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.
-
Long-term treatment with Peptide 6 enhances the pool of newborn neurons in the dentate gyrus, prevents neuronal loss in CA1 and parietal cortex, preserves the dendritic and synaptic architecture in the hippocampus, and improves performance on a hippocampus-dependent memory task in TBI mice.
Why it matters
In a mouse model of traumatic brain injury, a neurotrophic peptide increased newborn neurons and improved memory recall. These are animal results only, and the authors state that further inquiry into the therapeutic potential of such small molecules is needed.
-
The combination of a sedentary lifestyle and excess energy intake has led to an increased prevalence of obesity which constitutes a major risk factor for several co-morbidities including type 2 diabetes and cardiovascular diseases.
Why it matters
This review is about metabolic signals and innate immune activation in obesity and exercise, and it does not address Alzheimer's disease. It describes how free fatty acids can trigger inflammatory signaling that interferes with insulin signaling, and how exercise improves insulin sensitivity and reduces obesity-induced chronic inflammation.
-
The total number of neurons and glial cells in the mediodorsal thalamic (MDT) nucleus of four aged females with Down syndrome (DS; mean age 69years) was estimated and compared to six age- and sex-matched controls.
Why it matters
In four aged females with Down syndrome, the mediodorsal thalamic nucleus had an average of 3.41 million neurons compared with 5.97 million in controls, with no significant differences in glial cell populations. The authors state the cause of the reduced neuron numbers cannot be determined, and the study does not test any treatment or cure.
-
Oxidative stress is a phenomenon associated with imbalance between production of free radicals and reactive metabolites (e.g. superoxide and hydrogen peroxide) and the antioxidant defences.
Why it matters
This review links oxidative stress in Down syndrome to trisomy of chromosome 21 and increased superoxide dismutase activity, and discusses whether antioxidants might play a role in therapy. It presents no trial results, so whether antioxidants help patients is not established.
-
The plans are all normalized such that 50% of the PTV receives 30 Gy.
Why it matters
This study tested radiation treatment planning strategies to reduce dose to neural stem cells during whole-brain radiation. It is a physics planning study and does not test any treatment, cure, or prevention for Alzheimer's disease.
-
The microtubule-associated protein Tau promotes the assembly and stability of microtubules in neuronal cells.
Why it matters
In rat brain, inhibiting phospholipase A2 lowered total tau protein levels, and the authors note that reduced phospholipase A2 activity has been reported in Alzheimer's disease brain. This is animal and laboratory work, so it does not establish any treatment, cure or prevention for people.
-
We sought to examine the association of levels of total tau (t-tau) and phosphorylated tau 181 (p-tau181) protein with brain morphology in mild cognitive impairment, as defined by the concept of aging-associated cognitive decline (AACD) and Alzheimer disease.
Why it matters
In this small study, higher levels of total tau and phosphorylated tau 181 in cerebrospinal fluid were linked to lower grey matter density in several brain regions in people with aging-associated cognitive decline and Alzheimer disease. This supports using these fluid markers to track brain changes, but it does not show that measuring or lowering tau affects the disease course.
-
Cholesterol plays a crucial structural role in the brain and local synthesis covers almost all the requirements of the brain.
Why it matters
This review describes how the brain converts excess cholesterol into 24S-hydroxycholesterol and how this oxysterol enters the bloodstream. It is a general review and does not test any treatment, cure, or prevention for Alzheimer's disease.
-
This review discusses the laboratory and clinical research supporting the rationale for the efficacy of donepezil (Aricept USA) in enhancing cognition in autism, Alzheimer disease, Down syndrome, traumatic brain injury, Attention Deficit Hyperactivity Disorder (ADHD), and schizophrenia.
Why it matters
This review discusses laboratory and clinical research on donepezil for enhancing cognition in autism, Alzheimer's disease, Down syndrome, traumatic brain injury, ADHD and schizophrenia, and notes that human studies outside Alzheimer's disease are sparse. It calls for further study with reliable measures of attention and memory, but reports no new treatment result.
-
Myoclonic epilepsy is being increasingly recognized as a late-onset complication in middle-aged or elderly patients with Down syndrome, in association with cognitive decline.
Why it matters
This report describes two 56-year-old patients with Down syndrome who developed myoclonic epilepsy alongside cognitive decline and Alzheimer-type dementia. It concerns a clinical feature associated with dementia, not any treatment, cure or prevention.
