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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Corticobasal degeneration (CBD) is an adult-onset progressive neurodegenerative disorder characterized by L-dopa-resistant rigidity, focal cortical deficits, and variable dementia.
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Estrogen reduces the risk of Alzheimer's disease in post-menopausal women, beta-amyloid (Abeta) burden in animal models of Alzheimer's disease, and secretion of Abeta from neuronal cultures.
Why it matters
In cell-free systems from neuroblastoma cells and primary neurons, 17beta-estradiol stimulated formation of vesicles containing beta-amyloid precursor protein from the trans-Golgi network, which precluded maximal amyloid-beta generation there. This is laboratory cell work and does not establish that estrogen prevents or treats Alzheimer disease.
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The presence of a single APOE-epsilon4 allele is associated with an increased rate of hippocampal volume loss in healthy women in their sixth decade of life that is not related to any detectable memory changes.
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In major depression, decreased hippocampal volume has been attributed to hypercortisolemia, a frequent sign of the disorder, because in animals an excess of corticosteroids has led to dendritic atrophy, astrogliosis and loss of neurons in this brain region.
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The enzyme argininosuccinate synthetase (ASS) is the rate limiting enzyme in the metabolic pathway leading from L-citrulline to L-arginine, the physiological substrate of all isoforms of nitric oxide synthases (NOS).
Why it matters
In brain tissue from people who had died with Alzheimer's disease, neurons and glial cells showed increased levels of the enzyme ASS alongside increased iNOS. This is a tissue observation about inflammation-related enzymes and does not test any treatment, cure, or prevention.
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Chemokines are a family of proteins associated with the trafficking of leukocytes in physiological immune surveillance and inflammatory cell recruitment in host defence.
Why it matters
This review describes chemokines and their receptors in the central nervous system, where they are expressed by microglia, astrocytes and neurons. It is basic biology and reports no treatment, cure or prevention for Alzheimer's disease.
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To elucidate the mechanisms involved in beta-amyloid-mediated inflammation in Alzheimer's disease, transgenic Tg2576 mice containing as transgene the Swedish double mutation of human amyloid precursor protein 695, were examined for the expression pattern of various cytokines using double immunocytochemistry and laser scanning microscopy.
Why it matters
In aged transgenic Tg2576 mice with Alzheimer plaque pathology, beta-amyloid was associated with glial expression of both pro- and anti-inflammatory cytokines. This is animal research and does not test a treatment or show a benefit for patients.
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43/100
Immunohistochemical analysis of brains of patients with Alzheimer disease (AD) revealed that the cysteine proteinase inhibitor cystatin C colocalizes with amyloid beta-protein (Abeta) in parenchymal and vascular amyloid deposits.
Why it matters
This study found that cystatin C colocalizes with amyloid beta in parenchymal and vascular amyloid deposits in Alzheimer's brains and in transgenic mice, with no cerebral hemorrhage seen. It describes a protein found alongside amyloid and reports no treatment, cure or prevention.
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This study compared a fornix cross-sectional-area measurement and hippocampal volume in 86 traumatic brain injury (TBI) subjects with 46 normal controls.
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The authors tried to know specificity of aging in persons with Down syndrome (DS) from the aspect of electroencephalograph (EEG) frequency changes through the cross-sectional and longitudinal studies, in comparison with normal persons as well as those with mentally retardation except the Down syndrome (non-DS MR).
Why it matters
This cross-sectional and follow-up EEG study found that slowing of the basic brain rhythm began earlier in people with Down syndrome than in people with other intellectual disability. It describes a measure of aging in the brain and does not test any treatment, cure, or prevention.
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Deposition of beta-amyloid (A beta), a metabolite of approximately 4 kd of the amyloid precursor protein, is a critical pathological feature in Alzheimer disease.
Why it matters
This review proposes that the low-density lipoprotein receptor-related protein (LRP) helps clear beta-amyloid and that problems with this clearance could contribute to Alzheimer disease. It is a hypothesis based on existing data, not a test of any treatment, so it does not show that targeting LRP helps patients.
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43/100
Changes in human HFV associated with sustained hypercortisolemia are reversible, at least in part, once cortisol levels decrease.
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Despite these good results in the CAPIT scores, one patient experienced a partially regressive corticobulbar syndrome with dysphagia, dysarthria, and increased drooling.
Why it matters
This report of four cases found that bilateral simultaneous pallidotomy for Parkinson's disease can cause emotional, behavioral, and cognitive deficits as well as disabling swallowing and speech problems. It concludes this surgery is undesirable, and it does not address treating, curing, or preventing Alzheimer's disease.
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43/100
Hippocampal volume, while disproportionately small for brain size in individuals with Down's syndrome, remains fairly constant through the fifth decade of life in those without dementia.
