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 4,948 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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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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Previously, we found that amyloid beta-protein (Abeta)1-42 exhibits neurotoxicity, while Abeta1-40 serves as an antioxidant molecule by quenching metal ions and inhibiting metal-mediated oxygen radical generation.
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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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Studies in vitro have suggested that acetylcholinesterase (AChE) may interact with beta-amyloid to promote deposition of amyloid plaques in the brain of patients with Alzheimer's disease.
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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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Glial fibrillary acidic protein, GFAP, is a major intermediate filament protein of glial cells and major cytoskeletal structure in astrocytes.
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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.
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36/100
Within the brain, quinolinic acid (QUIN) is an important neurotoxin, especially in AIDS dementia complex (ADC).
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36/100
Proof that blood-brain barrier failure is key to these conditions could provide a target for new treatments to reduce the effects of vascular disease on the brain and prevent cognitive decline and dementia.
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Glutamate transport is central to neurotransmitter functions in the brain.
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The human immunodeficiency virus (HIV)-Tat protein has been implicated in the neuropathogenesis of HIV infection.
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Trisomy 21 (Down syndrome, DS) is the most common genetic cause of mental retardation, resulting from triplication of the whole or distal part of human chromosome 21.
Why it matters
This study found reduced levels of C21orf2 and CAF-1 p60 proteins in the brain of people with Down syndrome, but these proteins were comparable to controls in Alzheimer's disease. The findings challenge the simple gene dosage hypothesis and do not provide a treatment or prevention.
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These results suggest that alterations in amygdala:hippocampal volume ratios in pediatric MDD may more reflect severity of associated anxiety than depression.
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Schizophrenia is associated with structural deformities of the hippocampus, which suggest a disturbance of the connections between the hippocampus and the frontal cortex.
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The R406W tau mutation found in frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) causes a hereditary tauopathy clinically resembling Alzheimer's disease.
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Previous studies of Abeta-induced neuronal damage of hippocampal cells in culture have provided strong evidence that deregulation of the Cdk5/p35 kinase system is involved in the neurodegeneration pathway.
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Latent reservoirs of human immunodeficiency virus (HIV) present significant challenges for eradicating HIV from infected persons, particularly reservoirs in the brain established during acute infection.
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In recent years, oxidative stress has been implicated in a variety of degenerative processes, diseases, and syndromes.
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Our results replicate previous findings of reduced hippocampal volume in PTSD but also suggest independent, generalized, white matter atrophy.
From across this topic
10 of the 4,930 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.
- 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
- Increased CSF biomarkers of angiogenesis in Parkinson disease
- Activation of the CB2 receptor system reverses amyloid-induced memory deficiency
- Developmental neurobiology of childhood stress and trauma
- Amyloid-β pathology and APOE genotype modulate retinoid X receptor agonist activity in vivo
- NOTCH3 variants are more common than expected in the general population and associated with stroke and vascular dementia: an analysis of 200 000 participants