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 sought to identify the molecular basis of the autosomal dominant form of Kufs disease, an adult onset form of neuronal ceroid lipofuscinosis.
Why it matters
This study found that mutations in the DNAJC5 gene cause an inherited form of Kufs disease, which includes dementia among its symptoms, with onset around age 30. It identifies a genetic cause of a rare disease and does not test any treatment or prevention for Alzheimer's disease.
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A disintegrin and metalloprotease 10 (ADAM10) is a ubiquitous transmembrane metalloprotease that cleaves the extracellular regions from over 40 different transmembrane target proteins, including Notch and amyloid precursor protein.
Why it matters
This laboratory study describes how the TspanC8 subgroup of tetraspanins interacts with ADAM10 and regulates its maturation and cell surface expression. It is basic cell biology about a protein relevant to Alzheimer's disease and does not test any treatment or prevention.
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Lack of tau expression has been reported to protect against excitotoxicity and to prevent memory deficits in mice expressing mutant amyloid precursor protein (APP) identified in familial Alzheimer disease.
Why it matters
In mice expressing mutant APP and PS1, deleting tau rescued reduced survival, spatial memory deficits and motor impairments. This is animal work showing tau is needed for these deficits, and no treatment, cure or prevention in people is reported.
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Reactive microgliosis, hallmark of neuroinflammation, may contribute to neuronal degeneration, as shown in several neurodegenerative diseases.
Why it matters
Using PET imaging and spinal fluid markers, this small study of six people with dementia with Lewy bodies and six with Parkinson's disease measured microglia activation and oxidative stress. It involves only 12 participants and other diseases, so it does not provide a treatment or prevention for Alzheimer's disease.
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Abnormalities of functional connectivity in the default mode network (DMN) recently have been reported in patients with amnestic mild cognitive impairment (aMCI), Alzheimer's disease (AD) or other psychiatric diseases.
Why it matters
In this study of 30 amnestic mild cognitive impairment and 26 cognitively normal subjects, those with mild cognitive impairment showed reduced right posterior insula volumes and disrupted intrinsic connectivity of insula networks. The altered connectivity was linked to cognitive performance, but the study does not test any treatment or prevention.
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Pathogenic generation of amyloid β-peptide (Aβ) by sequential cleavage of β-amyloid precursor protein (APP) by β- and γ-secretases is widely believed to causally underlie Alzheimer disease (AD). β-Secretase initially cleaves APP thereby generating a membrane-bound APP C-terminal fragment, from which γ-secretase subsequently liberates 37-43-amino acid long Aβ species.
Why it matters
In a cell-free system, changing the thickness of model membranes directly affected gamma-secretase production of the pathogenic amyloid-beta 42 and 43 peptides. This identifies membrane thickness as a factor that can influence these peptides in the laboratory, but it is not a treatment or prevention for Alzheimer's disease.
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Few studies have examined connected speech in demented and non-demented patients with Parkinson's disease (PD).
Why it matters
Both demented and non-demented patients with Lewy body spectrum disorder showed reduced speech fluency, with slower overall speech rate and long pauses between sentences, and this was linked in part to disease in frontal brain regions. The study describes speech impairment only and does not test any treatment, cure or prevention.
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There has been no extensive characterization of the effects of Ginsenoside Rg1, a pharmacological active component purified from the nature product ginseng, in an Alzheimer's disease mouse model.
Why it matters
In transgenic Alzheimer mice, Ginsenoside Rg1 reduced cerebral amyloid-beta levels, reversed some neuropathological changes and preserved spatial memory. This is animal work and does not show benefit in patients.
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Pure vascular parkinsonism without evidence of nigral Lewy body pathology may occur as a distinct clinicopathological entity, but a much more frequent occurrence is the comorbid presence of age-associated white matter lesions (WMLs) in idiopathic Parkinson disease (PD).
Why it matters
This review suggests that age-associated white matter lesions may worsen or contribute to some motor and cognitive deficits in Parkinson disease. It concerns Parkinson disease and offers no treatment, cure, or prevention for Alzheimer's disease.
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Reducing the mammalian target of rapamycin (mTOR) activity increases lifespan and health span in a variety of organisms.
Why it matters
This study found increased mTOR activity and signaling in cells with mutant amyloid precursor protein and in the brains of 3xTg-AD mice, and showed mTOR activity could be reduced in those mice. It is animal and cell-based research and does not demonstrate a treatment, cure or prevention for Alzheimer's disease in people.
