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.
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A history of traumatic brain injury (TBI) is linked to an increased risk for the later development of dementia.
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Glucose and fructose metabolism originates the highly reactive byproduct methylglyoxal (MG), which is a strong precursor of advanced glycation end products (AGE).
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Osteoclasts require coordinated co-stimulation by several signaling pathways to initiate and regulate their cellular differentiation.
Why it matters
This review is about immune receptor regulation of osteoclasts, the bone cells that break down bone, not Alzheimer's disease. It provides no information on treating, curing or preventing Alzheimer's disease.
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Tyrosine hydroxylase (TH), a rate-limiting step in catecholamine synthesis in which its activity influences Alzheimer disease, Parkinson disease, and IQ of schizophrenia patients, has been studied for a long time.
Why it matters
This laboratory study used neuron-like cells grown on different self-assembling nanofibers to examine expression of the tyrosine hydroxylase gene, which the paper notes influences Alzheimer disease, Parkinson disease and IQ in schizophrenia. It is early cell-based work and does not test any treatment, cure or prevention of Alzheimer disease.
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Because of an extra copy of the Aβ precursor protein gene on chromosome 21, Down syndrome (DS) individuals develop high levels of Aβ peptides and Alzheimer disease-like brain amyloidosis early in life.
Why it matters
The γ-secretase activating protein was found to be increased in Down syndrome brains and regulated by the GATA1 transcription factor. The authors say pharmacological inhibition of GSAP is an attractive potential Aβ-lowering strategy, but this is a laboratory finding and no treatment was tested in patients.
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We studied with functional magnetic resonance imaging (fMRI) differences in resting-state networks between patients with mesial temporal lobe epilepsy (MTLE) and healthy subjects.
Why it matters
This small imaging study compared resting-state brain networks in 10 patients with mesial temporal lobe epilepsy and 10 healthy subjects. It is not about Alzheimer's disease and does not test any treatment, cure or prevention for it.
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The objective of this study was to evaluate the effect of apolipoprotein E (APOE) epsilon 4 allele on regional cerebral perfusion (rCBF) changes using arterial spin labeling (ASL) magnetic resonance imaging (MRI) in subjects who are carriers or noncarriers of this risk factor for Alzheimer disease (AD).
Why it matters
This imaging study found that in cognitively normal people and those with Alzheimer's disease, carriers of the APOE epsilon 4 allele had reduced regional cerebral blood flow in several brain areas compared with noncarriers. In people with mild cognitive impairment, carriers showed increased blood flow in some regions, so the pattern is not uniform.
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Expression of LRP1 by neurons in proximity to senile amyloid plaques does not appear to play a major role in modulating the formation of these proximal deposits or in the appearance of the associated neuritic pathology.
Why it matters
In this mouse study, reducing LRP1 levels in hippocampal neurons of an amyloid-forming transgenic model had no effect on the severity of amyloid deposition, the rate of amyloid accumulation, or plaque architecture. This is animal research and does not establish a treatment, cure or prevention for Alzheimer disease.
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Two genes on chromosome 21, namely dual specificity tyrosine phosphorylation-regulated kinase 1A (Dyrk1A) and regulator of calcineurin 1 (RCAN1), have been implicated in some of the phenotypic characteristics of Down syndrome, including the early onset of Alzheimer disease.
Why it matters
In this laboratory study, Dyrk1A was shown to directly interact with and phosphorylate RCAN1, which enhanced RCAN1's ability to inhibit calcineurin and led to enhanced tau phosphorylation. The authors suggest a direct link between these two chromosome 21 genes in pathways associated with Down syndrome features including early onset Alzheimer's disease.
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DYRK1A (dual specificity tyrosine phosphorylation-regulated kinase 1A) has been shown to be involved in learning and memory impairments in Alzheimer disease and Down syndrome.