-
Alzheimer disease (AD) and Down syndrome (DS) brains contain deposits of amyloid-beta peptide that are located extracellularly in the neuropil and in blood vessels walls.
Why it matters
This laboratory study produced extracellular deposits of amyloid-beta in primary cultures of vascular smooth muscle cells from Alzheimer's disease cases with cerebrovascular amyloid angiopathy, forming nonfibrillar granular deposits similar to early stages of vascular amyloidogenesis. It is a cell culture model and does not test any treatment, cure or prevention in patients.
-
An important lesion in Alzheimer's disease (AD) patient brains is the neurofibrillary tangle (NFT).
Why it matters
In a series of dogs of varying ages, this study found age-related increases in amyloid, oxidative damage markers and lipofuscin, with preliminary signs of cognitive loss in older dogs. This is animal research and does not show any treatment, cure or prevention for Alzheimer's disease in people.
-
Using immunohistochemical techniques we studied the light microscopic localization of ADAMs (A Disintegrin And Metalloprotease) 10 and 15 in different neocortical areas of the human brain during normal aging, and also in patients with Alzheimer disease (AD) and Down syndrome (DS).
Why it matters
This tissue study found ADAM 10 immunoreactivity associated with plaques in Alzheimer disease and Down syndrome brains and a significant reduction of ADAM 10 neurons in Alzheimer brains compared with controls. It is a descriptive pathology finding and does not test any treatment.
-
In Down syndrome, enhanced apoptosis (programmed cell death) may play a role in the pathogenesis of characteristic early mental retardation and precocious neurodegeneration of Alzheimer type.
Why it matters
In a single fetal Down syndrome brain at 35 weeks' gestation, Bax protein was at least fivefold elevated and Bcl-2 was decreased across cerebral regions, with reduced heat shock protein 70 and neuronal apoptosis inhibitory protein. The authors suggest developmental apoptosis may be inappropriately activated in Down syndrome, but this is a single-sample study and does not test any treatment or cure.
-
Apoptosis is the mechanism by which cells are programmed to die under a wide range of physiological and developmental stimuli.
Why it matters
In fetal Down syndrome brain tissue, no detectable changes were found in the expression of Fas, caspase-3, Bcl-2 and annexins compared with controls, and the neuronal marker NSE did not differ. The authors present this as evidence against increased apoptosis in fetal Down syndrome, and it reports no treatment, cure or prevention.
-
The present study examines N-myc and c-myc protein expression with Western blotting and single and double-labeling immunohistochemistry in the hippocampus in Alzheimer disease (AD), the striatum in Huntington disease (HD) and the substantia nigra in Parkinson disease (PD).
Why it matters
No changes in N-myc and c-myc expression were found in neurons in Alzheimer disease, Huntington disease or Parkinson disease, though strong expression occurred in reactive astrocytes. The study found no link between neuron death and these transcription factors and reports no treatment or prevention effect.
-
Down syndrome individuals develop abnormalities of most organs, including all the pathological and neurochemical features of Alzheimer's disease, by the early age of 30 yr. Here, we report the isolation and characterization of BACE2, a gene mapping on human chromosome 21q22.3, which is highly similar to a transmembrane aspartyl protease, BACE (for beta-site APP-cleaving enzyme), which is able to catalyze the beta-secretase cleavage of Alzheimer's amyloid precursor protein (APP).
Why it matters
A gene called BACE2 was identified on chromosome 21 and found to be similar to the enzyme BACE that cleaves amyloid precursor protein. The authors suggest BACE2 could be involved in the Alzheimer-like neuropathology of Down syndrome, but this is a gene characterization study with no treatment tested.
-
Age of onset (AO) of Huntington disease (HD) is known to be correlated with the length of an expanded CAG repeat in the HD gene.
Why it matters
In people with Huntington disease, the APOE epsilon2epsilon3 genotype was associated with significantly earlier age of onset in males than in females. This concerns Huntington disease, not Alzheimer disease, and offers no treatment or prevention.
-
35/100
The risk of developing AD definitely increases with (a) age, (b) head injuries, (c) family history of AD or Down syndrome, (d) sex (higher prevalence of AD in women), (e) vascular disease, (f) exposure to environmental toxins, (g) infectious processes, or (h) changes in immune function, and recent advances in molecular genetics have suggested that genetic predisposition (i) can be considered one of the most important risk factors in the development of AD.
Why it matters
This laboratory study found that serum from people with certain ApoE genotypes, mainly ApoE 3/4 and 4/4, contained factors that changed microglial cell proliferation and activation. It suggests immune-related processes may play a role in Alzheimer's disease, but it does not test or identify any treatment.
