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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We assessed the prevalence of common altered brain proteins in 296 cognitively unimpaired subjects ranging from age 50 to 102 years.
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The hyperphosphorylated microtubule-associated protein tau is present in several neurodegenerative diseases, although the causal relationship remains elusive.
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40/100
In view of its ability to explain the most frequent motor symptoms of Parkinson's Disease (PD), degeneration of dopaminergic neurons has been considered one of the disease's main pathophysiological features.
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40/100
These findings indicate that metformin pro-aggregation effects mitigate the potential benefits arising from its dephosphorylating action, possibly leading to an overall increase of the risk of tauopathy in elderly diabetic patients.
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The perforant pathway projection from layer II of the entorhinal cortex to the hippocampal dentate gyrus is especially important for long-term memory formation, and is preferentially vulnerable to developing a degenerative tauopathy early in Alzheimer's disease (AD) that may spread over time trans-synaptically.
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Alzheimer's disease (AD) increases dramatically in patients with ischaemic stroke.
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40/100
Exposure to stress is one of the best-known negative regulators of adult neurogenesis (AN).
Why it matters
This review discusses how stress, glucocorticoid hormones, and inflammation reduce adult neurogenesis, with lasting effects particularly from early-life stress, and notes that exercise, drugs targeting the stress system, and some antidepressants can partly overcome these reductions. It suggests a normalization of neurogenesis may be needed for successful treatment response in brain diseases like dementia, but no treatment is tested here.
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These data reveal a link between reduced glucocerebrosidase and the development of α-synucleinopathy and pathophysiological abnormalities in mice, and support the development of GCase therapeutics to reduce α-synucleinopathy in PD and related disorders.
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Advanced glycation end-products are toxic by-products of metabolism and are also acquired from high-temperature processed foods.
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40/100
Synaptic loss is one of the major features of Alzheimer's disease (AD) and correlates with the degree of dementia.
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The loss of synapses is a central event in neurodegenerative diseases.
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Hyperphosphorylation and dysregulation of exon 10 splicing of Tau are pivotally involved in pathogenesis of Alzheimer disease (AD) and/or other tauopathies.
Why it matters
In Alzheimer's disease brain, the kinase Dyrk1A was found to be truncated and overactivated by calpain I, which promoted tau exon 10 exclusion and tau hyperphosphorylation. This is a laboratory and animal study of a molecular mechanism and does not test any treatment in people.
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40/100
Alzheimer disease (AD) is characterized neuropathologically by synaptic disruption, neuronal loss, and deposition of amyloid β (Aβ) protein in brain structures that are critical for memory and cognition.
Why it matters
In cultures of human fetal astrocytes and in Alzheimer's disease transgenic mice, inhibiting or reducing PFKFB3 increased accumulation of amyloid β within and around astrocytes and made these cells more vulnerable to amyloid β toxicity. It is a laboratory and animal study and does not test any treatment, cure or prevention in people.
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Serotonin plays an important role in the etiology of depression.
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Alzheimer disease (AD) is a degenerative tauopathy characterized by aggregation of Tau protein through the repeat domain to form intraneuronal paired helical filaments (PHFs).
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Overexpression of apoE isoforms induces differential effects in the apoE4-TR background: apoE4 decreases apoE lipidation and enhances Aβ accumulation, whereas apoE2 has the opposite effects.
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The triggering receptor expressed on myeloid cells 2 (TREM2) is an immune-modulatory receptor involved in phagocytosis and inflammation.
Why it matters
This study shows that TREM2 with Nasu-Hakola disease mutations is impaired in the processing of N-linked oligosaccharides in the Golgi apparatus, and notes that the R47H variant increases Alzheimer's disease risk similar to ApoE4. It is a cell-based laboratory study of protein trafficking and does not test any treatment, cure, or prevention for Alzheimer's disease.
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As the number of people diagnosed with Alzheimer's disease (AD) reaches epidemic proportions, there is an urgent need to develop effective treatment strategies to tackle the social and economic costs of this fatal condition.
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Neuroinflammation occurs in Alzheimer's disease (AD).
Why it matters
This study exposed neuronal and microglial cell lines to mitochondrial lysates and found inflammation and Alzheimer's-relevant changes. It is a preliminary cell-based study, so it does not show how to treat, cure or prevent Alzheimer's.
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Alzheimer's disease is the most prevalent tauopathy and cause of dementia.
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Microglia play major roles in initiation, coordination and execution of innate immunity in the brain.
Why it matters
This review discusses how microglial TREM2 normally supports phagocytosis and homeostasis and how its role may change in Alzheimer's disease. It is a conceptual review and does not report a treatment, cure or prevention.
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Intraneuronal accumulation of abnormally hyperphosphorylated tau in the brain is a histopathological hallmark of Alzheimer's disease and a family of related neurodegenerative disorders collectively called tauopathies.
Why it matters
In a transgenic mouse model, passive immunization with tau antibodies reduced tau pathology and improved cognition. This is animal research and does not establish any treatment, cure, or prevention for people.
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Single, severe traumatic brain injury (TBI) which elevates CNS amyloid, increases the risk of Alzheimer's disease (AD); while repetitive concussive and subconcussive events as observed in athletes and military personnel, may increase the risk of chronic traumatic encephalopathy (CTE).
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Amyloid precursor protein (APP) has an important function in the generation of Alzheimer's disease (AD).
Why it matters
This laboratory and patient-sample study found that miR-193b can repress amyloid precursor protein and that exosomal miR-193b levels were lower in blood and cerebrospinal fluid of people with mild cognitive impairment and Alzheimer-type dementia. It identifies a possible biomarker but does not show that measuring or changing miR-193b treats or prevents Alzheimer disease.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is known to be involved in the anti-inflammatory response and osteoclast development.
Why it matters
This study found that TREM2 transgenic mice became much more obese than wild-type mice on a high-fat diet, showing TREM2 promotes adipogenesis and diet-induced obesity in mice. It does not test any treatment, cure, or prevention for 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.
- TREM2 modulates microglia phenotypes in the neuroinflammation of Parkinson's disease
- Tau pathology and neurodegeneration
- Investigating structural brain changes of dehydration using voxel-based morphometry
- CSF concentrations of soluble TREM2 as a marker of microglial activation in HIV-1 infection
- Population-based reference equations and Z-scores for blood biomarkers of neurodegenerative diseases
- Clearance of alpha-synuclein oligomeric intermediates via the lysosomal degradation pathway
- Development of language composites for enhanced sensitivity to multiple plasma biomarkers
- Circulating IL-6 and CRP are associated with MRI findings in the elderly: the 3C-Dijon Study
- Retraction: High-Affinity Naloxone Binding to Filamin A Prevents Mu Opioid Receptor-Gs Coupling / Retraction: Naloxone's Pentapeptide Binding Site on Filamin A Blocks Mu Opioid Receptor-Gs Coupling (among five Wang-authored papers retracted)
- Expression of human Cu-Zn superoxide dismutase gene in transgenic mice: model for gene dosage effect in Down syndrome