Why it matters
This laboratory study found that REST regulates DYRK1A transcription in a negative feedback loop, and that DYRK1A imbalance reduces REST protein stability. It is a cell and mouse study of neurodevelopment, and it does not test any treatment or prevention for Alzheimer disease.
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Hepatic encephalopathy (HE) is a serious neuropsychiatric complication of liver failure, characterized neuropathologically by astrocyte swelling, microglial activation and Alzheimer Type II astrocytosis.
Why it matters
This review describes altered astrocyte and microglia gene expression, glutamate handling and neurosteroid changes in hepatic encephalopathy brain. It is about liver failure-related brain changes and does not report a treatment, cure or prevention for Alzheimer's disease.
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Stem cells are central to the development and maintenance of many tissues.
Why it matters
This study looked at gene expression in stem cells from people with Down syndrome and found changes linked to aging, including Notch signaling. It is a laboratory study of cells and does not test any treatment or prevention for Alzheimer disease.
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38/100
Down syndrome, caused by the trisomy of chromosome 21, is a complex condition characterized by a number of phenotypic features, including reduced neuron number and synaptic plasticity, early Alzheimer disease-like neurodegeneration, craniofacial dysmorphia, heart development defects, increased incidence of childhood leukemia, and powerful suppression of the incidence of most solid tumors.
Why it matters
In mouse embryonic stem cells with an extra human chromosome 21, this study found 52 proteins that differed in expression, and some of these differences persisted into adult mice and appeared in human Down syndrome fetal tissue. This is early laboratory work and does not by itself show any treatment or prevention for Alzheimer's disease.
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Senile myoclonic epilepsy of Genton is a newer epileptic syndrome of the older patients with Down syndrome associated with an Alzheimer-type dementia.
Why it matters
This report describes two people with Down syndrome and dementia who developed senile myoclonic epilepsy of Genton, a syndrome associated with Alzheimer-type dementia. It is a description of two cases and does not test any treatment, cure, or prevention.
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Patients with advanced Parkinson's disease (PD) and motor complications can obtain significant symptom improvement by deep brain stimulation (DBS) of the subthalamic nucleus (STN).
Why it matters
In 22 Parkinson's disease patients with 4 years of bilateral subthalamic nucleus deep brain stimulation, dyskinesia and off periods were reduced and motor function improved, but axial symptoms and speech worsened from 1 to 4 years and five patients developed dementia. This concerns Parkinson's disease symptom management, not treating, curing, or preventing Alzheimer's disease.
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Traumatic brain injury (TBI) is a risk factors for Alzheimer's disease (AD), and repetitive TBI (rTBI) may culminate in dementia pugilistica (DP), a syndrome characterized by progressive dementia, parkinsonism, and the hallmark brain lesions of AD, including neurofibrillary tangles (NFTs), formed by abnormal tau filaments and senile plaques (SPs) composed of Abeta fibrils.
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Epidemiological and experimental studies have suggested that high dietary intake of fats is associated with cognitive decline and a significantly increased risk of dementia.
Why it matters
In rats, a high fat diet increased oxidative stress and inflammation in the cerebral cortex, which the authors suggest may contribute to dementia risk. This is animal research and does not show that dietary fat reduction prevents dementia in humans.
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The neurotrophin hypothesis proposes that repetitive neuronal activity enhances the expression, secretion and actions of neurotrophins to modify synaptic transmission and connectivity thereby providing a connection between neuronal activity and synaptic plasticity.
Why it matters
This review discusses the neurotrophin hypothesis, which proposes that neurotrophins link neuronal activity to synaptic plasticity and may have neuroprotective effects relevant to neurodegenerative diseases such as Alzheimer's disease. It is a discussion of a hypothesis and does not show that any treatment, cure or prevention works.
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The gene encoding the beta-site amyloid precursor protein cleaving enzyme 2 (BACE2) has been determined to be located on the long arm of chromosome 21 at 21q22.3.
Why it matters
This study found that BACE2 immunoreactivity was detected in neurons with neurofibrillary tangles in elderly Down syndrome brains with Alzheimer-type pathology, but not in those without. It suggests a possible involvement of BACE2, but it does not test any treatment or prevention.
