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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These findings suggest that in patients with schizophrenia spectrum disorders, hippocampal volume is influenced in part by schizophrenia susceptibility genes and an interaction of these genes with fetal hypoxia.
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The neuropeptide substance P and its receptor, the neurokinin 1 receptor (NK(1)R) have been proposed as possible targets for new antidepressant therapies.
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40/100
N-acetyl asparate and creatine reductions imply that there are hippocampal abnormalities in posttraumatic stress disorder.
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We report the first case of neuropathologically verified parkinsonism-dementia complex of the Kii peninsula, together with the patient's brother, who had amyotrophic lateral sclerosis.
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The objective of this study was to use high-resolution MRI techniques to determine whether children with Down syndrome exhibit decreases in hippocampal and amygdala volumes similar to those demonstrated in recent studies of adults with this condition.
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Increased SOD-1 levels in patients with DS may reflect the overexpression by the trisomic state, as a response to the oxidative stress, as has been proposed in DS by several authors.
Why it matters
In brain tissue from 9 controls, 9 adults with Down syndrome and 9 with Alzheimer's disease, SOD-1 levels were significantly increased in Down syndrome temporal, parietal and occipital cortex, decreased in Alzheimer's disease temporal cortex, and SOD-2 was comparable between all groups. The authors note the increase may reflect the trisomic state, oxidative stress, or increased glial proliferation.
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beta-Amyloid plaque deposition observed in brains from Alzheimer patients, might function as immune stimulus for glial/macrophages activation, which is supported by observations of activated microglia expressing interleukin (IL)-1beta and elevated IL-6 immunoreactivity in close proximity to amyloid plaques.
Why it matters
In transgenic mice with amyloid plaques, only IL-1beta was induced in reactive astrocytes near the plaques, while most other cytokines were not induced. This is animal research on inflammation around plaques and does not offer a treatment, cure, or prevention.
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This article reviews evidence for the occurrence of atypical parkinsonism in Afro-Caribbean and Indian ethnic minority subjects living in western countries, particularly the UK.
Why it matters
This review reports a three- to fourfold increase in atypical parkinsonism in Afro-Caribbean and Indian patients in the UK, and notes conflicting findings on Parkinson's disease prevalence in people of African origin. It does not test any treatment, cure or prevention for Alzheimer's disease.
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We report a patient with advanced Parkinson's disease, including severe and frequent off periods with freezing of gait, moderate dysphonia, and some cognitive impairment, who underwent bilateral subthalamic nucleus (STN) stimulation.
Why it matters
In one patient with Parkinson's disease, bilateral subthalamic nucleus stimulation improved mobility but was accompanied by cognitive decline and increased dependency. This case study is about Parkinson's disease surgery and does not address treating, curing, or preventing Alzheimer's disease.
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40/100
There is a reduction in the volume of amygdala and hippocampus in people with autism, particularly in relation to total brain volume.
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Hepatic encephalopathy (HE) is a neuropsychiatric disorder that occurs in both acute and chronic liver failure.
Why it matters
This review concerns hepatic encephalopathy, a neuropsychiatric disorder of liver failure, in which the astrocyte is the most vulnerable neural cell. It is not about Alzheimer's disease treatment, cure or prevention.
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Magnetic resonance imaging (MRI) studies have produced controversial results concerning the correlation of hippocampal volume loss with increasing age.
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In Down syndrome (DS), enhanced apoptosis (programmed cell death) may play a role in the pathogenesis of characteristic mental retardation and precocious dementia of Alzheimer-type.
Why it matters
In brain tissue from nine adults with Down syndrome and Alzheimer-like lesions, levels of two proteins linked to programmed cell death were higher than in controls. This is a small postmortem study and does not test any treatment.
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Ts65Dn mouse displays a partial triplication of chromosome 16 and is adopted as a model for Down syndrome (DS).
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In Down syndrome (DS), oxidative DNA-damage may play a role in the pathogenesis of characteristic mental retardation and precocious dementia of Alzheimer type.
Why it matters
This study found no significant increase in oxidative DNA damage in the brains of people with Down syndrome or Alzheimer disease compared to controls. It provides evidence against a role for this type of damage, and it does not test any treatment or prevention.
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Entry of the type 1 human immunodeficiency virus into most cells requires the presence of the CD4 protein in combination with one of several recently described co-receptors.
