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 showed that the sinergistic combination of the histone deacetilase inhibitor MS-275 with the sirtuin 1 activator resveratrol, at very low doses, restores normal RelA acetylation and elicit neuroprotection in mice subjected to transient middle cerebral artery occlusion (tMCAO) and primary cortical neurons exposed to oxygen-glucose-deprivation (OGD).
Why it matters
This study is about brain ischemia in mice, not Alzheimer's disease. It tested epigenetic drugs for neuroprotection after stroke, so it has no direct meaning for Alzheimer's treatment.
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Tauopathies are the most common type of neurodegenerative proteinopathy, being characterized by cytoplasmic aggregates of hyperphosphorylated tau protein.
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Tauopathies are a class of neurodegenerative diseases, including Alzheimer's disease (AD), Frontotemporal Dementia (FTD), Progressive Supranuclear Palsy (PSP), Corticobasal Degeneration (CBD), and many others where microtubule-associated protein tau (MAPT or tau) is hyperphosphorylated and aggregated to form insoluble paired helical filaments (PHFs) and ultimately neurofibrillary tangles (NFTs).
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Heterozygous, loss-of-function mutations in the granulin gene (GRN) encoding progranulin (PGRN) are a common cause of frontotemporal dementia (FTD).
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The blood-brain barrier (BBB) plays a crucial role in maintaining the specialized microenvironment of the central nervous system (CNS).
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Alzheimer's disease (AD) is the most prevalent type of dementia, characterized by the presence of amyloid-β (Aβ) plaques.
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Alzheimer's disease (AD) is the most common form of dementia characterized by progressive loss of cognitive functions due to neuronal death mainly in the hippocampal and cortical brain.
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41/100
The oral administration of P2RX7 inhibition mitigates disease phenotypes in P301S mice, likely by suppressing release of microglial exosomes.
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Age-related chronic inflammatory activation of microglia and their dysfunction are observed in many neurodegenerative diseases, and the potential contributions of these dysfunctional cells to neurodegeneration have been demonstrated recently.
Why it matters
This review describes how loss of normal microglial functions during neurodegenerative diseases can promote pathology by producing proinflammatory cytokines and increasing oxidative stress. It discusses mechanisms but does not test a treatment or cure.
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Chronic traumatic encephalopathy (CTE) is a tauopathy associated with repetitive head impacts (RHI) that has been neuropathologically diagnosed in American football players and other contact sport athletes.
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The objective was to compare the effect of HIV-1C and HIV-1B subtypes on neurofilament light (NfL) cerebrospinal fluid (CSF) levels and ratios of NfL to tau proteins.
Why it matters
This study compared cerebrospinal fluid nerve cytoskeleton proteins in people with HIV subtypes B and C, people with Alzheimer's disease, and HIV-negative controls. It is about biomarkers in HIV-related cognitive disorder, not about treating, curing or preventing Alzheimer's disease.
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Oxidative stress (OS) plays a critical role in the pathophysiology of several brain-related disorders, including neurodegenerative diseases and ischemic stroke, which are the major causes of dementia.
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The pathogenesis of Alzheimer's disease (AD) and the commonest cause of dementia in the elderly remain incompletely understood.
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Quercetin is a polyphenol with multiple biological activities, and results of our preliminary study showed that it could shorten the immobility time of mice in the forced swimming test and tail suspending test.
Why it matters
In rats given lipopolysaccharide, quercetin improved depression-like behaviors and affected BDNF-related copine 6 and TREM1/2 levels in the hippocampus and prefrontal cortex. This is animal work on depression-like behavior and does not show a treatment, cure, or prevention for Alzheimer's disease.
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We conclude that an inverse correlation between levels of inflammation in cortical areas and plasma NfL levels indicates that microglial activation may initially be protective to axons in AD.
Why it matters
In 27 people with mild cognitive impairment or early Alzheimer disease, higher brain inflammation in some cortical areas was linked to lower plasma neurofilament light, which the authors suggest means microglial activation may initially protect axons. They propose that stimulating microglial activity in early disease could be worth testing, but this was an observational study and no treatment was given.
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Neuroinflammation is a common feature shared by neurodegenerative disorders, such as Parkinson's disease (PD), and seems to play a key role in their development and progression.
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41/100
Alzheimer's disease (AD) is an aging-related neurological disorder characterized by synaptic loss and dementia.
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In neurodegenerative diseases, microglia-mediated neuroinflammation and oxidative stress are central events.
Why it matters
This review discusses disease-associated microglia and pro-oxidant microglia in neurodegeneration, challenging the classical M1/M2 polarization view. It is a conceptual review and does not report a treatment or cure.
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Aluminium (Al) is frequently accessible to animal and human populations to the extent that intoxications may occur.
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41/100
The fundamental role that alpha-synuclein (aSyn) plays in the pathogenesis of neurodegenerative synucleinopathies, including Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy, is a well-accepted fact.
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41/100
This article describes pathogenic concepts and factors, in particular glycolipid abnormalities, that create cell dysfunction and synaptic loss in neurodegenerative diseases.
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Innate immune responses are considered to play crucial roles in the progression of Alzheimer's disease (AD).
Why it matters
In APP/PS1 transgenic mice, the STING stimulator cGAMP improved cognitive deficits, reduced Aβ plaque load, and reduced neuron apoptosis by elevating TREM2. This is an early animal study, so it does not yet show that cGAMP treats Alzheimer's disease in people.
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Alzheimer's disease (AD) is the most common type of dementia and is the leading cause of disability in elderly people worldwide.
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Tau is a scaffolding protein that serves multiple cellular functions that are perturbed in neurodegenerative diseases, including Alzheimer's disease (AD) and frontotemporal dementia (FTD).
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41/100
The GGGGCC repeat expansion in C9ORF72 is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
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.
- Epilepsy in neurodegenerative diseases
- Advanced Glycation End Products Induce Microglial Activation and Impair Neurodevelopment in Human iPSC-Derived Brain Organoids
- Exercise, the Gut Microbiome and Gastrointestinal Diseases: Therapeutic Impact and Molecular Mechanisms
- Reversal of endothelial dysfunction reduces white matter vulnerability in cerebral small vessel disease in rats
- Association Between Midlife Risk Factors and Late-Onset Epilepsy: Results From the Atherosclerosis Risk in Communities Study
- RAGE mediates amyloid-beta peptide transport across the blood-brain barrier and accumulation in brain
- Acute function of secreted amyloid precursor protein fragment APPsα in synaptic plasticity
- A comparison of (99m)Tc-HMPAO SPET changes in dementia with Lewy bodies and Alzheimer's disease using statistical parametric mapping
- Imaging and plasma biomarkers for pathological accumulation in Down syndrome
- Extracellular vesicles in TDP-43 proteinopathies: pathogenesis and biomarker potential