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 4,766 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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Amyloid-β (Aβ) peptides, starting with pyroglutamate at the third residue (pyroGlu-3 Aβ), are a major species deposited in the brain of Alzheimer disease (AD) patients.
Why it matters
This comparative tissue study found that pyroGlu-3 amyloid-beta is deposited early in plaques and cerebral amyloid angiopathy in humans and non-human primates, but later in a subset of amyloid in Alzheimer-like transgenic mouse models. It describes a form of amyloid that may be more toxic and amyloidogenic, but reports no treatment, cure or prevention.
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Recent theories have suggested that chronic pain could be partly maintained by maladaptive physiological responses of the organism facing a recurrent stressor.
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Anatomical segmentation of structures of interest is critical to quantitative analysis in medical imaging.
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Amyloid precursor protein (APP) proteolysis is required for production of amyloid-β (Aβ) peptides that comprise β-amyloid plaques in brains of Alzheimer's disease (AD) patients.
Why it matters
In a transgenic mouse model of cerebral amyloidosis, six months of oral ferulic acid treatment reversed behavioral deficits and reduced Alzheimer-like pathology. This is animal research only and does not establish that ferulic acid treats or prevents Alzheimer's disease in people.
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Alzheimer's disease (AD) is the most common cause of dementia worldwide.
Why it matters
This study found that stimulating the immune system with monophosphoryl lipid A improved Alzheimer's-related pathology in a mouse model by helping clear amyloid beta. However, this is early animal research and does not yet show whether the approach would work or be safe in people.
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47/100
Kufs disease, an adult-onset neuronal ceroid lipofuscinosis, is challenging to diagnose and genetically heterogeneous.
Why it matters
Mutations in the CTSF gene were found in some families with Type B Kufs disease, an adult-onset neuronal ceroid lipofuscinosis that can present with dementia and motor features. This identifies a genetic cause in a minority of cases of this rare disease and does not provide a treatment, cure, or prevention for Alzheimer's disease.
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Triggering receptor expressed on myeloid cells-2 (TREM2) is a microglial surface receptor involved in phagocytosis.
Why it matters
In mice, researchers blocked a main brain artery for 30 minutes to mimic a stroke and checked the brain at times from 6 hours to 28 days afterwards; they found "a greatly increased transcription of TREM2", a microglial receptor involved in clearing debris. The title adds that mice lacking TREM2 had a weaker ("attenuated") inflammatory response after stroke, but the summary gives no details, numbers or recovery outcomes for that result. This is an animal stroke study: it does not mention Alzheimer's disease, and less inflammation should not be read as better recovery.
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There is growing evidence of activated microglia and inflammatory processes in the cerebral cortex in amyotrophic lateral sclerosis (ALS).
Why it matters
This study used the TSPO radioligand (18)F-DPA-714 to evaluate neuroinflammation in ten ALS patients and eight healthy controls. It concerns amyotrophic lateral sclerosis imaging and does not address treating, curing or preventing Alzheimer's disease.
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[(11)C](R)PK11195-PET measures upregulation of translocator protein, which is associated with microglial activation, [(11)C]PIB-PET is a marker of amyloid, while [(18)F]FDG-PET measures cerebral glucose metabolism (rCMRGlc).
Why it matters
This imaging study evaluated the relationship between microglial activation, amyloid deposition and glucose metabolism in 11 subjects with Parkinson's disease dementia, 8 with Parkinson's disease without dementia, and 24 controls. It examines disease processes in Parkinson's disease and does not test any treatment, cure or prevention for Alzheimer's disease.
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Microinfarcts are a common clinical feature of the aging brain, particularly in patients with cognitive decline or vascular or Alzheimer's dementia.
Why it matters
This study describes a mouse model of multiple small brain infarcts that produced cognitive deficits and delayed neuronal loss. It is animal research about vascular brain injury and does not test any treatment or prevention for Alzheimer's disease in people.
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Aggregation of amyloid-β (Aβ) peptides leads to synaptic disruption and neurodegeneration in Alzheimer disease (AD).
Why it matters
In this laboratory study, amyloid-β taken up by neurons trafficked to lysosomes for degradation, and apolipoprotein E accelerated this uptake, trafficking, and degradation in an isoform-dependent manner, with apoE3 more efficient than apoE4. These findings describe a possible clearance pathway and how apoE isoforms differ, but they are early laboratory work and do not show a treatment or prevention for Alzheimer's disease in people.
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47/100
Tauopathies are a class of neurodegenerative diseases marked by intracellular aggregates of hyperphosphorylated Tau.
Why it matters
This study asked whether disease-linked differences in the tau protein change how much tau is found outside cells. Its title reports that they do: "Extracellular Tau levels are influenced by variability in Tau that is associated with tauopathies." It starts from the known pattern that spinal-fluid tau is higher in Alzheimer's but only "slightly elevated" in inherited tau-gene FTD. It is basic tau-biology research and does not test any treatment, cure, or prevention.
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Pathogenic changes in the brain of a PARK2 patient were recapitulated using iPSC technology.
Why it matters
This study used stem cells from two PARK2 Parkinson's disease patients and found abnormal mitochondrial morphology, increased oxidative stress, and alpha-synuclein accumulation in their neurons. It is a small cell study and does not test any treatment or prevention for Alzheimer's disease, so it has no direct implications for treating, curing, or preventing the disease.
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C-reactive protein (CRP) is a systemic inflammation marker that predicts future cardiovascular risk.
