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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Imaging techniques are a potentially powerful method of identifying phenotypes that are associated with, or are indicative of, a vulnerability to developing major depressive disorder (MDD).
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This study demonstrates that the impact of the BDNF Val66Met polymorphism is not confined to the hippocampus but also extends to the parahippocampal gyrus and the amygdala.
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Brain-derived neurotrophic factor (BDNF) plays important roles in activity-dependent plasticity processes, such as long-term potentiation, learning, and memory.
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Chronic stress decreases neurogenesis in the adult brain, while exposure to enriched environment (EE) increases it.
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Adult neurogenesis, particularly in the subgranular zone, is thought to be linked with learning and memory.
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Oxidative stress has been implicated in the pathogenesis of several neurodegenerative diseases including Alzheimer's disease (AD).
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Chronic exposure to stress results in a reduction of hippocampal neurogenesis and of hippocampal volume.
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Loss of synapses has been correlated with dementia in Alzheimer's disease (AD) as an early event during the disease progression.
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Initial recruitment of leukocytes in inflammation associated with diseases such as multiple sclerosis (MS), ischemic stroke, and HIV-related dementia, takes place across intact, but activated brain endothelium.
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The mild cognitive impairment (MCI) stage of dementia with Lewy bodies (MCI-DLB) has not yet been defined, but is likely to differ in the MCI stage of Alzheimer's disease (MCI-AD).
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Epidemiological data suggest that omega-3 polyunsaturated fatty acids (PUFA) consumption may be inversely correlated to the prevalence and severity of depression but little is known about the underlying mechanisms.
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Frontotemporal lobar degenerations are a group of disorders characterized by circumscribed degeneration of the frontal and temporal lobes and diverse histopathologic features.
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Alzheimer's disease (AD) is a terminal age-associated dementia characterized by early synaptic dysfunction and late neurodegeneration.
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Dysregulation of genes that control cell-cycle progression and DNA repair is a hallmark of tumorigenesis.
Why it matters
This review discusses how genes involved in cancer and neurodegeneration overlap, noting that extra amyloid precursor protein in Down syndrome predisposes to Alzheimer-type dementia. It is a conceptual paper and offers no tested treatment, cure or prevention.
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Childhood trauma is a potent risk factor for developing depression in adulthood, particularly in response to additional stress.
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Glial activation and neuroinflammatory processes play an important role in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and HIV dementia.
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Notch signaling is critically important for proper architecture of the vascular system, and mutations in NOTCH3 are associated with CADASIL, a stroke and dementia syndrome with vascular smooth muscle cell (VSMC) dysfunction.
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Tau pathology is a hallmark of many neurodegenerative diseases including Alzheimer disease (AD) and frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17).
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Frontotemporal dementia with parkinsonism (FTDP) is a major neurodegenerative syndrome, particularly for those with symptoms beginning before age 65 years.
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The hippocampus is known to be vulnerable to hypoxia, stress, and undernutrition, all likely to be present in fetal intrauterine growth restriction (IUGR).
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The neurofibrillary-tangles (NTFs), characteristic of tauopathies including Alzheimer's-disease (AD), are the pathological features which correlate best with dementia.
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Glutamate is an essential neurotransmitter regulating brain functions.
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A dysregulated hypothalamic-pituitary-adrenal axis (HPA) has been implicated in major depressive disorder and most commonly used animal models of depression have been shown to elevate circulating levels of plasma corticosterone.
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Microglia are innate immune cells in the central nervous system.
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We describe two new transgenic mouse lines for studying pathological changes of Tau protein related to Alzheimer's disease.
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.
- A systems biology approach to Down syndrome: identification of Notch/Wnt dysregulation in a model of stem cells aging
- Functional screening of Alzheimer risk loci identifies PTK2B as an in vivo modulator and early marker of Tau pathology
- Effects of acute sleep loss on diurnal plasma dynamics of CNS health biomarkers in young men
- Overexpression of human apolipoprotein A-I preserves cognitive function and attenuates neuroinflammation and cerebral amyloid angiopathy in a mouse model of Alzheimer disease
- Phosphorylation of Ser-129 is the dominant pathological modification of alpha-synuclein in familial and sporadic Lewy body disease
- Soluble TREM2 ameliorates pathological phenotypes by modulating microglial functions in an Alzheimer's disease model
- Pharmacological modulation of cGAS-STING-NLRP3 signaling by nano-immunomodulators in Alzheimer and Parkinson disease
- An epigenetic signature in peripheral blood associated with the haplotype on 17q21.31, a risk factor for neurodegenerative tauopathy
- CSF Synaptic Biomarkers in AT(N)-Based Subgroups of Lewy Body Disease
- TREM2 Maintains Microglial Metabolic Fitness in Alzheimer's Disease