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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The beta-amyloid precursor protein (APP) represents a type I transmembrane glycoprotein that is ubiquitously expressed.
Why it matters
This study found that APP, a protein central to Alzheimer's disease, also plays an essential role in the growth of pancreatic and colon cancer cells. It does not test any treatment, cure, or prevention for Alzheimer's disease in people.
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Currently no specific biomarkers exist for the screening of pregnancies at risk for Down syndrome (DS).
Why it matters
Using iTRAQ labelling on plasma from six women with Down syndrome pregnancies and six with uncomplicated pregnancies, the study detected 178 proteins and found elevated Ig lambda chain C region, serum amyloid P-component and amyloid beta A4, and under expressed gamma-actin and titin. The authors say the approach may be useful for finding novel biomarkers, and these proteins are also found in the sera of patients with Alzheimer's disease.
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Caloric restriction (CR) mitigates neurological damage arising from aging and a variety of other sources, including neuropathology in young adult mice that express single and double transgenic (tg) mutations associated with Alzheimer disease (AD).
Why it matters
Middle-aged mice carrying APP and PS1 mutations fed a diet with 40% fewer calories than controls showed reduced amyloid-beta volume in the hippocampal formation and overlying neocortex after 18 weeks. This is animal research only and does not show that caloric restriction prevents or treats Alzheimer disease in people.
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The amyloid-beta precursor protein (AbetaPP) is a ubiquitously expressed transmembrane protein whose cleavage product, the amyloid-beta (Abeta) protein, is deposited in amyloid plaques in neurodegenerative conditions such as Alzheimer disease, Down syndrome, and head injury.
Why it matters
This laboratory study of human embryonic stem cells found that blocking cleavage of amyloid precursor protein reduced cell proliferation and promoted early neural precursor formation. These are cells in a dish, not people, so it says nothing yet about treating, curing or preventing Alzheimer's disease.
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Beta-amyloid (Abeta) is thought to be a key contributor to the pathogenesis of Alzheimer disease (AD) in the general population and in adults with Down syndrome (DS).
Why it matters
This study found that fibrillar amyloid deposits increase in Alzheimer disease and Down syndrome and correlate with dementia severity. It used a new antibody to detect these deposits in human tissue and a mouse model, but it did not test any treatment or show how to prevent the disease.
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The dietary essential PUFA docosahexaenoic acid [DHA; 22:6(n-3)] is a critical contributor to cell structure and function in the nervous system, and deficits in DHA abundance are associated with cognitive decline during aging and in neurodegenerative disease.
Why it matters
This review discusses the role of docosahexaenoic acid and its derivative neuroprotectin D1 in brain cell survival and repair, and their interactions with amyloid precursor protein mechanisms. It is a review and does not test any treatment, cure, or prevention.
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The dual-specific kinase DYRK1A (dual-specificity tyrosine phosphorylation-regulated kinase 1A) is the mammalian orthologue of the Drosophila minibrain (MNB) protein kinase and executes diverse roles in neuronal development and adult brain physiology.
Why it matters
In transfected cells and mouse brain tissue, the DYRK1A kinase was found to interact with and phosphorylate the protein SEPT4, which has been found in neurofibrillary tangles of Alzheimer's disease brains. This is a laboratory study suggesting a possible link to neurodegeneration, not a treatment or cure.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder primarily characterized by excessive deposition of amyloid-beta (Abeta) peptides in the brain.
Why it matters
This laboratory study examined how amyloid beta reduces glutamate uptake in cultured astrocytes, possibly through oxidative stress and MAP kinase pathways. Being cell-based work, it is preliminary and does not show that targeting this process would treat or prevent Alzheimer's disease in people.
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As mosaicism for trisomy 21 can present with no or minimal manifestations of Down syndrome, it may be underdiagnosed as a cause of early-onset AD.
Why it matters
This case report describes a 55-year-old man with young-onset Alzheimer's disease who was found to have trisomy 21 in 10% of his peripheral lymphocytes, a mosaicism that had not been diagnosed as Down syndrome. The authors suggest screening for such mosaicism in selected patients with mild developmental delay or young-onset Alzheimer's disease, but this is a single case and does not establish a treatment or cure.
