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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HIV-1 Nef is expressed in astrocytes, but a contribution to neuropathogenesis and the development of HIV-associated dementia (HAD) remains uncertain.
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Neurofibrillary tangles (NFTs) are a pathological hallmark of many neurodegenerative diseases including Alzheimer's disease (AD), Parkinson's disease (PD), and frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP17).
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Neurofibrillary tangles (NFTs), which are composed of hyperphosphorylated and ubiquitylated tau, are exhibited at regions where neuronal loss occurs in neurodegenerative diseases; however, the mechanisms of NFT formation remain unknown.
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36/100
Alzheimer's disease (AD) is characterized histopathologically by beta-amyloid-containing plaques, neurofibrillary tangles (NFT), reduced synaptic density, and neuronal loss in selected brain areas.
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Our results are consistent with previous findings of structural abnormalities of amygdala and hippocampus in subjects with recent-onset major depression.
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L-Glutamate serves as a major excitatory neurotransmitter in the mammalian central nervous system (CNS) and is stored in synaptic vesicles by an uptake system that is dependent on the proton electrochemical gradient (VGLUTs).
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36/100
Intracellular accumulations of filamentous tau inclusions are neuropathological hallmarks of neurodegenerative diseases known as tauopathies.
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In the dentate gyrus of the hippocampus, cell birth and maturation into neurons, or neurogenesis, occur throughout the lifetime of animals and humans.
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36/100
Mitochondriopathies (MCPs) are either due to sporadic or inherited mutations in nuclear or mitochondrial DNA located genes (primary MCPs), or due to exogenous factors (secondary MCPs).
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Aberrant mitosis occurs in many tauopathy-related neurodegenerative diseases and is believed to precede the formation of neurofibrillary tangles.
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Animal studies on the effects of chronic variable stress during the peripubertal-juvenile period on hippocampal structure and function are lacking.
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Acute stress suppresses new cell birth in the hippocampus in several species.
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Hypoxia damages multiple organ systems especially those with high oxygen utilization such as the central nervous system.
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Excitotoxicity, defined as excessive exposure to the neurotransmitter glutamate or overstimulation of its membrane receptors, has been implicated as one of the key factors contributing to neuronal injury and death in a wide range of both acute and chronic neurologic disorders.
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In Alzheimer's disease and related disorders, the microtubule-associated protein Tau is abnormally hyperphosphorylated and aggregated into neurofibrillary tangles.
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These findings indicate that the prenatal environment can alter behavior, dysregulate neuroendocrine systems, and affect the hippocampal structure of primates in a persistent manner.
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Astrocytes are the most numerous cell type in the brain, and their physiological roles are essential for normal brain function.
Why it matters
Post-mortem brain tissue from people with AIDS showed that a small proportion of astrocytes were infected by HIV-1, which is linked to HIV-associated dementia. Astrocyte infection in the body is generally non-productive and only detectable with sensitive tests, so its role in causing dementia remains unclear.
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The receptor for advanced glycation end products (RAGE) is known to be causally involved in a variety of pathophysiological processes, e.g. immune/inflammatory disorders, Alzheimer disease, tumors, and abnormalities associated with diabetes as arteriosclerosis or disordered wound healing.
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Neurodegeneration, synaptic alterations, and gliosis are prominent features of human immunodeficiency virus (HIV) encephalitis, but HIV encephalitis is distinct from other viral encephalitides because neurodegeneration occurs in uninfected neurons at anatomical sites that are often distant from the site of viral replication.
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36/100
Frontotemporal dementia with parkinsonism chromosome 17 type (FTDP-17) is caused by mutations in MAPT, the gene encoding tau.
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MRI studies using the manual tracing method have shown a smaller-than-normal hippocampal volume in patients with posttraumatic stress disorder (PTSD).
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Patients with Parkinson's disease (PD) may have hippocampal atrophy compared with controls.
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Plasma amyloid beta protein 1-40 (Abeta40) and Abeta42 levels were quantitated from 28 young Down syndrome (DS) (20-40 years old), 28 age-matched controls, 32 old DS (41-65 years old) and 32 age-matched controls in a sandwich enzyme-linked immunosorbent assay.
Why it matters
This study found that plasma amyloid beta 42 levels are higher in older people with Down syndrome than in controls or younger people with Down syndrome. It suggests this increase happens alongside Alzheimer disease neuropathology, but it does not show that measuring or lowering this protein treats or prevents the disease.
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These results are consistent with deficits in hippocampal function and structure in abuse-related PTSD.
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36/100
We immunohistochemically studied the expression of beta-amyloid precursor protein (APP), Abeta40, Abeta42, and Abeta43 in the frontal lobes of 20 Down syndrome (DS) patients and 13 controls.
Why it matters
This study describes the order in which different amyloid beta proteins appear in the brains of people with Down syndrome, with Abeta43 and 42 appearing in diffuse plaques from age 32. It suggests a time course related to Alzheimer-type dementia, but it does not test any treatment or cure.
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.
- TREM2 macrophage promotes cardiac repair in myocardial infarction by reprogramming metabolism via SLC25A53
- Glymphatic System Impairment in Alzheimer's Disease and Idiopathic Normal Pressure Hydrocephalus
- Cell type- and tau lesion-specific accumulation of phospho-Ser65 ubiquitin in primary tauopathies
- Increased expression of TREM2 in peripheral blood of Alzheimer's disease patients
- Cerebral white matter changes in acquired immunodeficiency syndrome dementia: alterations of the blood-brain barrier
- Differential role of C-terminal truncations on alpha-synuclein pathology and Lewy body formation
- Diffusible, nonfibrillar ligands derived from Aβ 1–42 are potent central nervous system neurotoxins
- Multi-organ distribution of phosphorylated alpha-synuclein histopathology in subjects with Lewy body disorders
- A proteomic network approach across the ALS-FTD disease spectrum resolves clinical phenotypes and genetic vulnerability in human brain
- Prior activation state shapes the microglia response to antihuman TREM2 in a mouse model of Alzheimer's disease