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The amyloid precursor protein (APP) is cleaved by β- and γ-secretases to generate the β-amyloid (Aβ) peptides, which are present in large amounts in the amyloid plaques of Alzheimer disease (AD) patient brains.
Why it matters
In mouse and human neural cells, activating the P2X7 receptor increased release of the neuroprotective sAPPα fragment. These are cell and animal findings, so it is not yet known whether this could be used to treat or prevent Alzheimer's disease in people.
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Scavenger receptor class B type I (SR-BI) is a high-density lipoprotein receptor that regulates cholesterol efflux from the peripheral tissues to the liver.
Why it matters
In an Alzheimer's mouse model, reducing or deleting the SR-BI gene increased perivascular macrophages and modified amyloid pathology and cerebral amyloid angiopathy. This is animal work and reports no treatment, cure or prevention for people.
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Recent studies indicate that the deposition of β-amyloid peptide (Aβ) is related to the pathogenesis of Alzheimer disease (AD); however, the underlying mechanism is still not clear.
Why it matters
In SH-SY5Y cells overexpressing the Swedish mutant form of human amyloid precursor protein and in a Caenorhabditis elegans amyloid-expressing strain, amyloid-beta increased iron content and oxidative stress. This is cell and worm research on a mechanism and does not show any treatment, cure or prevention for patients.
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Deposition of amyloid β (Aβ) in the brain is closely associated with Alzheimer disease (AD).
Why it matters
This laboratory study shows that brain endothelial cells express APP770 and produce amyloid beta, preferentially secreting an O-glycosylated form. It addresses how amyloid beta may accumulate in blood vessels but does not test or establish a treatment, cure or prevention for Alzheimer's disease.
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The presence of Met-BDNF allele, particularly in association with APOE*E4, may predict a worse cognitive outcome in patients with MCI.
Why it matters
In 160 older adults followed for up to 60 months, mean serum brain-derived neurotrophic factor levels were reduced in people with mild cognitive impairment and Alzheimer's disease compared with controls. The authors conclude that decreased neurotrophic support may play a role in the neurodegenerative processes from mild cognitive impairment to Alzheimer's disease, but this is an observational study and no treatment is tested.
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Epidemiological studies suggest that statins (hydroxymethylglutaryl-CoA reductase inhibitors) could reduce the risk of Alzheimer disease.
Why it matters
In mice, fluvastatin reduced brain amyloid-beta and APP C-terminal fragment levels, and this effect was blocked by lysosomal inhibitors. This is an animal study and does not establish any treatment, cure, or prevention for Alzheimer's disease in humans.
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The amyloid precursor protein (APP) and its proteolytic product amyloid beta (Abeta) are associated with both familial and sporadic forms of Alzheimer disease (AD).
Why it matters
In rat hippocampal neurons grown in the lab, the researchers found a site in the amyloid precursor protein (APP) gene's message where the microRNA miR-101 acts: blocking the cells' own miR-101 raised APP, while adding extra miR-101 "significantly reduced APP and Abeta load." This shows one way cells may control the protein that amyloid comes from, but it is a cell-culture result with no human or animal testing and does not show that changing miR-101 treats or prevents Alzheimer's.
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Previous studies indicated increased levels of protein oxidation in brain from subjects with Alzheimer's disease (AD), raising the question of whether oxidative damage is a late effect of neurodegeneration or precedes and contributes to the pathogenesis of AD.
Why it matters
Researchers asked whether oxidative damage to brain proteins is just a late result of Alzheimer's or appears earlier. In post-mortem brain tissue (inferior parietal lobule) they found raised oxidation ("carbonylation") of four proteins in mild cognitive impairment — including Hsp70 and carbonic anhydrase II — and three different proteins in early Alzheimer's, compared with age-matched controls. The authors say this suggests "a possible involvement" of protein oxidation in disease progression; it does not show cause, test a treatment, or offer a test for living patients.
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Alzheimer's disease (AD) is the most common form of dementia and is pathologically characterized by senile plaques, neurofibrillary tangles, synaptic disruption and loss, and progressive neuronal deficits.
