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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Theories of the pathophysiology of schizophrenia have implicated the hippocampus, but controversy remains regarding hippocampal abnormalities in patients with schizophrenia.
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Cytokines and chemokines have been implicated in contributing to the initiation, propagation and regulation of immune and inflammatory responses.
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A group of similar autosomal dominant hereditary neurodegenerative disorders have been linked to chromosome 17 in thirteen kindreds.
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In an attempt to elucidate the pathological implications of intracellular accumulation of the amyloid precursor protein (APP) in postmitotic neurons in vivo, we transferred APP695 cDNA into rat hippocampal neurons by using a replication-defective adenovirus vector.
Why it matters
In rats, overexpressing wild-type amyloid precursor protein in hippocampal neurons caused degeneration of some of those neurons. This is animal work on the effects of amyloid precursor protein accumulation and does not test any treatment, cure, or prevention.
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Frontotemporal dementia is a neurological disorder characterised by personality changes, deterioration of memory and executive functions as well as stereotypical behaviour.
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Nitric oxide (NO) is a unique biological messenger molecule which mediates diverse physiologic roles.
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Neurofibrillary lesions made of hyperphosphorylated microtubule-associated protein tau constitute not only one of the defining neuropathological features of Alzheimer disease but also are present in a number of other neurodegenerative diseases with dementia.
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High alcohol consumption for long periods of time causes significant hippocampal neurodegeneration in rodents.
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NAA-relative signal intensity reductions in schizophrenia appear to be remarkably localized, involving primarily the hippocampal region and the dorsolateral prefrontal cortex, two regions implicated prominently in the pathophysiology of this disorder.
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Individual differences in the development of neurofibrillary changes were examined in eight cortical regions in the brains of 43 subjects with Down syndrome (DS; age range, 15-69 years) using sections stained with monoclonal antibodies (mAb) tau-1 and 3-39.
Why it matters
Among 43 people with Down syndrome, neurofibrillary pathology was found in all 20 cases above 36 years of age, with wide variation in severity between individuals. The authors suggest this indicates differing susceptibility to Alzheimer-type changes, but no treatment, cure, or prevention was tested.
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The most important new development during recent years in the field of degenerative dementia concerns synaptic pathology.
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Possible roles of the complement (C) system in the normal and injured brain were explored with inbred mice that carried a frameshift mutation in the C5 gene.
Why it matters
In mice with a C5 gene mutation, kainic acid caused more hippocampal neuron death and greater astrocyte mRNA induction than in C5-sufficient mice, and astrocyte cultures produced more IL-6 and TNF after an inflammatory stimulus. These are animal and cell-culture findings about complement C5 and neurodegeneration, not a treatment or prevention for Alzheimer's disease.
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This study examined relations of mesiotemporal lobe tissue volumes with neuropsychological (NP) functions in a sample of patients with first episode schizophrenia.
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Black-capped chickadees (Parus atricapillus) in upstate New York show a peak in food-hoarding intensity in October.
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Progressive multifocal leukoencephalopathy, a formerly rare disease that chiefly occurred in persons with underlying lymphoma and chronic lymphocytic leukemia, is now seen with increasing frequency in the era of acquired immunodeficiency syndrome.
Why it matters
This review is about progressive multifocal leukoencephalopathy, a disease that increased with AIDS, and its diagnosis and therapy. It is not about Alzheimer's disease and does not test any treatment, cure, or prevention for it.
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We studied a synatophysin-like immunoreactivity in the hippocampal formation of patients with definite Alzheimer's disease, multi-infarct dementia, patients with no evidence of clinical dementia with neuropathological findings fulfilling the criteria of possible Alzheimer's disease, and age-matched nondemented controls.
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The stability of proteins that constitute the neurofibrillary tangles and senile plaques of Alzheimer disease suggests that they would be ideal substrates for nonenzymatic glycation, a process that occurs over long times, even at normal levels of glucose, ultimately resulting in the formation of advanced glycation end products (AGEs).
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Frequencies of chromatid aberrations in response to G2-phase x-irradiation were compared in PHA-stimulated blood lymphocytes from healthy control subjects, Down syndrome (DS) patients, and Alzheimer disease (AD) patients.
Why it matters
This laboratory study found that cells from Down syndrome patients had deficient repair of X-ray-induced DNA damage compared to Alzheimer's disease and control cells. It describes a cellular difference but does not test any treatment, cure, or prevention for Alzheimer's disease.
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The hippocampus plays an essential role in spatial learning.
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It has been suggested that microglia, a type of glial cells in the central nervous system, play various important roles in normal and pathologic brains.
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This finding is consistent with the notion that schizophrenia involves pathology of and dysfunction within a widely distributed neocortical-limbic neural network that has been implicated in, among other activities, the performance of cognitive tasks requiring working memory.
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36/100
The structure and function of the chemicals contributing to the three main peaks seen with 1H NMR spectroscopy, N-acetyl-L-aspartate (NAA), creatine/phosphocreatine (Cr), and choline-containing compounds (Cho) is reviewed and the changes seen with these compounds in various disease states are briefly outlined.
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Review of the clinical cytogenetic literature provides compelling evidence for a specific relationship between imbalance of particular chromosomes or chromosomal regions and the appearance of defined patterns of phenotypic abnormalities.
Why it matters
This review of cytogenetic literature states that the regions responsible for many aspects of the Down syndrome phenotype, including Alzheimer's disease, have not been defined, and that loci on many parts of chromosome 21 likely play a role. It reports no treatment, cure, or prevention.
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36/100
Alzheimer disease (AD) as well as other dementing disorders are characterized by a continuous loss of neurons in cortical and subcortical areas and probably by an extensive synaptic loss.
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A sequential light and electron microscopic study of cerebral cortex was performed in a rat model of portal-systemic encephalopathy produced by creating a portacaval shunt and followed by ammoniate resin feedings.
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.
- Cyclooxygenase-2 (COX-2) in inflammatory and degenerative brain diseases
- Familial Alzheimer disease-linked mutations specifically disrupt Ca2+ leak function of presenilin 1
- FMRP mediates mGluR5-dependent translation of amyloid precursor protein
- Spectrum of human immunodeficiency virus-associated neocortical damage
- Neuro-Cells Mitigate Amyloid Plaque Formation and Behavioral Deficits in the APPswe/PS1dE9 Model of Alzheimer Disease While Also Reducing IL-6 Production in Human Monocytes
- Elevated methylation levels, reduced expression levels, and frequent contractions in a clinical cohort of C9orf72 expansion carriers
- C9orf72 suppresses systemic and neural inflammation induced by gut bacteria
- Retinal vessel density using optical coherence tomography angiography as a potential biomarker in patients with cerebral small vessel disease
- Microglia: Agents of the CNS Pro-Inflammatory Response
- The touchscreen operant platform for testing learning and memory in rats and mice