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Current therapeutic approaches for Alzheimer and Parkinson disease (AD and PD, respectively) are merely symptomatic, intended for the treatment of symptoms, but offer only partial benefit, without any disease-modifying activity.
Why it matters
This review discusses green tea catechins and other plant compounds as potential neuroprotective strategies for Alzheimer and Parkinson diseases, noting that current therapies are only symptomatic. It is a summary of possible approaches and does not report a proven treatment, cure or prevention.
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Down syndrome (DS) is the most common human chromosomal abnormality caused by an extra copy of chromosome 21.
Why it matters
In fetal Down syndrome brain, BACE2 and APP protein levels were comparable to controls and BACE1 was increased but not significantly, while in adult Down syndrome brain APP was significantly increased but BACE1 and BACE2 were comparable to controls. The authors conclude that APP overexpression appears absent during early development but is present in adult Down syndrome brain.
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Advanced age and presence of intracerebral amyloid deposits are known to be major risk factors for development of neurodegeneration in Alzheimer's disease (AD), and both have been associated with microglial activation.
Why it matters
This study reports telomere shortening and reduced telomerase activity in microglia with normal aging in rats, and a tendency toward telomere shortening with dementia in humans, along with more microglial dystrophy in brains with high amyloid loads. It states that the specific role of activated microglia in Alzheimer's disease remains unresolved and offers no treatment, cure or prevention.
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6-[(3-Cyclobutyl-2,3,4,5-tetrahydro-1H-3-benzazepin-7-yl)oxy]-N-methyl-3-pyridinecarboxamide hydrochloride (GSK189254) is a novel histamine H(3) receptor antagonist with high affinity for human (pK(i) = 9.59 -9.90) and rat (pK(i) = 8.51-9.17) H(3) receptors.
Why it matters
This paper describes a compound, GSK189254, that binds histamine H3 receptors in human Alzheimer's brain tissue and improves cognitive performance in preclinical models. It is preclinical research, so it does not show benefit in people with Alzheimer's disease.
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The over expression of APP gene in DS leads to increases in plasma Abeta40 and Abeta42 levels before plaque formation in DS brain.
Why it matters
This study found higher plasma amyloid beta 40 and 42 levels in children and adolescents with Down syndrome than in their siblings, with a lower ratio of amyloid beta 42 to 40. The authors state that further studies are needed to know whether these children are at increased risk of later Alzheimer disease, so this is not a treatment or prevention finding.
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The human and rat hippocampus is highly susceptible to iron deficiency (ID) during the late fetal, early neonatal time period which is a peak time of regulated brain iron uptake and utilization.
Why it matters
In rats, perinatal iron deficiency altered expression of genes involved in energy metabolism and neuronal development in the hippocampus, including a gene network implicated in Alzheimer's disease. This is an animal study of early-life iron deficiency and does not show that iron deficiency causes Alzheimer's or that any intervention prevents it in people.
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Amyloidogenic processing of the amyloid precursor protein (APP) results in the generation of beta-amyloid, the main constituent of Alzheimer plaques, and the APP intracellular domain (AICD).
Why it matters
Using a human neural cell culture system, this study found that the APP intracellular domain affects gene expression and cytoskeletal dynamics. This is laboratory cell work and does not test any treatment or show a benefit for patients.
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The neuronal ceroid-lipofuscinoses (NCLs) are inherited lysosomal storage diseases and constitute the most common group of children's progressive encephalopathies.
Why it matters
This review discusses the neuronal ceroid-lipofuscinoses, a group of inherited lysosomal storage diseases that are the most common cause of progressive encephalopathies in children. It notes that the rare adult forms are dominated by dementia, and that mutations in at least seven different genes have been shown to underlie the multiple forms of NCL.
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Cardiovascular and cerebrovascular disorders are the main cause of death and permanent disability worldwide.
Why it matters
This review is about silent brain ischaemic lesions seen on MRI after invasive heart and blood vessel procedures, not about treating or curing Alzheimer's disease. It notes that a cumulative burden of ischaemic brain injury may cause neuropsychological deficits or aggravate vascular dementia, but it does not test any treatment or prevention for Alzheimer's disease.
