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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In addition to the full-length beta-amyloid peptides (Aβ 1-40/42), several Aβ variants, truncated at their N- or C-termini and bearing different post-translational modifications, have been detected in the brain of Alzheimer´s disease (AD) patients.
Why it matters
This study generated a mouse monoclonal antibody, 3B8, that recognizes amyloid aggregates in brain tissue from Alzheimer's disease patients and from 3xTg-AD transgenic mice, and appears to bind two conformational epitopes in AβN3(pE) and Aβ 3-42. The authors say the antibody may be useful in future therapeutic and diagnostic applications, but no treatment or diagnostic use has yet been established.
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Previously, we found that circadian desynchrony was involved in isoflurane-induced cognitive impairment.
Why it matters
In mice, feeding only during the active phase reduced memory deficits after isoflurane anaesthesia, while feeding during the rest phase prolonged them. This is animal research, so it does not yet show whether meal timing affects memory problems in people.
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It should be noted that by improving the neuronal connectivity in AM rat brains, the transplanted NLCs rescue Alzheimer's cognition.
Why it matters
In a rat model, transplanted neuron-like cells derived from mouse embryonic stem cells were studied for effects on memory and brain tissue after a lesion. This is early animal cell-therapy research and does not establish any treatment, cure, or prevention for Alzheimer's disease in people.
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32/100
Notch signaling is a master controller of the neural stem cell and neural development maintaining a significant role in the normal brain function.
Why it matters
This review discusses the role of Notch signaling in normal brain function and its possible involvement in sporadic Alzheimer's disease and other neurodegenerative diseases including Down syndrome. It presents a research perspective and does not test any treatment, cure, or prevention.
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The precise regulation of DSCR gene expression is crucial to maintain the brain homeostasis, especially in those areas with high levels of gene expression associated with a remarkable process of learning and cognition.
Why it matters
This database analysis correlated the transcription levels of 19 genes in the Down Syndrome Critical Region with their expression across 42 normal human brain substructures, finding highest expression in the caudate nucleus, nucleus accumbens, and putamen. The authors conclude that precise regulation of these genes is crucial to maintain brain homeostasis, but the study examined normal brain tissue and did not test any treatment or prevention.
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Down syndrome (DS) is one of the most common genetic diseases.
Why it matters
In cell and mouse experiments, BACE1 but not BACE2 was associated with increased SET protein, and both BACE1 and SET levels were increased in Down syndrome patients. The authors suggest BACE1-induced SET upregulation may contribute to growth delay and cognitive impairment in Down syndrome, but this is laboratory work and no treatment was tested in people.
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Nardilysin is a metalloprotease that cleaves peptides, such as dynorphin-A, α-neoendorphin, and glucagon, at the N-terminus of arginine and lysine residues in dibasic moieties.
Why it matters
This review summarizes current knowledge on possible roles of nardilysin in brain diseases including Alzheimer disease and Down syndrome, describing it as possibly neuropathogenic in some diseases and neuroprotective in others. It is a review and does not present a treatment or cure.
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Down's syndrome (DS) is characterized by several pathological aspects leading to an increased susceptibility to cardiovascular diseases, infections, leukemia, endocrine alterations.
Why it matters
In laboratory studies of skin fibroblasts, cells from people with Down syndrome showed more baseline apoptosis and greater susceptibility to okadaic acid than normal fibroblasts. This is cell-level research and does not establish a treatment or prevention for Alzheimer's disease.
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Features of multipotentiality of engineered NSC-derived cell lines versus naive cells (control-NSC) were assessed by immunocytochemical analysis in differentiation conditions.
Why it matters
Mouse neural stem cells engineered to express human NGF released active NGF and increased axonal sprouting in vitro. This is early laboratory work, and the authors only suggest these cells may prospectively be candidates for treating neurodegenerative diseases such as Alzheimer's disease.
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The present findings demonstrate several fundamental parallels between lens and neuron vesicle trafficking cell biology and development, and suggest that more extensive AbetaPP related vesicle trafficking disease mechanisms may be shared by lens and brain.
Why it matters
This laboratory study in mouse and rat lenses examined proteins involved in vesicle transport, including amyloid precursor protein, which the authors previously linked to early-onset cataract and Alzheimer's disease in Down syndrome. The work is in lens tissue and does not test any treatment for Alzheimer's disease.
