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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Higher cognitive inhibitory and attention functions have been shown to develop throughout adolescence, presumably concurrent with anatomical brain maturational changes.
Why it matters
This brain imaging study found that adults showed more activation than children in frontostriatal networks during tasks of cognitive control. It concerns normal cognitive development and does not address treating, curing or preventing Alzheimer's disease.
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These CSF A beta 42 findings are consistent with acceleration by the APOE*4 allele of pathogenic A beta 42 brain deposition starting in later middle age in persons with normal cognition.
Why it matters
Among 184 people with normal cognition aged 21 to 88, levels of beta-amyloid 42 in spinal fluid fell with age, with a sharp drop starting in the sixth decade in those carrying the APOE4 allele. This suggests that amyloid plaque deposition in the brain begins years before dementia symptoms appear, and that APOE4 speeds this process.
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Recently, we have shown that green tea polyphenol (-)-epigallocatechin-3-gallate (EGCG) exerts a beneficial role on reducing brain Abeta levels, resulting in mitigation of cerebral amyloidosis in a mouse model of Alzheimer disease.
Why it matters
This laboratory study found that green tea compound EGCG increased alpha-secretase cleavage of amyloid precursor protein, with no significant change in beta- or gamma-secretase activity. It is cell-based mechanistic work and does not show that EGCG treats or prevents Alzheimer's disease in people.
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Neurofibrillary degeneration in the nucleus basalis and a loss of its cortical cholinergic projections are prominent components of the neuropathology in Alzheimer's disease (AD).
Why it matters
This study examined tissue from a small number of cognitively normal controls and subjects with mild cognitive impairment or early Alzheimer's disease to see whether the locus coeruleus shows neurofibrillary abnormalities early. It is a small tissue study of disease processes, not a treatment, cure, or prevention study.
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Dysfunction of cholinergic basal forebrain (CBF) neurons of the nucleus basalis (NB) is a cardinal feature of Alzheimer's disease (AD) and correlates with cognitive decline.
Why it matters
In single cholinergic basal forebrain neurons, expression of trkA, trkB and trkC was significantly reduced during progression of Alzheimer's disease, with an intermediate reduction in mild cognitive impairment, while p75(NTR) expression was not regulated. The authors suggest trk defects may be a molecular marker for the transition from no cognitive impairment to mild cognitive impairment and from mild cognitive impairment to Alzheimer's disease, but this is not a treatment finding.
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The results demonstrate that functional connectivity can be an effective marker for the detection of changes in brain function in MCI subjects.
Why it matters
This study found that measuring functional connectivity in the fusiform gyrus can detect changes in brain function in people with mild cognitive impairment. It is about a possible diagnostic marker, not about treating, curing, or preventing Alzheimer's disease.
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The clinical, laboratory, and radiologic findings associated with SREAT are more varied than previously reported.
Why it matters
This review of 20 patients describes a treatable encephalopathy tied to autoimmune thyroiditis that is often misdiagnosed, including as degenerative dementia. Recognizing it matters because it is treatable, but this is a small retrospective case series, not a study of Alzheimer's disease itself.
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Locus ceruleus (LC) degeneration and loss of cortical noradrenergic innervation occur early in Alzheimer's disease (AD).
Why it matters
In APP23 transgenic mice, damaging the locus ceruleus led six months later to more glial inflammation, more amyloid plaques, and greater neurodegeneration and neuronal loss. This is animal evidence that locus ceruleus degeneration may contribute to Alzheimer's progression, not a proven treatment for people.
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IL-6 levels were negatively associated with performance on the MMSE in this multiethnic cohort.
Why it matters
This cross-sectional study found that higher interleukin-6 levels were associated with lower Mini Mental State Exam scores in a multiethnic cohort. It is observational and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Trafficking and proteolytic processing of amyloid precursor protein (APP) have been the focus of numerous investigations in the past two decades, since the identification of Abeta as the principal component of brain senile plaques and the cloning of APP cDNA.
Why it matters
This is a review of how amyloid precursor protein is trafficked and cut inside cells to make amyloid beta, the main component of senile plaques. It summarizes knowledge about the beta- and gamma-secretases involved, but reports no treatment, cure or prevention.
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Encephalitis and dementia associated with acquired immunodeficiency syndrome (AIDS) are characterized by leukocyte infiltration into the CNS, microglia activation, aberrant chemokine expression, blood-brain barrier (BBB) disruption, and eventual loss of neurons.
Why it matters
This laboratory study shows that HIV-infected leukocytes move more readily across a tissue culture model of the human blood-brain barrier in response to CCL2 and disrupt that barrier. It concerns HIV-related brain disease, not Alzheimer's disease, and reports no Alzheimer's treatment or prevention finding.
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The majority of clinical trials of N-methyl d-aspartate antagonists have been conducted in the fields of stroke, traumatic brain injury (TBI) and dementia.
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The human G-protein-coupled formyl peptide receptor-like 1 (FPRL1) and its mouse homologue mFPR2 mediate the chemotactic activity of a variety of polypeptides associated with inflammation and bacterial infection, including the 42-amino acid form of amyloid beta peptide (Abeta42), a pathogenic factor in Alzheimer disease.
Why it matters
In mouse microglial cells, activating Toll-like receptor 2 increased a receptor that promotes uptake of amyloid beta peptide. This is cell-based laboratory work, so it is early and does not establish a therapy for Alzheimer's disease.
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47/100
ABCA1 (ATP-binding cassette transporter A1) is a major regulator of cholesterol efflux and high density lipoprotein (HDL) metabolism.
