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 4,948 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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Mild cognitive impairment (MCI) represents a transitional stage between normal aging and dementia, often considered critical for dementia prevention.
Why it matters
This review describes an association between the gut microbiota-derived metabolite TMAO and mild cognitive impairment, and explores therapeutic strategies targeting TMAO. No effective clinical treatment for mild cognitive impairment has yet been established.
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Gastrointestinal (GI) involvement in Lewy body diseases (LBDs) has been observed since the initial descriptions of patients by James Parkinson.
Why it matters
This review discusses evidence that alpha-synuclein pathology may develop in the gut and spread to the brain in Lewy body diseases, and highlights critical knowledge gaps. It concerns Lewy body diseases rather than Alzheimer's disease and reports no treatment, cure or prevention.
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Mutations in the ANXA11 gene, encoding an RNA-binding protein, have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS), but the underlying in vivo mechanisms remain unclear.
Why it matters
This study developed a knock-in mouse model carrying the ANXA11 p.P36R mutation, which exhibited late-onset motor dysfunction, abnormal aggregates, and cytoplasmic TDP-43 mislocalization. These findings describe a gain-of-function mechanism for late-onset ALS, but the work is in mice and not yet applicable to human treatment.
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43/100
None of the genetically proxied functional network features were significantly associated with neurodegenerative outcomes (adjusted P value >0.05), despite sufficient calculated power.
Why it matters
This genetic analysis found no evidence that resting-state functional network features cause neurodegenerative diseases. The results do not support a causal role for the tested associations.
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43/100
Amyloid‐reactive T cell polyfunctional response distinguishes MCI from normal aging and could serve as a novel MCI biomarker.
Why it matters
This study found that amyloid-reactive T cell responses were higher in people with mild cognitive impairment than in controls and outperformed plasma p-tau181 in discriminating mild cognitive impairment. This could serve as a novel biomarker, but no treatment or cure is tested.
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Klebsiella pneumoniae is infamous for hospital-acquired infections and sepsis, which have also been linked to Alzheimer disease (AD)-related neuroinflammatory and neurodegenerative impairment.
Why it matters
In this mouse model, Klebsiella pneumoniae gut infection, especially after antibiotic-induced disruption of gut bacteria, moved from the gut into the bloodstream and worsened brain inflammation and behavior in Alzheimer-model mice. This is early animal work, so it does not yet show that such infections affect Alzheimer's disease in people or that treating them would help.
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Our findings point to the involvement of increased levels of Aβ42 and/or Aβ40 in contributing to several molecular and cognitive traits associated with DS-AD.
Why it matters
In a mouse model of Down syndrome, the compound BPN15606 lowered levels of Aβ42 and Aβ40 and normalized several Alzheimer-related cellular changes. This is an animal study, so it does not yet show any treatment, cure or prevention of Alzheimer's disease in people.
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43/100
Macroautophagy/autophagy is the intracellular degradation process of cytoplasmic content and damaged organelles.
Why it matters
In a 5×FAD mouse model, conditional knockout of Atg5 in microglia inhibited postnatal neurogenesis in the dentate gyrus of the hippocampus but not in the subventricular zone, and this protection of neurogenesis by Atg5 in microglia was only observed in female Alzheimer mice. Depleting ATG5-deficient microglia with a CSF1R antagonist restored hippocampal neurogenesis, but these are animal findings and do not establish a treatment, cure, or prevention for human Alzheimer's disease.
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Intranasal administration of ahaMSCs-Exos was safe and well tolerated, and a dose of at least 4×10 8 particles could be selected for further clinical trials.
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In aging, mitochondrial dysfunction may play a vital role in AD pathological changes and neuroinflammation.
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High-intensity interval training (HIIT) alleviates cognitive dysfunction in STZ-induced AD-like rat models and provides neuroprotection against neurodegeneration, neuronal damage, and neuronal loss.
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Aging is a multi-faceted process caused by the accumulation of cellular damage over time, associated with a gradual reduction of physiological activities in cells and organs.
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43/100
Idiopathic pulmonary fibrosis (IPF) is a lung disease with high mortality, limited treatment options and an unknown aetiology.
