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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47/100
In the past, the role of physical activity as a life-style modulating factor has been considered as that of a tool to balance energy intake.
Why it matters
This review notes accumulating epidemiological evidence that a physically active life plays an independent role in protection against several conditions including dementia, and proposes that muscle-released myokines may contribute to this protection. It reports no tested treatment, cure or prevention for Alzheimer's disease.
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TDP-43, or TAR DNA-binding protein 43, is a pathological marker of a spectrum of neurodegenerative disorders, including amyotrophic lateral sclerosis and frontotemporal lobar degeneration with ubiquitin-positive inclusions.
Why it matters
In cultured cells, sorbitol stress sent TDP-43 into stress granules, and mutant TDP-43 formed larger granules and entered them earlier than wild-type TDP-43. This is cell-culture work on a possible disease mechanism, not a treatment or prevention study.
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Neuroprotection alone is not sufficient to rescue tau-induced memory loss in a transgenic mouse model.
Why it matters
In a mouse model, neuroprotection alone was not enough to rescue cognition; cognitive improvement was only observed when soluble tau levels were also reduced by a very high concentration of methylene blue. This is early animal research and does not yet show a treatment for people.
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To date there is no effective therapy for Alzheimer disease (AD).
Why it matters
In a mouse model of Alzheimer's disease, overexpressing human apolipoprotein A-I preserved cognitive function and attenuated neuroinflammation and cerebral amyloid angiopathy. This is animal work, so it does not show that raising apoA-I or HDL treats or prevents Alzheimer's disease in people.
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These findings suggest that there is reduced chaperone-mediated autophagy activity in the PD brain, provide evidence for the role of autophagy in PD pathogenesis and Lewy body formation, and suggest that this pathway may be a suitable therapeutic target in PD.
Why it matters
In postmortem brain samples, levels of the chaperone-mediated autophagy proteins LAMP2A and hsc70 were reduced in Parkinson disease brains compared with Alzheimer disease and control brains, and lowering LAMP2A in cells increased the half-life of α-synuclein. This points to autophagy as a possible target in Parkinson disease, not a treatment or cure for Alzheimer's disease.
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RNA-binding protein TDP-43 has been associated with multiple neurodegenerative diseases, including amyotrophic lateral sclerosis and frontotemporal lobar dementia.
Why it matters
This study engineered worms to express human TDP-43 and found an uncoordinated phenotype and abnormal motorneuron synapses, work relevant to ALS and frontotemporal lobar dementia. It is an animal model study and reports nothing about treating, curing or preventing Alzheimer's disease.
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VCP (VCP/p97) is a ubiquitously expressed member of the AAA(+)-ATPase family of chaperone-like proteins that regulates numerous cellular processes including chromatin decondensation, homotypic membrane fusion and ubiquitin-dependent protein degradation by the proteasome.
Why it matters
In cell experiments, this work found that VCP is needed for autophagosome maturation and that disease-causing VCP mutations impair this function. It is laboratory research, so it does not yet show any treatment, cure or prevention for Alzheimer's disease.
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TDP-43 is a highly conserved and ubiquitously expressed member of the heterogeneous nuclear ribonucleoprotein (hnRNP) family of proteins.
Why it matters
This laboratory study found that TDP-43 interacts with many proteins involved in RNA metabolism, clustering into nuclear/splicing and cytoplasmic/translation networks, and that it is recruited to stress granules. It does not test any treatment or show a way to cure or prevent Alzheimer's disease.
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TDP-43 is a DNA/RNA-binding protein implicated in multiple steps of transcriptional and post-transcriptional regulation of gene expression.
Why it matters
Mice lacking the TDP-43 gene died early in embryonic development, showing the protein is required for normal development. This is animal developmental biology and does not test any treatment, cure or prevention for Alzheimer's disease.
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47/100
Transactive response DNA-binding protein 43 pathology occurs in FAD and DS, similar to that observed in sporadic Alzheimer disease.
Why it matters
In brain tissue from 42 people with familial Alzheimer's disease and 14 with Down syndrome, pathological TDP-43 aggregates were found in 14.0% of participants, most often in the amygdala and hippocampus with none in neocortical regions. The authors conclude that TDP-43 pathology may contribute to cognitive impairment in familial and sporadic Alzheimer's disease.
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Numerous studies have demonstrated oxidative damage in the central nervous system in subjects with Alzheimer disease and in animal models of this dementing disorder.
Why it matters
Transgenic mice modeling Alzheimer's disease developed oxidative damage in the brain, and this damage was completely prevented when a single methionine at position 35 of amyloid beta-peptide was mutated. These are findings in mice about a mechanism of oxidative stress and do not show that targeting this process helps patients.
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47/100
Astrocyte infection with human immunodeficiency virus (HIV) is considered rare, so astrocytes are thought to play a secondary role in HIV neuropathogenesis.
Why it matters
This study found extensive HIV infection of astrocytes, up to 19% of GFAP+ cells, in subjects with HIV-associated dementia, correlating with severity of neuropathological changes. It concerns HIV dementia and provides no findings about treating, curing or preventing Alzheimer's disease.
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The blood-brain barrier (BBB) represents a considerable obstacle to brain entry of the majority of drugs and thus severely restricts the therapy of many serious CNS diseases including brain tumours, brain HIV, Alzheimer and other neurodegenerative diseases.
Why it matters
In this mouse and in vitro study, human serum albumin nanoparticles with covalently bound apolipoprotein E were detected in brain capillary endothelial cells and neurones after intravenous injection, while nanoparticles without apolipoprotein E showed no uptake into the brain. This describes a possible way to deliver drugs across the blood-brain barrier, but it is early animal and laboratory work and does not itself treat, cure, or prevent Alzheimer disease.