Why it matters
This study found that CXCR-4, a co-receptor for type 1 human immunodeficiency virus, is expressed in the human brain in several cell types including microglia and neurons. It reports no treatment, cure, or prevention for Alzheimer's disease.
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We examined the relation of APOE-epsilon 4, hippocampal volume, and cognitive performance in ten pairs of cognitively normal twins who had a mean age of 62.5 years (SD = 7.8).
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Plasma-membrane composition plays a crucial role in most of the cellular functions that depend on membrane processes.
Why it matters
In COS cells, raising cellular cholesterol reduced the processing of amyloid precursor protein into soluble APP. This is laboratory cell work and does not show a treatment, cure, or prevention for Alzheimer's disease.
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Early outcome measures of experimental traumatic brain injury (TBI) are useful for characterizing the traumatic severity as well as for clarifying the pathomechanisms underlying patterns of neuronal vulnerability.
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One hundred patients with intractable temporal lobe epilepsy and 22 control subjects were scanned on a 1.5-T Siemens SP63 Magnetom scanner.
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40/100
To identify changes in brain functions associated with the development of dementia, brain metabolism and cognition were assessed repeatedly in 12 adults with Down syndrome (DS) using positron emission tomography and neuropsychological tests.
Why it matters
In 12 adults with Down syndrome followed over time, the 10 who did not develop dementia showed no significant changes in cognition or brain metabolism, while the 2 who developed dementia declined rapidly afterward. This small study suggests brain function stays stable until dementia begins, which may help with timing of future treatments.
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The purpose of this study was to determine cerebral myo-inositol (mI) in adults with Down syndrome (DS), and to trace the chronobiology of DS to Alzheimer disease (AD).
Why it matters
Elevated cerebral myo-inositol was found in 23 young people with Down syndrome without dementia and in one person with Down syndrome and dementia, resembling the pattern seen in Alzheimer's disease. The authors suggest this may reflect a progressive neurochemical disorder, but the study is small and does not test any treatment or prevention.
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We describe a clinico-pathological variant of a degenerative disorder involving Broca's, Wernicke's, and supplementary motor areas, which presented as primary progressive aphasia, dysarthria, bucco-facial apraxia, and hearing loss as initial symptoms, followed by organic personality changes.
Why it matters
This is a clinico-pathological case description of a degenerative disorder presenting as primary progressive aphasia, with postmortem findings of focal atrophy and argyrophilic neuronal inclusions. It describes one variant's pathology and does not report a treatment, cure or prevention for Alzheimer's disease.
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Five patients developed a stereotyped syndrome of progressive akinesia of gait, speech, and hand-writing without rigidity, tremor, or dementia.
Why it matters
Five patients with pure akinesia of gait, speech, and handwriting without rigidity, tremor, or dementia are described, and the syndrome may represent a form of progressive supranuclear palsy. This is a small clinical description and reports no treatment or cure.
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The major component of senile plaques found in the brains of Alzheimer disease patients is the beta-amyloid peptide, which is derived from a larger amyloid precursor protein (APP).
Why it matters
This work identified a gene in the nematode Caenorhabditis elegans, called apl-1, that encodes a protein related to the human amyloid precursor protein. It is basic biology in a worm and has no direct implications for treating, curing, or preventing Alzheimer's disease in humans.
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.
- Dystrophic (senescent) rather than activated microglial cells are associated with tau pathology and likely precede neurodegeneration in Alzheimer's disease
- Calcium-mediated transient phosphorylation of tau and amyloid precursor protein followed by intraneuronal amyloid-beta accumulation
- A hypothalamic circuit for the circadian control of aggression
- Tau depletion prevents progressive blood-brain barrier damage in a mouse model of tauopathy
- Amyloid-β Dynamics Are Regulated by Orexin and the Sleep-Wake Cycle
- Cerebrovascular co-pathology and cholinergic white matter pathways along the Lewy body continuum
- Mechanisms, pathophysiology, and therapy of arterial stiffness
- TREM2 expression in the human brain: a marker of monocyte recruitment?
- Loss-of-function mutations in TYROBP (DAP12) result in a presenile dementia with bone cysts
- Molecular modeling to simulation: insights into Gaussian QSAR, molecular docking, and DFT for identification of HDAC3 inhibitors for neurocognitive vascular dementia