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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41/100
The secondary structures in solution of the synthetic, naturally occurring, amyloid beta peptides, residues 1 to 42 [beta (1-42)] and beta (1-39), and related fragments, beta (1-28) and beta (29-42), have been studied by circular dichroism and two-dimensional nuclear magnetic resonance spectroscopy.
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The amyloid beta peptide (A beta P) is a small fragment of the much larger, broadly distributed amyloid precursor protein (APP).
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41/100
The beta-amyloid protein (beta/A4), derived from a larger amyloid precursor protein (APP), is the principal component of senile plaques in Alzheimer's disease.
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Amyloid deposition in senile plaques and the cerebral vasculature is a marker of Alzheimer's disease.
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The clinical manifestations of AIDS (acquired immune deficiency syndrome) often include neuropsychiatric and neurological deficits, including early memory loss and progressive dementia.
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The formation of clusters of altered axons and dendrites surrounding extracellular deposits of amyloid filaments (neuritic plaques) is a major feature of the human brain in both aging and Alzheimer's disease.
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Both Alzheimer's disease and senile dementia of the Alzheimer type (AD/SDAT) are progressive dementias characterized neuropathologically by the presence in the cerebral cortex of numerous neurofibrillary tangles and neuritic plaques.
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Adult hippocampal neurogenesis declines with aging and in neurological disorders, leading to cognitive impairment.
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Brain derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase B (TrkB) play crucial roles in neuronal development, synaptic transmission, and neuroplasticity.
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40/100
Tau protein aggregation is a hallmark of neurodegenerative diseases, including Alzheimer's disease, making the development of anti-aggregation therapeutics a critical area of research.
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Alzheimer disease (AD) is the most common cause of dementia in older individuals.
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Therapeutics based on short interfering RNAs (siRNAs) delivered to hepatocytes have been approved, but new delivery solutions are needed to target additional organs.
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As the number of patients with Alzheimer's disease (AD) increases, it brings great suffering to their families and causes a heavy socioeconomic burden to society.
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Converging evidence continues to point towards Tau aggregation and pathology formation as central events in the pathogenesis of Alzheimer's disease and other Tauopathies.
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Tau immunotherapies have advanced from proof-of-concept studies to over a dozen clinical trials for Alzheimer's disease (AD) and other tauopathies.
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Tau has become an attractive alternative target for passive immunotherapy efforts for Alzheimer's disease (AD).
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Traumatic brain injury (TBI) is the largest non-genetic, non-aging related risk factor for Alzheimer's disease (AD).
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Butyrylcholinesterase (BChE) is an essential human cholinesterase relevant to liver conditions and neurodegenerative diseases, which makes it a pivotal biomarker of health.
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BACE1 (beta-site amyloid precursor protein cleaving enzyme 1) was initially cloned and characterized in 1999.
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Alzheimer's disease (AD) is a common, chronic expensive debilitating neurodegenerative disease with no current treatments to prevent the physical deterioration of the brain and the consequent cognitive deficits.
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Alzheimer's Disease (AD) is an age-related neurodegenerative disorder in which aggregation-prone neurotoxic amyloid β-peptide (Aβ) accumulates in the brain.
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The dismal success rate of clinical trials for Alzheimer's disease (AD) motivates us to develop model systems of AD pathology that have higher predictive validity.
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Mutations in the amyloid precursor protein (APP) gene and the aberrant cleavage of APP by γ-secretase are associated with Alzheimer's disease (AD).
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Parkinson's disease (PD) is characterized by the progressive appearance of intraneuronal Lewy aggregates, which are primarily composed of misfolded α-synuclein (α-syn).
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Down syndrome (DS) is one of the leading causes of intellectual disability, and patients with DS face various health issues, including learning and memory deficits, congenital heart disease, Alzheimer's disease (AD), leukemia, and cancer, leading to huge medical and social costs.
From across this topic
10 of the 1,352 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.
- Proteolytic α-Synuclein Cleavage in Health and Disease
- Neuronal uptake and neuroprotective effect of curcumin-loaded PLGA nanoparticles on the human SK-N-SH cell line
- GLT-1 loss accelerates cognitive deficit onset in an Alzheimer's disease animal model
- Fibrils formed in vitro from alpha-synuclein and two mutant forms linked to Parkinson's disease are typical amyloid
- Aβ induces astrocytic glutamate release, extrasynaptic NMDA receptor activation, and synaptic loss
- Patient-Derived PSEN1 Cerebral Organoids Revealed Parallel Development of Amyloid-β Accumulation and Network Dysfunction
- Transient sleep apnea results in long-lasting increase in β-amyloid generation and tau hyperphosphorylation
- beta-Amyloid precursor protein-deficient mice show reactive gliosis and decreased locomotor activity
- Increased H-Bond Stability Relates to Altered ε-Cleavage Efficiency and Aβ Levels in the I45T Familial Alzheimer's Disease Mutant of APP
- Complement C3 Is Activated in Human AD Brain and Is Required for Neurodegeneration in Mouse Models of Amyloidosis and Tauopathy