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Alzheimer's disease (AD) is the commonest form of adult onset dementia and is characterised neuropathologically by the accumulation of plaques containing beta-amyloid (A beta) fibrils, reactive astrocytes, activated microglia, and leukocytes.
Why it matters
In laboratory experiments, beta-amyloid activated astrocytes and oligodendrocytes to produce chemokines that attract microglia and macrophages. This is early cell research and does not show any treatment or prevention for Alzheimer's disease.
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43/100
Recent studies have shown that deficient functioning of glutamate transporters (GTs) in Alzheimer disease (AD) might lead to neurodegeneration via excitotoxicity; however, the characteristics of cell death and pathways involved are not yet clear.
Why it matters
This study examined whether poor glutamate transporter function in Alzheimer's disease is linked to cell damage and activation of caspase enzymes. It reports an association between these processes, but the work is descriptive and does not test any treatment or show that blocking caspases would help patients.
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Measurement of regional abnormalities of HT2 along the length of the hippocampus provides further refinement to the MRI assessment of the hippocampi in patients with temporal lobe epilepsy and is complementary to volumetric and morphological data.
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The amygdala is a key structure in the brain's integration of emotional meaning with perception and experience.
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43/100
The clbC form of methylmalonic acidaemia is a rare and poorly understood condition which results from impaired biosynthesis of methylcobalamin and adenosylcobalamin.
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The pathogenesis of HIV-associated cognitive changes is poorly understood.
Why it matters
In brain tissue from 12 people with AIDS, 8 of whom had dementia, compared with 6 controls, cells producing the inflammatory molecule TNF-alpha became more numerous as cognitive impairment worsened, in parallel with astrocyte activation (astrogliosis). The authors say this supports the idea that TNF-alpha-driven white matter damage and widespread immune activation contribute to HIV-associated dementia. The work concerns HIV-related dementia rather than Alzheimer's.
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HIV-1 invades the central nervous system early during viral infection, but neurologic impairment usually occurs years later.
Why it matters
This laboratory study built an artificial blood-brain barrier model to study how monocytes migrate into the brain during HIV-1 encephalitis, a condition different from Alzheimer's disease. It does not provide evidence about treating, curing, or preventing Alzheimer's disease.
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We have previously reported smaller hippocampal volume and deficits in short-term memory in patients with combat-related posttraumatic stress disorder (PTSD) relative to comparison subjects.
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A 62-year-old right-handed man gradually experienced increasing difficulty with speech and manual dexterity.
Why it matters
This clinicopathologic report describes a man with apraxia of speech, buccofacial apraxia and complex limb apraxia who developed terminal dementia, with Pick bodies found diffusely in the temporal and posterior frontal lobes and, to a lesser degree, in the superior parietal lobule. It is a single case report linking the distribution of Pick's pathology to apraxic impairments and reports no treatment, cure or prevention.
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Two chemokine (chemoattractant cytokines) beta peptides, macrophage inflammatory proteins 1 alpha and 1 beta (MIP-1 alpha and MIP-1 beta), were induced in human monocyte cultures following infection with the human immunodeficiency virus type 1 (HIV-1).
Why it matters
This study found that HIV-1 infection of human monocytes in culture induced chemokine beta peptides and changed their response to TNF. It concerns HIV and immune cell behavior, not Alzheimer's disease, so it has no direct implications for treating, curing or preventing Alzheimer's.
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Senile plaques found in the brains of patients with Alzheimer's disease (AD) are surrounded by clusters of reactive microglia.
Why it matters
This laboratory study found that isolated human microglia in contact with senile plaques released a neurotoxin also found in Alzheimer's brain tissue, and that infusing it into rat hippocampus damaged neurons. It is early experimental work and does not test any treatment, cure or prevention for Alzheimer's disease in people.
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.
- Transfer of beta-amyloid precursor protein gene using adenovirus vector causes mitochondrial abnormalities in cultured normal human muscle
- ESO Guideline on covert cerebral small vessel disease
- Insulin receptor dysfunction impairs cellular clearance of neurotoxic oligomeric a{beta}
- Alzheimer-mutant γ-secretase complexes stall amyloid β-peptide production
- Phylogenetic diversity of the expression of the microtubule-associated protein tau: implications for neurodegenerative disorders
- Hypocretin and brain β-amyloid peptide interactions in cognitive disorders and narcolepsy
- Sympathetic and parasympathetic subtypes of body-first Lewy body disease observed in postmortem tissue from prediagnostic individuals
- High expression on Kunitz-type protease inhibitor-containing substances in the cerebral vessels of patients with Down syndrome
- Direct Comparison of the Tau PET Tracers 18F-Flortaucipir and 18F-MK-6240 in Human Subjects
- Parkinson risk in idiopathic REM sleep behavior disorder: preparing for neuroprotective trials