Why it matters
In a mouse model of pulmonary fibrosis, reducing TREM2 with TREM2-specific siRNA protected against lung fibrosis by inhibiting M2 macrophage polarization. This is an animal study of lung disease, not Alzheimer's disease, so it does not show a treatment or prevention for Alzheimer's disease.
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Complement overactivation mediates microglial synapse elimination in neurological diseases such as Alzheimer's disease (AD) and frontotemporal dementia (FTD), but how complement activity is regulated in the brain remains largely unknown.
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Vascular dementia (VD) is the second most common dementia syndrome worldwide, and effective treatments are lacking.
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Lipopolysaccharide (LPS) is a cell-wall immunostimulatory endotoxin component of Gram-negative bacteria.
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CSF biomarkers measured with the LUMIPULSE system showed good agreement with amyloid PET imaging.
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Regulatory T cells (Tregs) play a neuroprotective role by suppressing microglia and macrophage-mediated inflammation and modulating adaptive immune reactions.
Why it matters
In an immunodeficient mouse model of Alzheimer's disease, human regulatory T cells expanded outside the body were tested for whether they could suppress neuroinflammation and amyloid pathology. This is animal research only and reports no treatment, cure or prevention for people.
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Oral infection with F. nucleatum could contribute to abnormalities in cognitive ability and pathological change in the brain of AD-like rats, which may be related to abnormal gut microbiota composition.
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Postoperative cognitive dysfunction (POCD) is a common postoperative complication involving the central nervous system, but the underlying mechanism is not well understood.
Why it matters
In a mouse model of postoperative cognitive dysfunction, activating TREM2 reduced neuroinflammation and improved cognitive problems. This is early animal work on a complication of surgery and does not show that any treatment prevents or cures Alzheimer's disease in people.
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A recent study showed that TREM2 is a receptor for mycolic acids in the mycobacterial cell wall and inhibits macrophage activation.
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Down syndrome (DS) is a complex genetic condition due to an additional copy of human chromosome 21, which results in the deregulation of many genes.
Why it matters
This cross-sectional study in adults with Down syndrome examined DYRK1A and ADNP in CSF and plasma across stages of Alzheimer-related cognitive impairment, with supporting mouse work. It is about biomarker evaluation and does not test any treatment, cure or prevention.
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Alzheimer's disease (AD) is the most common dementia in the world.
Why it matters
In an Alzheimer's mouse model, exosomes from hypoxia-pretreated adipose-derived stem cells improved cognition, apparently by delivering circ-Epc1 and shifting microglial polarization. This is animal research only and reports no treatment, cure or prevention for people.
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Our results indicate that glycosphingolipids regulated by GCS are important modulators of Aβ neuropathology and that glycosphingolipid homeostasis plays a critical role in the consolidation of remote memories.
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HIV-associated neurocognitive disorders (HAND) is a term used to describe a variety of neurological impairments observed in HIV-infected individuals.
From across this topic
9 of the 4,930 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 9. The same 9 appear here every time.
- Human Interleukin-34 facilitates microglia-like cell differentiation and persistent HIV-1 infection in humanized mice
- Mitochondrial ATP-synthase in the entorhinal cortex is a target of oxidative stress at stages I/II of Alzheimer's disease pathology
- Modelling synaptic dysfunction in childhood dementia using human iPSC-derived cortical networks
- Disrupted Calcium Dynamics in Reactive Astrocytes Occur with End Feet–Arteriole Decoupling in an Amyloid Mouse Model of Alzheimer's Disease
- Rapid and ultra-sensitive quantitation of disease-associated α-synuclein seeds in brain and cerebrospinal fluid by αSyn RT-QuIC
- The exposome and pancreatic cancer, lifestyle and environmental risk factors for PDAC
- Mutations in LRRK2 cause autosomal-dominant parkinsonism with pleomorphic pathology
- Opposing roles of the triggering receptor expressed on myeloid cells 2 and triggering receptor expressed on myeloid cells-like transcript 2 in microglia activation
- C9orf72 deficiency promotes microglial-mediated synaptic loss in aging and amyloid accumulation