-
Growth inhibitory factor, a new metallothioneinlike protein, was investigated at postmortem examination in the brains of 18 patients with Down syndrome ranging in age from 18 weeks gestation to 50 years of age and in 20 age-matched normal controls by developmental immunohistochemistry.
Why it matters
This developmental study describes how growth inhibitory factor in astrocytes changes with age and around senile plaques in Down syndrome brains. It suggests a possible link to dendritic maturation and plaque formation but does not test any treatment, cure, or prevention.
-
Cerebral amyloid angiopathy (CAA) is caused by the cerebrovascular deposition of Alzheimer amyloid beta protein (Abeta) and shows an increased incidence in carriers of the apolipoprotein E (APOE) epsilon4 genotype.
Why it matters
In cultured smooth muscle cells from blood vessels, amyloid-beta was taken up through a lipoprotein receptor pathway involving APOE and LRP. This is laboratory cell work proposing a model for cerebral amyloid angiopathy and does not show a treatment for people.
-
In order to study whether phosphokinases might be involved in the neuropathology of Down Syndrome (DS) and Alzheimer disease (AD), cyclin dependent kinase (CDK) activity and protein, phosphokinase C (PKC) and phosphokinase A (PKA) activities have been determined in frontal lobes of DS, AD and control brains.
Why it matters
This study found a significant decrease in cyclin dependent kinase protein and activity in the brains of people with Down syndrome compared with Alzheimer's disease and control brains, while PKC and PKA were unaffected. This is laboratory brain tissue work and does not show a treatment or cure.
-
IgG subclasses were measured in sera from 33 persons with Down syndrome (DS) (mean age 55 +/- 7 years) and 33 age- and sex-matched control individuals using a mouse monoclonal antibody based sandwich enzyme linked immunosorbent assay.
Why it matters
In 33 older people with Down syndrome, levels of IgG1 and IgG3 were higher and IgG2 and IgG4 lower than in matched controls, a pattern seen in autoimmune diseases and chronic infections. There were no significant differences in IgG subclass levels between those with signs of Alzheimer-type dementia and those without, and the authors speculate these levels may have little or no relationship to the brain lesions of Alzheimer's disease.
-
Brain spectrin is a major membrane skeleton protein that participates in cellular transport, cell morphogenesis, neurotransmitter release and growth cone adhesion.
Why it matters
This study found abnormal brain spectrin immunoreactivity in neuronal processes in Alzheimer's disease brain tissue, possibly from sprouting neurons or degeneration products. It is a descriptive pathology study and does not test any treatment, cure, or prevention for Alzheimer's disease.
-
Serum tests of thyroid function were compared in Down syndrome (DS) patients with and without manifestations of Alzheimer disease (AD).
Why it matters
This study found that adults with Down syndrome often had autoimmune thyroiditis with mild subclinical hypothyroidism, and this was more pronounced in those with Alzheimer's disease symptoms. The authors suggest this mild hypothyroidism may contribute to cognitive deficits, but no treatment trial was conducted.
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.
- Brain interleukin 1 and S-100 immunoreactivity are elevated in Down syndrome and Alzheimer disease
- The Co-oligomers of Aβ42 and Human Islet Amyloid Polypeptide Exacerbate Neurotoxicity and Alzheimer-like Pathology at Cellular Level
- First-in-Humans Evaluation of 18F-SMBT-1, a Novel 18F-Labeled Monoamine Oxidase-B PET Tracer for Imaging Reactive Astrogliosis
- ApoE4 and Connectivity-Mediated Spreading of Tau Pathology at Lower Amyloid Levels
- Promoting the clearance of neurotoxic proteins in neurodegenerative disorders of ageing
- An Altered Relationship between Soluble TREM2 and Inflammatory Markers in Young Adults with Down Syndrome: A Preliminary Report
- Automated Detection of Speech Timing Alterations in Autopsy-Confirmed Nonfluent/Agrammatic Variant Primary Progressive Aphasia
- Progressive language disorder due to lobar atrophy
- Chronic lithium administration to FTDP-17 tau and GSK-3beta overexpressing mice prevents tau hyperphosphorylation and neurofibrillary tangle formation, but pre-formed neurofibrillary tangles do not revert
- The Microglial Innate Immune Receptor TREM2 Is Required for Synapse Elimination and Normal Brain Connectivity