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Astaxanthin (1), a red-orange carotenoid pigment, is a powerful biological antioxidant that occurs naturally in a wide variety of living organisms.
Why it matters
This review describes astaxanthin as an antioxidant with potential health effects, including neuroprotective effects seen in animal models of stroke and vascular dementia. It provides no evidence from human trials that astaxanthin treats, cures or prevents Alzheimer's disease.
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Neuronal oxidative stress occurs early in the progression of Alzheimer disease (AD), significantly before the development of the pathologic hallmarks, neurofibrillary tangles, and senile plaques.
Why it matters
This review proposes that oxidative stress occurs early in Alzheimer disease and that amyloid-beta and tau changes may be compensatory responses. It discusses a similar process in a muscle disease, but it does not report a treatment or cure.
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The 5-year cumulative incidence of neurotoxicity was 24%; this incidence increases over time.
Why it matters
This retrospective review describes delayed neurotoxicity, including a rapidly progressive subcortical dementia, in patients treated for primary central nervous system lymphoma. It aims to generate hypotheses for future studies on preventing and treating this complication of successful lymphoma therapy, not Alzheimer's disease.
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Interaction of the amino- and carboxyl-terminal domains in apolipoprotein (apo) E, referred to as domain interaction, is predicted to be more pronounced in apoE4 than in apoE3 and to underlie the association of apoE4 with Alzheimer and cardiovascular diseases.
Why it matters
Using spectroscopy methods, this laboratory study found that the two domains of apolipoprotein E4 are closer together than in apolipoprotein E3, supporting the idea of domain interaction. This is basic structural research and does not show any treatment or prevention for Alzheimer disease.
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42/100
Cotton wool plaques (CWPs) are round lesions that lack a central amyloid core.
Why it matters
In one person with familial Alzheimer's disease carrying a PSEN1 mutation, the cotton wool plaques were found to be made mainly of amyloid β peptides shortened at the amino end. This is a single-case pathology description and does not test any treatment, cure, or prevention.
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In most neurodegenerative disorders, including multiple sclerosis, Parkinson disease, and Alzheimer disease, a massive neuronal cell death occurs as a consequence of an uncontrolled inflammatory response, where activated astrocytes and microglia and their cytotoxic agents play a crucial pathological role.
Why it matters
In cultured brain astrocytes and microglia, thiadiazolidinone derivatives inhibited inflammatory activation by diminishing lipopolysaccharide-induced interleukin 6, tumor necrosis factor alpha, and inducible nitric oxide synthase. This is an in vitro study, so it does not establish a treatment or cure for Alzheimer's disease.
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Gamma-secretase cleavage of beta-amyloid precursor protein (APP) is crucial in the pathogenesis of Alzheimer disease, because it is the decisive step in the formation of the C terminus of beta-amyloid protein (Abeta).
Why it matters
This study identified a new presenilin-dependent zeta-cleavage site within the transmembrane domain of the amyloid precursor protein. It is basic molecular work and does not test any 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.
- Spatial and Temporal Mapping of Breast Cancer Lung Metastases Identify TREM2 Macrophages as Regulators of the Metastatic Boundary
- Ordered Assembly of Tau Protein and Neurodegeneration
- Pathways to neuronal injury and apoptosis in HIV-associated dementia
- In silico structure-based multi-targeted molecular docking analysis of ginkgo biloba phytocompounds against Alzheimer’s disease associated proteins
- Modified titration of donanemab reduces ARIA risk and maintains amyloid reduction
- Cognitive dysfunction associates with white matter hyperintensities and subcortical atrophy on magnetic resonance imaging of the elderly diabetes mellitus Japanese elderly diabetes intervention trial (J-EDIT)
- Multi-Omics Analysis of Microglial Extracellular Vesicles From Human Alzheimer's Disease Brain Tissue Reveals Disease-Associated Signatures
- Left anterior temporal cortex actively engages in speech perception: A direct cortical stimulation study
- Neuropeptide Y immunoreactive neurons in murine trisomy 16 cortical cultures. Plasticity of expression and differentiation
- TREM2: Potential therapeutic targeting of microglia for Alzheimer's disease