Why it matters
This genome-wide association study in African American and Hispanic American women found a CRP-associated variant in TREM2. It concerns C-reactive protein and cardiovascular risk, not the treatment, cure, or prevention of Alzheimer's disease.
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In Alzheimer disease (AD), the perturbation of the endoplasmic reticulum (ER) calcium (Ca²⁺) homeostasis has been linked to presenilins, the catalytic core in γ-secretase complexes cleaving the amyloid precursor protein (APP), thereby generating amyloid-β (Aβ) peptides.
Why it matters
In cells and in Tg2576 mice, APP overexpression increased ryanodine receptor expression and ER calcium release, and lowering this release with dantrolene reduced amyloid-beta load and memory impairments. This is animal and cell research, so it does not yet show a treatment for people.
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The RNA-binding proteins TDP-43 and FUS form abnormal cytoplasmic aggregates in affected tissues of patients with amyotrophic lateral sclerosis and frontotemporal lobar dementia.
Why it matters
In motoneuron-like cells, TDP-43 and FUS were found to bind different sets of cytoplasmic messenger RNAs while converging on common cellular pathways. This is laboratory cell work on ALS and frontotemporal lobar dementia and does not show any treatment, cure or prevention for Alzheimer's disease.
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Neuroplasticity may have a core role in the pathophysiology of major depressive disorder (MDD), a concept supported by experimental studies that found that excessive cortisol secretion and/or excessive production of inflammatory cytokines impairs neuronal plasticity and neurogenesis in the hippocampus.
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The objective of the present study was to assess the neuroprotective role of rutin (vitamin P) and delineate the mechanism of action.
Why it matters
In a rat model of Alzheimer-type dementia, the plant compound rutin improved cognitive performance and reduced markers of oxidative stress and inflammation in the hippocampus. This is early animal research, so it does not yet show that rutin treats or prevents Alzheimer's disease in people.
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These results suggest that 4-O-methylhonokiol inhibits LPS-induced amyloidogenesis via anti-inflammatory mechanisms.
Why it matters
In mice given lipopolysaccharide and in cultured cells, 4-O-methylhonokiol reduced memory impairment and inflammatory and amyloid-related markers. This is early animal and cell work and does not show that this substance treats, cures, or prevents Alzheimer's disease in people.
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Amyloid β-peptide (Aβ), the pathogenic agent of Alzheimer disease, is a physiological metabolite whose levels are constantly controlled in normal brain.
Why it matters
This laboratory study reports that neuron-derived exosomes drive amyloid-beta into nontoxic fibrils and promote its uptake by microglia. It is a cell-level mechanism study and reports no treatment, cure or prevention for Alzheimer's disease.
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Amyloid precursor protein (APP) proteolysis is essential for production of amyloid-β (Aβ) peptides that form β-amyloid plaques in brains of Alzheimer disease (AD) patients.
Why it matters
In transgenic PSAPP mice, six months of oral tannic acid prevented some behavioral impairment and reduced Alzheimer-like pathology. This is animal research and does not show that tannic acid treats, cures, or prevents Alzheimer's disease in people.
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Allelic variation in the apolipoprotein E (APOE) gene is the major risk factor of sporadic Alzheimer disease.
Why it matters
In laboratory work, apoE helped microglia break down amyloid-beta by lowering cellular cholesterol and speeding delivery of amyloid-beta to lysosomes. This is a mechanistic, cell-level finding and does not establish any treatment or prevention in people.
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Oxidative stress is closely linked to the pathogenesis of neurodegeneration.
Why it matters
In a mouse model, deficiency of the antioxidant enzyme SOD1 drove amyloid beta oligomerization and memory loss. This is an animal study and does not show that targeting oxidative stress treats or prevents Alzheimer's disease in people.
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Down syndrome (DS) is the most common genetic cause of intellectual disability in children, and the number of adults with DS reaching old age is increasing.
Why it matters
In 70 autopsy cases, this study found that soluble and insoluble amyloid beta and oligomers increase with age in the frontal cortex of people with Down syndrome, and that one marker of oxidative damage, HNE-bound proteins, was increased overall. It suggests oxidative damage, but not nitrosative stress, may contribute to Alzheimer's disease in Down syndrome, but it is an observational tissue study and tests no treatment.
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Apolipoprotein E (apoE) is a major apolipoprotein in the brain.
Why it matters
In this laboratory cell model, astrocytes carrying the apoE4 form weakened the blood-brain barrier's tight junctions compared with apoE3, and mice with apoE4 had leakier barriers. This is early, in-vitro and animal work, so it does not yet show that repairing the barrier would treat or prevent Alzheimer's in people.
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.
- Pathological alpha-synuclein propagates through neural networks
- Dopaminergic changes in the subgenual cingulate cortex in dementia with lewy bodies associates with presence of depression
- Olfactory bulb involvement in neurodegenerative diseases
- A Stochastic Landscape Approach for Protein Folding State Classification
- Degradation and Transmission of Tau by Autophagic-Endolysosomal Networks and Potential Therapeutic Targets for Tauopathy
- Increased iron deposition in putamen and substantia nigra correlates with cognitive function in cerebral small vessel disease: A quantitative susceptibility mapping study
- Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy maps to chromosome 19q12
- Structural determinants of the cellular localization and shuttling of TDP-43
- Calpain activation promotes BACE1 expression, amyloid precursor protein processing, and amyloid plaque formation in a transgenic mouse model of Alzheimer disease
- Oxidative stress and Down syndrome. Do antioxidants play a role in therapy?