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 4,766 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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With increased life expectancy worldwide, there is an urgent need for improving preventive measures that delay the development of age-related degenerative diseases.
Why it matters
This study reports evidence from mouse and human studies that maintaining optimal hydration throughout life may delay age-related degenerative diseases. It found that restricting drinking water shortened mouse lifespan and caused metabolic and inflammatory changes.
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38/100
Tau inclusions are a shared feature of many neurodegenerative diseases, among them frontotemporal dementia caused by tau mutations.
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Accumulation of abnormal tau in neurofibrillary tangles (NFT) occurs in Alzheimer disease (AD) and a spectrum of tauopathies.
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Small vessel diseases (SVDs) are a group of disorders that result from pathological alteration of the small blood vessels in the brain, including the small arteries, capillaries and veins.
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Impaired glucose metabolism, decreased levels of thiamine and its phosphate esters, and reduced activity of thiamine-dependent enzymes, such as pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase and transketolase occur in Alzheimer's disease (AD).
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Though emerging evidence indicates that the pathogenesis of Parkinson's disease is strongly correlated to the accumulation 1,2 and transmission 3,4 of α-synuclein (α-syn) aggregates in the midbrain, no anti-aggregation agents have been successful at treating the disease in the clinic.
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Dementia is a major social and economic problem for our aging population.
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Dysfunction of the autonomic nervous system afflicts most patients with Parkinson disease and other synucleinopathies such as dementia with Lewy bodies, multiple system atrophy, and pure autonomic failure, reducing quality of life and increasing mortality.
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AAV-mediated progranulin delivery reduced lipofuscinosis in Grn -/- mice even after the onset of pathology.
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Chronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy associated with repetitive head trauma, including concussion and subconcussion.
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The accumulation of aberrantly aggregated MAPT (microtubule-associated protein Tau) defines a spectrum of tauopathies, including Alzheimer's disease.
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The monoamine hypothesis has been accepted as the most common hypothesis of major depressive disorder (MDD) for a long period because of its simplicity and understandability.
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Type 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer disease (AD).
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Aggregates of the microtubule-associated protein tau are a defining feature of several neurodegenerative diseases that are collectively known as tauopathies, and constitute one of the hallmark lesions of Alzheimer disease (AD).
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Lipocalin-2 (LCN2) has diverse functions in multiple pathophysiological conditions; however, its pathogenic role in vascular dementia (VaD) is unknown.
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Hyperexcitable neuronal networks are mechanistically linked to the pathologic and clinical features of Alzheimer's disease (AD).
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Our observations suggest functional tau disturbance in DS brains during development, rather than axonal loss.
Why it matters
This brain tissue study found that the normal phosphorylation of the tau protein was critically changed in fetal Down syndrome brains, suggesting tau problems begin early in development. The findings are from tissue analysis and suggest tau may play a role in cognitive impairment in Down syndrome and related Alzheimer's disease, but no treatment was tested.
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The findings suggest that adult neurogenesis is required to maintain hippocampal volume but is not responsible for stress-induced volume loss.
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In Alzheimer's disease (AD), insoluble and fibrillary amyloid-β (Aβ) peptide accumulates in plaques.
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Tau is a microtubule-associated protein that functions in regulating cytoskeleton dynamics, especially in neurons.
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Histone deacetylase 2 (HDAC2) plays a major role in the epigenetic regulation of gene expression.
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Psychosocial stress and physical, cognitive, and social activity predict the risk of cognitive decline and dementia.
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Accumulation of hyperphosphorylated tau directly correlates with cognitive decline in Alzheimer's disease and other primary tauopathies.
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Here, we show that the dendrite lengths and spine densities are reduced significantly in hippocampal CA1 pyramidal neurons, but increased in spinal neurokinin-1-positive neurons in mice after SNI, indicating that the excitatory synaptic connectivity is reduced in hippocampus but enhanced in spinal dorsal horn in this neuropathic pain model.
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Progressive supranuclear palsy is associated with an elevated [ 18 F]AV-1451 signal in a characteristic and distinct regional pattern that correlates with disease severity and differs from the patterns observed in Alzheimer's dementia. © 2016 International Parkinson and Movement Disorder Society.
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.
- Downregulation of TREM2 expression exacerbates neuroinflammatory responses through TLR4-mediated MAPK signaling pathway in a transgenic mouse model of Alzheimer's disease
- Novel monoclonal antibody 3B8 specifically recognizes pyroglutamate-modified amyloid β 3-42 peptide in brain of AD patients and 3xTg-AD transgenic mice
- Presynaptic alpha-synuclein aggregates, not Lewy bodies, cause neurodegeneration in dementia with Lewy bodies
- Molecular mechanisms of cognitive dysfunction following traumatic brain injury
- Evaluation of a Sensitive Visual Read Algorithm for Assessing 3R/4R Tau PET Images
- Microtubule-associated protein tau. A component of Alzheimer paired helical filaments.
- Modification of the relationship of the apolipoprotein E ε4 allele to the risk of Alzheimer disease and neurofibrillary tangle density by sleep
- Regional selectivity of rab5 and rab7 protein upregulation in mild cognitive impairment and Alzheimer's disease
- Phenotypic and biochemical analyses of BACE1- and BACE2-deficient mice
- Factors regulating microglia activation