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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Diseases of the central nervous system (CNS) pose a significant health challenge, but despite their diversity, they share many common features and mechanisms.
Why it matters
This review describes how endothelial dysfunction and breakdown of the blood-brain barrier are early events in several central nervous system disorders, including Alzheimer's disease. It reports no new treatment, cure or prevention and is a summary of existing evidence.
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Parkinson's disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA) are adult onset neurodegenerative disorders characterised by prominent intracellular α-synuclein aggregates (α-synucleinopathies).
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Changes of the microtubule-associated protein tau are central in Alzheimer's disease (AD) and frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17).
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Recent neuroimaging studies proposed the importance of the anterior auditory pathway for speech comprehension.
Why it matters
Direct electrical cortical stimulation in two epilepsy patients identified a language area in the left anterior temporal cortex involved in auditory sentence comprehension. This is a small anatomical study about speech perception, not about treating, curing or preventing Alzheimer's disease.
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Synaptic loss is the best pathological correlate of the cognitive decline in Alzheimer's disease; however, the molecular mechanisms underlying synaptic failure are unknown.
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Alzheimer's disease (AD) is characterized by the extracellular deposition of β-amyloid in senile plaques, the intraneuronal accumulation of hyperphosphorylated tau aggregates as neurofibrillary tangles, and progressive neuronal loss leading to the onset of dementia.
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Nasu-Hakola disease (NHD) was first reported separately by Nasu and Hakola around the same time in the 1970s. It is an autosomal recessive inherited disorder characterized by progressive dementia and repeated pathological fractures during adolescence.
Why it matters
This paper reviews Nasu-Hakola disease, which is caused by mutations in TREM2 or DAP12 and features progressive dementia. It is a case report and review, not a study of Alzheimer's treatment or prevention.
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Melatonin is mainly produced in the mammalian pineal gland during the dark phase.
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Diabetic encephalopathies are now accepted complications of diabetes.
Why it matters
This review discusses how type 2 diabetes, with insulin resistance and high blood sugar, is linked to higher rates of Alzheimer disease, while type 1 diabetes more often causes different cognitive problems. It is based on epidemiological and experimental data and does not test a treatment.
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Neurogenesis in the hippocampus occurs throughout life in a wide range of species and could be associated with hippocampus-dependent learning and memory.
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40/100
Selective loss of neurons, abnormal protein deposition and neuroinflammation are the common pathological features of neurodegenerative diseases, and these features are closely related to one another.
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TDP-43 is characteristically accumulated in TDP-43 proteinopathies such as frontotemporal lobar degeneration and motor neurone disease, but is also present in some tauopathies, including Alzheimer's disease, argyrophilic grain disease, and corticobasal degeneration (CBD).
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Tauopathies are neurodegenerative diseases, sporadic or familial, mainly characterized by dementia and parkinsonism associated to atrophy of the frontotemporal cortex and the basal ganglia, with deposition of abnormal tau in brain.
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Delirium is an acute, severe neuropsychiatric syndrome, characterized by cognitive deficits, that is highly prevalent in aging and dementia and is frequently precipitated by peripheral infections.
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Neurodegenerative pathologies associated with aging exhibit clinical and morphological features that are relatively specific to humans.
Why it matters
This study compared microRNA expression in the aging brains of humans, chimpanzees and macaques, and found that miR-144 is linked to aging and regulates the gene that causes spinocerebellar ataxia type 1. In cells, blocking miR-144 and miR-101 raised ATXN1 levels, suggesting that miRNA activity in the aging brain may help reduce the toxic effects of this protein, though this is early laboratory work.
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40/100
These data suggest that low-grade inflammation as assessed by high-sensitivity C-reactive protein is associated with cerebral microstructural disintegration that predominantly affects frontal pathways and corresponding executive function.
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Endocytic alterations are one of the earliest changes to occur in Alzheimer's disease (AD), and are hypothesized to be involved in the selective vulnerability of specific neuronal populations during the progression of AD.
Why it matters
This study found that the proteins rab5 and rab7 were elevated in certain brain regions of people with mild cognitive impairment and Alzheimer's disease. The findings describe a biological change associated with disease progression but do not test any treatment or prevention.
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The white matter (WM) of the adult human neocortex contains the so-called "interstitial neurons".
Why it matters
This paper describes interstitial neurons in the white matter of the adult human cortex and notes their heterogeneity may be relevant to Alzheimer's disease. It is a descriptive anatomy paper with no experiments on Alzheimer's, so it offers no direct implications for treating, curing or preventing the disease.
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Hyperhomocysteinemia and beta-amyloid (Abeta) overproduction are critical etiological and pathological factors in Alzheimer disease, respectively; however, the intrinsic link between them is still missing.
Why it matters
In rats, high homocysteine raised amyloid-beta levels and increased presenilin-1, part of gamma-secretase. This is an animal finding about a possible mechanism and does not show that lowering homocysteine treats or prevents Alzheimer's disease in people.
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Our data shows that early environment has a critical influence on establishing sex differences in neural plasticity and supports the concept that the setpoint for neurogenesis may be determined during perinatal life.
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40/100
Our results demonstrate that prenatal inflammation is sufficient to induce synaptic alterations with delay.
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Elevated plasma lipopolysaccharide (LPS), an indicator of microbial translocation from the gut, is a likely cause of systemic immune activation in chronic HIV infection.
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This is the first study to show aberrant regulation of the protein synthesis machinery in the suicide brain.
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There is a high incidence on Guam of a severe tauopathy known as the Parkinson- dementia complex (PDC).
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Most psychiatric disorders are associated with increased oxidative stress.
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 lexical semantic hub for heteromodal naming in middle fusiform gyrus
- Astrocytic α2-Na+/K+ ATPase inhibition suppresses astrocyte reactivity and reduces neurodegeneration in a tauopathy mouse model
- Utilization of P2Y12 Inhibitors in Older Adults With ST-Elevation Myocardial Infarction and Frailty
- Characterizing the distinct neuroanatomical phenotypes, cognitive profiles, and transcriptomic signatures of brain structural subtypes in Parkinson's disease with mild cognitive impairment
- ATG5 (autophagy related 5) in microglia controls hippocampal neurogenesis in Alzheimer disease
- Association of Plasma Phosphorylated Tau With the Response to Neflamapimod Treatment in Patients With Dementia With Lewy Bodies
- TREM2 and β-catenin regulate bone homeostasis by controlling the rate of osteoclastogenesis
- Adaptation of a Protocol for Disclosure of Amyloid PET Results for Adults with Down Syndrome and Their Caregivers
- Neural stem cells improve cognition via BDNF in a transgenic model of Alzheimer disease
- Reactive microglia are positive for HLA-DR in the substantia nigra of Parkinson's and Alzheimer's disease brains