test any treatment or prevention.
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We identified specific miRNA groups, mRNA targets, and signaling pathways distinguishing AD, MCI, resilience, ante mortem neuropsychological test performance, post mortem neuropathological burden, and AD risk.
Why it matters
This study identified specific microRNAs and their target pathways that differ among people with Alzheimer's disease, mild cognitive impairment, and cognitive resilience. The findings suggest that manipulating microRNA activity could potentially modify disease pathways, but this is early research and no treatment is tested.
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41/100
The advanced glycation end-products (AGEs) are toxic molecules result from non-enzymatic interactions of sugar with lipids or proteins.
Why it matters
This review discusses how advanced glycation end-products may contribute to ischemic stroke and whether inhibitors of them could help manage stroke. It concerns stroke, not treating, curing or preventing Alzheimer's disease.
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Stereotyped mutations in NOTCH3 drive CADASIL, the leading inherited cause of stroke and vascular dementia.
Why it matters
This laboratory study describes a new assay to distinguish harmful NOTCH3 mutations that cause CADASIL, an inherited small vessel disease. It suggests the assay could be used to screen for compounds that suppress harmful NOTCH3 shapes, but this is early laboratory work and no treatment is proven.
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The mean age of the 3 women and 18 men was 50 years (range, 26-68 years).
Why it matters
In this small study of 21 patients, endovascular stent placement of moderate to high-grade azygos vein stenosis resulted in improvement of symptoms in some patients, but the yield of finding a clinically important treatable venous lesion was relatively low at 15%. This is a small, preliminary study and does not establish a treatment, cure or prevention for frontotemporal dementia.
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Alzheimer's disease (AD) is the most common form of dementia, marked by progressive brain degeneration and cognitive decline.
Why it matters
A newly made heparan sulfate mimetic compound protected cells against hyperphosphorylated tau and reduced tau-induced ER stress and inflammation in laboratory experiments. This is early, cell-based work, and the authors present it only as a foundation for further investigation of tau-heparan sulfate interactions.
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Recent advancements in molecular biomarkers and therapeutic options for Alzheimer's disease have brought into focus the need for greater progress in the second most common cause of dementia, vascular cognitive impairment and dementia (VCID).
Why it matters
This review argues that studying inherited small vessel diseases such as CADASIL and Fabry disease could help explain vascular cognitive impairment and dementia more broadly. It does not report any new treatment or cure, only that these conditions may be useful models for finding biomarkers and targets.
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HEK293, Neuro2a and SH-SY5Y expressing increased levels of α-synuclein were treated with sonicated α-synuclein pre-formed fibrils, to model seeded aggregation.
Why it matters
This laboratory study used Raman spectroscopy and machine learning to examine lipid changes during alpha-synuclein aggregation in cells, which is relevant to Lewy body diseases. It is early cell-based work and does not test any treatment, cure or prevention in people.
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• Executive dysfunction is a key characteristic of bvFTD. • Network de-differentiation reflects loss of specialized networks. • De-differentiation of the salience network relates to executive dysfunction in bvFTD. • Reduced network capacity for specialized processing may mediate emergence of executive dysfunction.
Why it matters
In 90 patients with behavioral variant frontotemporal dementia and 71 controls, de-differentiation of the salience network related to worse executive function. This concerns understanding of brain network changes, not treatment, cure or prevention.
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• Anterior cingulate cortex (ACC) hypometabolism is a non-specific finding in many brain disorders. • ACC hypometabolism was more common in vascular cognitive impairment and dementia (VCID) than Alzheimer dementia (AD). • ACC hypometabolism correlated with cerebral small vessel disease markers. • ACC hypometabolism may be associated with motor stereotypies in VCID. • FDG-PET patterns of hypometabolism may identify vascular contributions to cognitive impairment The anterior cingulate cortex (ACC) is an important hub in the executive and salience networks.
Why it matters
Reduced metabolism in the anterior cingulate cortex on FDG-PET was more common in vascular cognitive impairment and dementia than in Alzheimer's dementia and correlated with small vessel disease markers. This was a retrospective review and does not provide a treatment, cure, or prevention.