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Nascent polypeptide-associated complex (NAC) protein, a heterodimeric complex of alpha- and beta-subunits, prevents mistargeting of nascent polypeptide chains to the endoplasmic reticulum membranes. alpha-NAC has sequence similarities with transcription-regulating proteins and has been reported to function as a transcriptional coactivator potentiating c-Jun-mediated transcription.
Why it matters
This study found reduced levels of a protein called alpha-NAC in the frontal cortex of people who had died with Alzheimer's disease and Down syndrome. It suggests this decrease may be involved in the disease process, but it does not test any treatment or show that raising this protein would help patients.
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Complex interactions and interconnectivity between neurons are hallmarks of normal neuronal differentiation and development.
Why it matters
This paper proposes a hypothesis that deficient glial support in Down syndrome contributes to cognitive limitation and early Alzheimer's disease. It is a theoretical discussion without experimental treatment or prevention data.
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The mechanisms responsible for the pathological deposition of brain iron in Parkinson's disease, Alzheimer's disease and other human neurodegenerative disorders remain poorly understood.
Why it matters
In rat astrocyte cultures, dopamine and other agents triggered HO-1 expression and mitochondrial iron buildup, and HO-1 inhibitors blocked this iron trapping. Astrocytes co-expressing HO-1 were increased in Parkinson's substantia nigra and Alzheimer's hippocampus compared with age-matched controls, suggesting a possible role for HO-1 in iron deposition in these diseases.
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We recently identified a cDNA encoding a human brain specific trypsinogen (trypsinogen IV).
Why it matters
In transgenic mice expressing human brain-specific trypsinogen IV, astrocytes showed increased GFAP expression and one-year-old mice showed an intracellular beta-amyloid-like signal in neurons. This is an animal study from 1998 and does not demonstrate any treatment or prevention for Alzheimer's disease in people.
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Tau protein promotes microtubule assembly.
Why it matters
This immunohistochemistry study found beta-tubulin immunoreactive structures resembling neurofibrillary tangles in Alzheimer's disease and, more frequently, in parkinsonism dementia complex of Guam and Down syndrome. The structures were intracellular and appeared at an early stage of tangle development, which the authors say may indicate tubulin is involved in tangle formation.
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Monoclonal antibodies (mAbs) D3G6 and C8A5, specific for amino acid residues 160-168 of S182 protein, immunolabeled neurons, ependymal and choroid plexus cells, and myocytes in brain sections from normal subjects and people with Alzheimer disease or Down syndrome and in rats and mice.
Why it matters
Antibodies to the presenilin-1 protein labelled neurons and some other cells in brain tissue from normal people and people with Alzheimer's disease or Down syndrome. The protein detected was not part of amyloid-beta deposits or tangles, so this describes where the protein is found rather than any treatment or prevention.
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32/100
On the basis of what is known about the neural circuitry essential or normally involved in eyeblink classical conditioning (EBCC), the pattern of neurodegeneration in Huntington's disease (HD) would not appear to interfere with this type of learning.
Why it matters
In seven patients with Huntington's disease, the ability to acquire conditioned eyeblink responses was normal but the timing of the response was abnormal, and performance was significantly better than in patients with probable Alzheimer's disease or Down syndrome over age 35. This study is about Huntington's disease and does not test or propose any treatment, cure or prevention for Alzheimer's disease.
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32/100
B/A4 is the major component of brain amyloid plaque, one of the hallmarks of Alzheimer's disease (AD).
Why it matters
In gerbils after transient forebrain ischemia, levels of apolipoprotein E and GFAP mRNA increased in the hippocampus while APP mRNA did not. This is an animal study about gene responses to injury and does not test any treatment or prevention for Alzheimer's disease.
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It has been suggested that this increment, by accelerating hydrogen peroxide formation, might promote oxidative damage within DS cells and might be involved in the various neurobiological abnormalities found in DS such as premature aging and Alzheimer-type neurological lesions.