Why it matters
In hippocampus tissue from people with amnestic mild cognitive impairment, levels of the synaptic protein PSD95 and two associated proteins were decreased compared with controls. The authors suggest these proteins may be involved in synaptic changes and memory loss in progression from mild cognitive impairment to Alzheimer's disease, but this is a tissue study and not a treatment or cure.
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Abnormal processing of the amyloid precursor protein (APP) and beta-amyloid (Abeta) plaque accumulation are defining features of Alzheimer disease (AD), a genetically complex neurodegenerative disease that is characterized by progressive synapse loss and neuronal cell death.
Why it matters
In laboratory work, Reelin prevented the suppression of long-term potentiation and NMDA receptors caused by amyloid-beta levels comparable to those in an Alzheimer's-afflicted brain, but at high amyloid-beta concentrations Reelin could no longer overcome this suppression. This is a mechanistic model of synaptic function and does not test any treatment, cure, or prevention in people.
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For decades, astrocytes have been regarded as passive partners of neurons in central nervous system (CNS) function.
Why it matters
This review discusses how astrocytes respond to neurotransmitters with calcium signals and release glutamate, and how this may relate to neurodegeneration. It is a mechanistic overview and does not report any treatment, cure or prevention for Alzheimer's disease.
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Although frontotemporal lobar degeneration with ubiquitin/TDP-43-positive inclusions (FTLD-TDP) and Pick's disease are common pathological substrates in sporadic FTLD, clinical differentiation of these diseases is difficult.
Why it matters
This study found clinical differences between Pick's disease and frontotemporal lobar degeneration with ubiquitin/TDP-43-positive inclusions, such as asymmetric motor disturbances being more frequent in the latter. These findings are for pathological characterization and do not address treating, curing, or preventing Alzheimer's disease.
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A genome-wide screen using 382 STR markers to localize and identify the gene implicated in early-onset dementia (EOD) without bone cysts in a Lebanese family with three affected subjects was conducted.
Why it matters
In a Lebanese family with three members affected by early-onset dementia but no bone cysts, a genome-wide search pointed to one region on chromosome 6, where the researchers found a new small deletion at a splicing signal in the TREM2 gene. TREM2 was already known to cause Nasu-Hakola disease (PLOSL), which includes bone cysts, so this study links the same gene to dementia without bone disease; a computer prediction suggested the mutated splice site is weaker, and the authors report confirming its effect with RNA tests. This comes from one family, does not concern common late-onset Alzheimer's disease, and does not show any treatment or prevention.
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The beta-amyloid peptide (Abeta) is the major constituent of the amyloid core of senile plaques found in the brain of patients with Alzheimer disease.
Why it matters
This laboratory study found that amyloidogenic processing of APP requires a precisely oriented APP dimer formed by transmembrane GXXXG motifs. It identifies a mechanism of amyloid-beta production and does not test any treatment or prevention in people.
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Elucidation of Abeta-lowering agents that inhibit processing of the wild-type (WT) beta-secretase amyloid precursor protein (APP) site, present in most Alzheimer disease (AD) patients, is a logical approach for improving memory deficit in AD.
Why it matters
This study found that cathepsin B inhibitors improved memory and reduced amyloid-beta in transgenic mice expressing the wild-type beta-secretase site, but not in mice with the Swedish mutant site. It is animal research and does not establish that these inhibitors treat or prevent Alzheimer's disease 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.
- Visual Classification of Tau-PET Detects 4 Subtypes With Different Long-Term Outcomes
- Cardiovascular Risk Reduction in Metabolic Dysfunction-Associated Steatotic Liver Disease and Metabolic Dysfunction-Associated Steatohepatitis
- Intravenous chaperone treatment of late-stage Alzheimer´s disease (AD) mouse model affects amyloid plaque load, reactive gliosis and AD-related genes
- Immunoglobulin G subclasses in older persons with Down syndrome
- Perivascular macrophages mediate the neurovascular and cognitive dysfunction associated with hypertension
- Quantitative susceptibility mapping reveals differences between subtypes of Lewy body dementia
- Perceptions of non-invasive brain stimulation and barriers to it's clinical translation: a multi-stakeholder focus group study
- Chronic alcohol consumption does not cause hippocampal neuron loss in humans
- Alpha-synuclein is part of a diverse and highly conserved interaction network that includes PARK9 and manganese toxicity
- Cyclic 2.5D Perceptual Loss for Cross‐Modal 3D Medical Image Synthesis: T1w MRI to Tau PET