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Down syndrome (DS) is a genetic disease with developmental brain abnormalities resulting in early mental retardation and precocious, age dependent Alzheimer-type neurodegeneration.
Why it matters
In post-mortem brain tissue, serotonin was significantly decreased in the caudate nucleus and temporal cortex of adults with Down syndrome in an age-dependent way. This describes brain chemistry changes and does not test any treatment, cure, or prevention.
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Trisomy 21 (Down syndrome) is associated with a high incidence of Alzheimer disease and with deficits in cholinergic function in humans.
Why it matters
In this mouse cell study, cholinergic neurons from trisomy 16 mice worked normally when grown with normal glia, and normal neurons lost function when grown with trisomy 16 glia. This points to astroglia as a possible contributor to cholinergic problems, but it is a laboratory finding in a mouse model and does not establish a treatment for people.
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In order to study whether Alzheimer-like neuropathological changes involve the central histaminergic system we measured the concentration of histamine, its precursor histidine as well as the activity of histidine decarboxylase (HDC) and histamine-N-methyl-transferase (HMT) in frontal cortex of aging Down syndrome (DS) patients, Alzheimer patients and control individuals.
Why it matters
In frontal cortex from aging Down syndrome and Alzheimer's disease patients, histidine decarboxylase and choline acetyltransferase activity were reduced compared with controls, and histamine levels were significantly decreased in the Down syndrome group. This is a post-mortem biochemical study showing similar deficits in both conditions and does not test treatment.
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38/100
Neuritic pathology is a major neuroanatomical correlate of dementia in Alzheimer disease (AD).
Why it matters
In brain tissue from people who died with end-stage Alzheimer's disease, the enzyme ceNOS was reduced in cortical neurons and appeared in abnormal locations, including glial cells. The authors suggest this abnormal ceNOS behavior may play a role in the neuritic pathology of Alzheimer's disease, but the study does not test any treatment or show that changing ceNOS alters the disease course.
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We report on the clinical and cytogenetic assessment of five cases of Down syndrome phenotype with either a partial duplication of chromosome 21 or a normal karyotype, and we quote a case of del (21q) syndrome.
Why it matters
This report presents a study protocol and a call for collaboration to collect cases of Down syndrome with partial duplication of chromosome 21 or del (21q) syndrome, aiming to find genes involved in traits including Alzheimer disease. It is a protocol and does not report treatment, cure, or prevention results.
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38/100
The survival of cultured mouse hippocampal neurons was found to be greatly enhanced by micromolar concentrations of the excitatory neurotransmitter glutamate.
Why it matters
In cultured mouse hippocampal neurons, glutamate at low concentrations helped neurons survive, but hippocampal neurons from mice with the trisomy 16 genetic defect died 2-3 times faster than normal and did not respond to glutamate at any concentration. This is a cell-culture and animal study, so it does not show a treatment for 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.
- Autosomal dominant leukoencephalopathy and subcortical ischemic stroke. A clinicopathological study
- Measurement of GFAP in hepatic encephalopathy by ELISA and transblots
- Redox proteomics identification of oxidatively modified hippocampal proteins in mild cognitive impairment: insights into the development of Alzheimer's disease
- A deep dive into statistical modeling of RNA splicing QTLs reveals variants that explain neurodegenerative disease
- Traumatic brain injury in later life increases risk for Parkinson disease
- Proteoform-resolved neoGFAP as a diagnostic and prognostic biomarker across the TBI--MCI--AD continuum in Veterans
- STAT1 signaling modulates HIV-1-induced inflammatory responses and leukocyte transmigration across the blood-brain barrier
- Mutations in progranulin cause tau-negative frontotemporal dementia linked to chromosome 17
- Impact of regional white matter hyperintensity patterns on cognitive trajectories in NACC
- Toxoplasmic encephalitis in AIDS