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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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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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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Lipopolysaccharide (LPS) is a cell-wall immunostimulatory endotoxin component of Gram-negative bacteria.
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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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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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43/100
The human tau protein is implicated in a wide range of neurodegenerative "tauopathy" diseases, consisting of Alzheimer's disease (AD) and frontotemporal lobar degeneration which includes progressive supranuclear palsy, corticobasal degeneration, Pick's disease, and FTLD-tau (frontotemporal dementia with parkinsonism caused by MAPT mutations).
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We previously demonstrated that PNA5, a novel glycosylated angiotensin 1-7 (Ang-(1-7)) Mas receptor (MasR) agonist peptide, is an effective therapy to rescue cognitive impairment in our preclinical model of VCID.
Why it matters
In a mouse model of vascular contributions to cognitive impairment and dementia, treatment with Ang-(1-7)/MasR agonist peptides reversed cognitive impairment and lowered neurofilament light levels, which were negatively correlated with cognitive scores. This is preclinical animal work, so it does not yet show that this treatment helps people with Alzheimer's disease or related dementias.
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These data suggested that METTL3 reduction-mediated m 6 A dysregulation likely contributes to neurodegeneration in AD which may be a therapeutic target for AD.
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Patients with essential tremor (ET) frequently develop concurrent dementia, which is often assumed to represent co-morbid Alzheimer disease (AD).
Why it matters
This study examined brain tissue after death and found that the pattern of tau protein in people with essential tremor was different from the pattern in people with Alzheimer's disease. This suggests that dementia in essential tremor may not simply be co-occurring Alzheimer's disease, but the finding does not directly lead to a treatment or cure.
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Abbreviations Aβ: β-amyloid; AD: Alzheimer disease; AIF1/IBA1: allograft inflammatory factor 1; ALP: autophagy-lysosomal pathway; APP: amyloid beta precursor protein; ATP6V1B1/V-ATPase V1b1: ATPase H+ transporting V1 subunit B1; AVs: autophagy vacuoles; BAF: bafilomycin A 1 ; CFC: contextual/cued fear conditioning assay; CHX: Ca 2+ /H + exchanger; CTF-β: carboxy-terminal fragment derived from β-secretase; CTSD: cathepsin D; fAD: familial Alzheimer disease; GFAP: glial fibrillary acidic protein; LAMP1: lysosomal associated membrane protein 1; LTP: long-term potentiation; MCOLN1/TRPML1: mucolipin 1; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MAPT: microtubule associated protein tau; MWM: Morris water maze; NFT: neurofibrillary tangles; PFC: prefrontal cortex; PSEN1: presenilin 1; SQSTM1/p62: sequestosome 1; TBS: theta burst stimulation; TEM: transmission electronic microscopy; TPCN2/TPC2: two pore segment channel 2; WT: wild-type; V-ATPase: vacuolar type H + -ATPase.
Why it matters
This study reports that inhibiting lysosomal two pore segment channels reduced beta-amyloid pathology and mitigated memory impairment in an Alzheimer's disease model. The available summary does not state whether this was done in animals or cells, so it is early work and does not show a treatment for people.
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Our results suggest significant mechanistic overlap between AD and COVID-19, centered on neuroinflammation and microvascular injury.
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43/100
These data demonstrate the neuroprotective effects of systemic administration of stem cell-derived EVs for remediation of behavioral and molecular AD neuropathologies.
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.
- Fructose-2,6-bisphosphate restores TDP-43 pathology-driven genome repair deficiency in motor neuron diseases
- Assessing the role of the TREM2 p.R47H variant as a risk factor for Alzheimer's disease and frontotemporal dementia
- APOE and TREM2 regulate amyloid-responsive microglia in Alzheimer's disease
- NAD+ improves cognitive function and reduces neuroinflammation by ameliorating mitochondrial damage and decreasing ROS production in chronic cerebral hypoperfusion models through Sirt1/PGC-1α pathway
- Prolonged coenzyme Q10 treatment in Down syndrome patients: effect on DNA oxidation
- Clinical spectrum of Kufor-Rakeb syndrome in the Chilean kindred with ATP13A2 mutations
- Translocator Protein-18 kDa (TSPO) Positron Emission Tomography (PET) Imaging and Its Clinical Impact in Neurodegenerative Diseases
- Total Tau and Phosphorylated Tau Protein Serum Levels in Patients with Schizophrenia Compared with Controls
- Increased cerebral microbleeds and cortical superficial siderosis in pediatric patients with Down syndrome
- TREM2 deficiency exacerbates tau pathology through dysregulated kinase signaling in a mouse model of tauopathy