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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This study proposes TLR2 immunotherapy as a novel therapeutic strategy for synucleinopathies of the aging population.
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41/100
Frontotemporal dementia and amyotrophic lateral sclerosis patients with C9orf72 mutation show cytoplasmic poly-GR and poly-PR aggregates.
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Diffusion-tensor imaging (DTI) is a noninvasive medical imaging tool used to investigate the structure of white matter.
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Regulation of astrocytic mitochondrial function and redox status by IGF-1 is essential to maintain astrocytic function and coordinate hippocampal-dependent spatial learning.
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Prolonged intake of excessive amounts of ethanol is known to have adverse effects on the central nervous system (CNS).
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In vivo 11 C-PBB3 binding to the rTg4510 neocortex/hippocampus was increased relative to controls and correlated with local atrophy.
Why it matters
This study in tauopathy mouse models compared in-vitro and in-vivo measures of tau deposits and their link to brain atrophy. It is animal research into how tau relates to nerve cell loss and does not test a treatment, cure or prevention for Alzheimer's disease in people.
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Accumulating evidence suggests that brain-derived neurotrophic factor (BDNF) is associated with the pathophysiology of major depressive disorder (MDD).
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Overall, these results support the vervet as a non-human primate model of amyloid-related neurodegeneration, such as Alzheimer's disease and cerebral amyloid angiopathy, and highlight Aβ 1-40 and p-tau 181 as potentially valuable biomarkers of these processes.
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Alzheimer's disease (AD) is the most common cause of dementia in the elderly.
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Aging is a major driving force underlying dementia, such as that caused by Alzheimer's disease (AD).
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Synucleinopathies, such as Parkinson's disease and dementia with Lewy bodies, are neurodegenerative disorders that are characterized by the accumulation of α-synuclein (aSyn) in intracellular inclusions known as Lewy bodies.
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Clearance of amyloid-beta (Aβ) from the brain is an important therapeutic strategy for Alzheimer's disease (AD).
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Myeloperoxidase (MPO) is a key enzyme in inflammatory and degenerative processes, although conflicting reports have been presented concerning its expression in the brain.
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In vivo exploration of activated microglia in neurodegenerative diseases is achievable by Positron Emission Tomography (PET) imaging, using dedicated radiopharmaceuticals targeting the translocator protein-18 kDa (TSPO).
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Apolipoprotein E4 (E4) and type 2 diabetes are major risk factors for cognitive decline and late onset Alzheimer's disease (AD).
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It is well-established that inflammation plays an important role in Alzheimer's disease (AD) and frontotemporal lobar dementia (FTLD).
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Gliomas are the most common and aggressive type of primary adult brain tumors.
Why it matters
This study is about glioma, a type of brain tumor, not Alzheimer's disease. It found TREM2 overexpressed in glioma tissues and linked to tumor grade and survival, which does not inform Alzheimer's treatment.
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Between 1992 and 2000, 8 women developed dementia (4 AD, 3 vascular dementia, 1 mixed vascular dementia and AD).
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The chemokine/chemokine receptor CCL2/CCR2 axis was impaired in BDMs from AD and MCI patients, causing a deficit in cell migration.
Why it matters
In blood-derived monocytes and macrophages from people with Alzheimer's disease and mild cognitive impairment, this study found impaired CCL2/CCR2 chemotaxis and altered phagocytosis of amyloid beta fibrils. These are laboratory observations about immune cell behavior, not a demonstrated treatment or cure.
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41/100
Many insults, including trauma, ischemia, infection, inflammation, and neurodegeneration, result in irreversible damage to the central nervous system.
Why it matters
This is a review of naturally occurring antibodies as possible treatments for several neurologic diseases, including Alzheimer's disease, not a test of a treatment in patients. It notes that many approaches that work in animal models fail in humans due to lack of efficacy or toxic effects, so no treatment benefit is established here.
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Attention deficit is one of the core symptoms of the attention-deficit/hyperactivity disorder (ADHD).
Why it matters
This genetic study of attention function in adults with ADHD found no variants reaching genome-wide significance, though one suggestive signal was in the SORCS2 gene, previously linked to Alzheimer disease among other conditions. The findings are preliminary and do not directly address treating, curing, or preventing Alzheimer disease.
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Alzheimer's disease is a severe neurodegenerative disorder of the brain, pathologically characterized by extracellular beta-amyloid plaques, intraneuronal Tau inclusions, inflammation, reactive glial cells, vascular pathology and neuronal cell death.
Why it matters
In cultured brain slices from adult Alzheimer's model mice, the proteases neprilysin, insulysin, and MMP-9 degraded beta-amyloid plaques, but only at the highest concentration tested. This is an in vitro model, so it does not show that these proteases could clear plaques or improve outcomes in living patients.
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Bach1, among the genes encoded on chromosome 21, is a transcription repressor, which binds to antioxidant response elements of DNA thus inhibiting the transcription of specific genes involved in the cell stress response including heme oxygenase-1 (HO-1).
Why it matters
In brain tissue from all Down syndrome cases studied, total Bach1 protein levels were increased along with reduced induction of HO-1, and the development of Alzheimer's disease in Down syndrome was characterized by increased Bach1, increased HO-1 and increased nitration of BVR-A with reduced activity. The findings were also examined in the Ts65Dn mouse model at 3 and 15 months of age.
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Previous data demonstrate that bexarotene (Bex), retinoid X receptor (RXR) agonist, reduces soluble and insoluble amyloid-β (Aβ) in Alzheimer disease (AD)-transgenic mice either by increasing the levels of mouse apolipoprotein E (apoE) or increasing ABCA1/ABCG1-induced apoE lipoprotein association/lipidation.
Why it matters
In mice carrying the human APOE4 gene, which is the strongest genetic risk factor for Alzheimer's, short-term treatment with retinoid X receptor drugs (bexarotene or LG100268) raised the fat-carrying ("lipidated") form of apoE4 and lowered soluble amyloid in the hippocampus. The same short-term treatment raised soluble amyloid in the cortex, possibly because the drugs enlarged the liver, and a prevention schedule showed no benefit. This is mouse research only. It suggests the APOE4 problem may be too little lipidated apoE4, but it does not show that these drugs help people.
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An imbalance of tau isoforms containing either three or four microtubule-binding repeats causes frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17) in families with intronic mutations in the MAPT gene.
From across this topic
10 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 10. The same 10 appear here every time.
- Impaired synaptic function in the microglial KARAP/DAP12-deficient mouse
- Increased plasma DOPA decarboxylase levels in Lewy body disorders are driven by dopaminergic treatment
- 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
- Galectin-3 promotes Aβ oligomerization and Aβ toxicity in a mouse model of Alzheimer's disease