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41/100
Robust structural remodeling and synaptic plasticity occurs within spinal autonomic circuitry after severe high-level spinal cord injury (SCI).
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Functional loss of TDP-43, an RNA binding protein genetically and pathologically linked to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), leads to the inclusion of cryptic exons in hundreds of transcripts during disease.
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Many epidemiological studies have shown the beneficial effects of a largely plant-based diet, and the strong association between the consumption of a Mediterranean-type diet with healthy aging including a lower risk of cognitive decline.
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Hypertension is a global health problem, with >1.3 billion individuals with high blood pressure worldwide.
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Semaglutide is a potent glucagon-like peptide 1 receptor agonist for the management of type 2 diabetes mellitus.
Why it matters
This paper concerns semaglutide, a diabetes drug, and its emerging potential clinical implications, including preliminary data in type 1 diabetes. It does not report any finding about treating, curing or preventing Alzheimer's disease.
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Our studies point to increased APP gene dose as a compromising retromer function in DS and suggest a causal role for Aβ42 and Aβ40.
Why it matters
Levels of some retromer proteins were reduced in Down syndrome and Down syndrome with Alzheimer disease, and this reduction required increased App gene dose in mice. In Dp16 mice, a γ-secretase modulator prevented these reductions, but this is animal and tissue research, not a demonstrated treatment for people.
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The results of the present study suggest that increased 18 F-THK5351 uptake might be a useful predictor of poor prognosis among Aβ- aMCI patients, which might be associated with increased neuroinflammation (ClinicalTrials.gov NCT02656498).
Why it matters
In 25 people with amnestic mild cognitive impairment but no amyloid on brain scans, 10 (40.0%) were positive on 18F-THK5351 PET, a scan whose signal may reflect neuroinflammation as well as tau. That group was older and deteriorated at a faster rate over follow-up than the scan-negative group. The authors suggest increased uptake on this scan might be a useful predictor of a poorer outlook in such patients, possibly linked to increased neuroinflammation.
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Alzheimer's disease is a progressive neurodegenerative disease characterized by the presence of amyloid-β plaques in the extracellular environment and aggregates of Tau protein that forms neurofibrillary tangles (NFTs) in neuronal cells.
Why it matters
This review describes how GPCR, PI3K, and Rho signaling pathways, including signaling through TREM2, regulate Tau and amyloid-β cascades in Alzheimer's disease. It summarizes mechanisms but does not test any treatment, cure, or prevention.
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Traumatic brain injury (TBI) is a major cause of morbidity and mortality, both in adult and pediatric populations.
Why it matters
This study analyzed gene expression changes after traumatic brain injury and identified functional gene modules. It is about traumatic brain injury biology and does not report a treatment, cure or prevention for Alzheimer's disease.
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41/100
Intracellular protein trafficking via the endosomes plays a key role in the maintenance of normal neuronal function.
Why it matters
This review describes how the endosome system, which moves proteins inside cells, is abnormal in Down syndrome and may contribute to Alzheimer's-like pathology. It discusses possible mechanisms but reports no treatment or cure.
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.
- Distinct subcellular localization of tau and alpha-synuclein in lewy body disease
- The neural cell adhesion molecules L1 and CHL1 are cleaved by BACE1 protease in vivo
- Genetic drivers of hippocampal atrophy highlight the role of APOE functional variants and AD polygenicity in Mild Cognitive Impairment
- Neuropathology underlying clinical variability in patients with synucleinopathies
- Profiling characteristics of plasma exosomal miRNAs across cognitive stages: from normalcy to mild cognitive impairment and Alzheimer's disease
- Association of REM sleep behavior disorder and neurodegenerative disease may reflect an underlying synucleinopathy
- Enriched environment restores hippocampal cell proliferation and ameliorates cognitive deficits in chronically stressed rats
- Temporal progression of auditory brainstem dysfunction and behavioral phenotypes in mouse models of tauopathy
- Impaired synaptic function in the microglial KARAP/DAP12-deficient mouse
- Increased plasma DOPA decarboxylase levels in Lewy body disorders are driven by dopaminergic treatment