Why it matters
This paper discusses the idea that increased copper-zinc superoxide dismutase in Down syndrome may accelerate hydrogen peroxide formation and oxidative damage, possibly contributing to premature aging and Alzheimer-type neurological lesions. In transgenic mice overexpressing CuZnSOD in the brain, MnSOD activity was also increased; this is animal and conceptual work with no treatment tested in people.
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Immunohistochemical staining with polyclonal antibodies to synthetic amyloid (residues 1-28 of A4) was performed on normal and Down syndrome brains from fetuses to adults.
Why it matters
This brain tissue study found that amyloid protein appears in developing brains and reappears in elderly brains, including in people with Down syndrome at an earlier age. The authors suggest this reappearance may relate to a regeneration process, but the study does not test any treatment.
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Studies of Alzheimer amyloid protein precursor mRNA expression in the human brain have provided compelling evidence for a neural origin of beta amyloid.
Why it matters
This early work found altered levels of amyloid precursor mRNA specifically in neurons at risk in Alzheimer's disease and Down syndrome, suggesting a neuronal source of beta amyloid. It raises the possibility that a shift toward the transcript containing the protease inhibitor domain may explain beta amyloid accumulation, but no treatment or prevention is tested here.
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Digital and palmar dermatoglyphics were examined in 29 men and 27 women with dementia of the Alzheimer type (DAT) and 112 age-, sex-, and racial group-matched controls.
Why it matters
This study found no dermatoglyphic differences between men with Alzheimer-type dementia and controls, and only limited differences in women, so it did not confirm earlier reports of such differences. It also failed to confirm a reported similarity between the dermatoglyphic pattern in Alzheimer's disease and that in Down syndrome, and it tests no treatment.
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31/100
In addition, we found sex-associated changes in the abundances of several proteins previously reported to be involved in tau pathology, such as Reelin, DARPP-32, Zyxin, Tbce, and Gng5, in JNPL3 mice.
Why it matters
In JNPL3 tauopathy mice, proteomics revealed altered membrane protein abundance in the prefrontal cortex, differing between males and females, including reduced levels of the drug efflux transporter ABCB1 in males. This is animal tissue analysis and identifies no treatment, cure or prevention.
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Neurodegenerative disorders (NDDs), primarily alzheimer, dementia, parkinson, and rare NDD disease, present an escalating global health crisis, currently affecting over 55 million older adults worldwide.
Why it matters
This is a plan for a scoping review that will map existing observational studies of GLP-1 receptor agonists in neurodegenerative disorders. It reports no new results and therefore cannot say whether these drugs treat or prevent Alzheimer's disease.
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Down syndrome (DS), caused by trisomy of chromosome 21, is characterized by early-onset oxidative stress, impaired neuronal development, and an increased risk of Alzheimer's disease (AD)-like neuropathology.
Why it matters
This review proposes that dysregulation of the BACH1/HO-1 axis links Down syndrome to Alzheimer-like neurodegeneration and discusses BACH1 inhibitors and NRF2 activators as emerging strategies. These are proposed approaches only, with no tested treatment or cure 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.
- Glial fibrillary acidic protein in the cerebrospinal fluid of patients with dementia
- Prenatal activation of microglia induces delayed impairment of glutamatergic synaptic function
- Stem Cell-Derived Extracellular Vesicles Ameliorate the Neuron Mitochondrial Damage Induced by ROS-, LPS-Exposure: In Vitro Model of Neuron, Microglia, and Astrocyte Triple Co-Culture
- Plaque-associated human microglia accumulate lipid droplets in a chimeric model of Alzheimer's disease
- beta Subunits of voltage-gated sodium channels are novel substrates of beta-site amyloid precursor protein-cleaving enzyme (BACE1) and gamma-secretase
- Presenilin 2 regulates corticosterone-induced autophagic death of adult hippocampal neural stem cells
- Progression of tau pathology in cholinergic Basal forebrain neurons in mild cognitive impairment and Alzheimer's disease
- ω-3 PUFA for Secondary Prevention of White Matter Lesions and Neuronal Integrity Breakdown in Older Adults: A Randomized Clinical Trial
- Alzheimer patients and Down patients: abnormal presynaptic terminals are related to cerebral preamyloid deposits
- Reduced FDG-PET brain metabolism and executive function predict clinical progression in elderly healthy subjects