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The colonic epithelial lining undergoes constant replacement, driven by epithelial stem cells in crypts of Lieberkühn.
Why it matters
This study found that colonic mucosal wound repair in mice requires Trem2 signaling. It concerns the colon, not the brain, and does not address treating, curing or preventing Alzheimer's disease.
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47/100
The results suggest that structural compromise to multiple fiber tracts is associated with memory and language impairments in patients with temporal lobe epilepsy.
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Alzheimer disease amyloid beta-peptide (Abeta) is generated via proteolytic processing of the beta-amyloid precursor protein by beta- and gamma-secretase.
Why it matters
This cell study found that generation of Abeta38 and Abeta42 occurs independently, and that sulindac sulfide selectively reduced the aggregation-prone Abeta42 while increasing Abeta38. It is laboratory work on gamma-secretase modulation and does not demonstrate a treatment or cure for Alzheimer's disease.
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Compelling evidence indicates that excess consumption of sugar-sweetened beverages plays an important role in the epidemic of obesity, a major risk factor for type 2 diabetes mellitus.
Why it matters
Mice bred to develop Alzheimer-like brain changes were given 10% sugar water alongside a normal diet. They gained weight, became insulin resistant, and had worse memory and 2–3 times more insoluble amyloid-beta in the brain than mice given plain water. The amyloid-making machinery was unchanged, but brain apoE was 2.5 times higher, which the authors propose sped up amyloid clumping. This is a single mouse study: it raises the question of whether sugary drinks matter for Alzheimer's risk, but it does not show that cutting them prevents the disease in people.
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The combined advances of a new, protease-resistant SDF-1 and nanofiber-mediated delivery promoted recruitment of stem cells and improved cardiac function after myocardial infarction.
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Epidemiological evidence suggests that long term treatment with hydroxymethylglutaryl-CoA reductase inhibitors, or statins, decreases the risk for developing Alzheimer disease (AD).
Why it matters
This cell study found that statins reduced amyloid-beta production through inhibition of protein isoprenylation, not just through cholesterol lowering. It is laboratory work on a possible mechanism and does not show that statins treat or prevent Alzheimer's disease.
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Amyloid precursor protein (APP) metabolism is central to the pathogenesis of Alzheimer disease.
Why it matters
This cell study found that alkalizing drugs cause APP by-products to accumulate in luminal vesicles of multivesicular bodies. It is laboratory research on cell biology and does not test any treatment, cure, or prevention.
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The underlying cause of sporadic Alzheimer disease (AD) is unknown, but a number of environmental and genetic factors are likely to be involved.
Why it matters
In the 3xTg-AD mouse model, dietary DHA reduced intraneuronal accumulation of amyloid-beta and tau, but combining DHA with n-6 fatty acids diminished the effect. This is animal research, so it does not show that these dietary changes treat or prevent Alzheimer's disease in people.
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The s allele variant of the serotonin transporter gene (5-HTT) has recently been observed to moderate the relationship of stress to depression and anxiety.
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Chronic cerebral hypoperfusion has been associated with cognitive decline in aging and Alzheimer's disease.
Why it matters
This review describes a rat model of permanent bilateral common carotid artery occlusion used to study chronic cerebral hypoperfusion and related cognitive and neurodegenerative changes. It is an animal model review and reports no treatment, cure or prevention for Alzheimer's disease.
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In response to oxidative stress, the nuclear factor E2-related factor 2 (Nrf2) transcription factor translocates from the cytoplasm into the nucleus and transactivates expression of genes with antioxidant activity.
Why it matters
In Alzheimer's disease and Lewy body variant of Alzheimer's disease, Nrf2 was predominantly cytoplasmic in hippocampal neurons and nuclear Nrf2 levels were significantly decreased in Alzheimer's cases, suggesting Nrf2-mediated transcription is not induced despite oxidative stress. In Parkinson's disease, Nrf2 was strongly nuclear in nigral neurons, but this response may be insufficient to protect neurons from degeneration.
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An inflammatory process in the central nervous system (CNS) is believed to play an important role in the pathway leading to neuronal cell death in a number of neurodegenerative diseases including Parkinson's disease, Alzheimer's disease, prion diseases, multiple sclerosis and HIV-dementia.
Why it matters
This review describes how activated microglia mediate the inflammatory response in the central nervous system and notes that it remains controversial whether microglia have beneficial or detrimental functions, with chronic activation possibly causing neuronal damage. It reports no 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.
- Increased level of active GSK-3beta in Alzheimer's disease and accumulation in argyrophilic grains and in neurones at different stages of neurofibrillary degeneration
- Soluble TREM2: Innocent bystander or active player in neurological diseases?
- SGLT2 Inhibitor Use and Risk of Dementia and Parkinson Disease Among Patients With Type 2 Diabetes
- TREM2, a DAP12-associated receptor, regulates osteoclast differentiation and function
- Evidence against increased oxidative DNA-damage in Down syndrome
- RBM3 mediates structural plasticity and protective effects of cooling in neurodegeneration
- Amyloid precursor protein processing is stimulated by metabotropic glutamate receptors
- Diffusion tensor imaging (DTI)-based white matter mapping in brain research: a review
- Age-dependent emergence and progression of a tauopathy in transgenic mice overexpressing the shortest human tau isoform
- High-fat diet-induced deregulation of hippocampal insulin signaling and mitochondrial homeostasis deficiences contribute to Alzheimer disease pathology in rodents