Why it matters
In this mouse study, targeted disruption of ABCA1 increased amyloid deposition in APP23 mice, increased cerebral amyloid angiopathy and related microhemorrhage, and dramatically decreased the level of soluble brain apoE. This is animal work describing how loss of ABCA1 affects amyloid, and it does not show that any treatment, cure, or prevention works in people.
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Inflammatory processes may be involved in the pathogenesis of cerebral small-vessel disease, in particular, the development of white matter lesions.
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47/100
Magnetic resonance (MR) imaging studies have identified hippocampal structural alterations in the pathogenesis of schizophrenia.
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Apolipoprotein E (apoE), a chaperone for the amyloid beta (Abeta) peptide, regulates the deposition and structure of Abeta that deposits in the brain in Alzheimer disease (AD).
Why it matters
In mice, the low density lipoprotein receptor regulated levels of apolipoprotein E in the brain and cerebrospinal fluid, but lacking this receptor did not significantly change brain amyloid-beta levels or plaque pathology in the PDAPP mouse model. This animal work clarifies how apoE is regulated but does not show a way to treat or prevent Alzheimer's disease.
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A glia-mediated, inflammatory immune response is an important component of the neuropathophysiology of Alzheimer's disease, of the midlife neurodegeneration of Down's syndrome, and of other age-related neurodegenerative conditions.
Why it matters
This review discusses how glial cells and their cytokines contribute to inflammation in Alzheimer's disease and other neurodegenerative conditions. It describes a possible role for inflammation in disease progression but does not test any treatment.
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Recent evidence suggests that statin use may be associated with a decreased risk for Alzheimer disease, although the mechanisms underlying this apparent risk reduction are poorly understood.
Why it matters
This laboratory work indicates statins can activate alpha-secretase-type shedding of sAPPalpha, with ROCK modulating this effect. It is cell-based research and does not show that statins treat, cure, or prevent Alzheimer's disease.
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A generally similar pattern of cerebral hypometabolism was detected in APOE epsilon4-positive and -negative patients with Alzheimer disease.
Why it matters
In 83 people with Alzheimer's disease matched for age, disease duration and cognitive impairment, brain glucose metabolism was reduced in similar regions in APOE4 carriers and non-carriers. Carriers showed stronger abnormalities in some cortical regions, but this imaging study does not test any treatment or prevention.
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Anti-Abeta immunotherapy in transgenic mice reduces both diffuse and compact amyloid deposits, improves memory function and clears early-stage phospho-tau aggregates.
Why it matters
In aged APP-transgenic mice, anti-Abeta antibody treatment reversed cognitive deficits and reduced parenchymal amyloid deposits but increased vascular amyloid and microhemorrhage. This is an animal study, and the findings do not establish a safe or effective treatment, cure, or prevention for people.
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Several proteins are expressed in both immune and nervous systems.
Why it matters
Mice lacking KARAP/DAP12, a protein linked in humans to a rare presenile dementia, showed impaired synaptic function. This is animal and genetic work on a different condition, so it does not provide a treatment or prevention for Alzheimer's disease.
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Degeneration of cholinergic nucleus basalis (NB) cortical projection neurons is associated with cognitive decline in late-stage Alzheimer's disease (AD).
Why it matters
Cortical TrkA levels were reduced by about 50% in mild/moderate and severe Alzheimer's disease compared with no cognitive impairment and mild cognitive impairment, while p75(NTR) levels were stable across groups. The authors say this selective reduction may have important consequences for cholinergic nucleus basalis function during the transition from mild cognitive impairment to Alzheimer's disease.
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Accumulation of amyloid beta-peptide (Abeta) in the central nervous system (CNS) may initiate pathogenic cascades mediating neurovascular and neuronal dysfunctions associated with the development of cerebral beta-amyloidosis and cognitive decline in patients with Alzheimer disease (AD) and with related familial cerebrovascular disorders.
Why it matters
This review summarizes evidence that the receptors RAGE and LRP1 at the blood-brain barrier control amyloid-β levels in the brain, and that altered activity of these two receptors may contribute to amyloid-β accumulation. It is a summary of evidence rather than a clinical trial, and it does not establish that targeting these receptors reverses disease in people.
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To better understand the pathogenesis of brain dysfunction in Gaucher disease (GD), we studied brain pathology in seven subjects with type 1 GD (four also exhibited parkinsonism and dementia), three with type 2 GD and four with type 3 GD.
Why it matters
This brain pathology study in people with Gaucher disease found specific patterns of neuronal loss and astrogliosis and argued for a common cytotoxic mechanism linking glucocerebrosidase activity, neuronal damage and Lewy body formation. It describes disease mechanisms, not a treatment, cure or prevention for Alzheimer's disease.
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.
- Curcumin inhibits LPS-induced neuroinflammation by promoting microglial M2 polarization via TREM2/ TLR4/ NF-κB pathways in BV2 cells
- TREM2 is associated with increased risk for Alzheimer's disease in African Americans
- Lipopolysaccharide exposure during late embryogenesis triggers and drives Alzheimer-like behavioral and neuropathological changes in CD-1 mice
- Morphometric and histologic substrates of cingulate integrity in elders with exceptional memory capacity
- Tau Isoform Profile in Essential Tremor Diverges From Other Tauopathies
- Associations between intrinsic capacity, plasma p-tau181 and cognitive function over a 5-year follow-up among community-dwelling older adults: a secondary analysis of the MAPT Study
- Novel Galectin-3 Roles in Neurogenesis, Inflammation and Neurological Diseases
- Trisomy 21 and the brain
- Neuropathological fingerprints of survival, atrophy and language in primary progressive aphasia
- Sensitivity and specificity of dopamine transporter imaging with 123I-FP-CIT SPECT in dementia with Lewy bodies: a phase III, multicentre study