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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The notion of uncontrollable stress causing reduced hippocampal size remains controversial in the posttraumatic stress disorder literature, because human studies cannot discern the causality of effect.
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Frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS) are neurodegenerative diseases that show considerable clinical and pathologic overlap, with no effective treatments available.
Why it matters
Mice expressing mutant human TDP-43 developed a progressive fatal disease resembling ALS and FTLD-U, yet cytoplasmic TDP-43 aggregates were absent. This animal work suggests altered protein function rather than aggregation drives disease, and no treatment was tested.
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Accumulation of the synaptic protein alpha-synuclein (alpha-syn) is a hallmark of Parkinson's disease (PD) and Lewy body disease (LBD), a heterogeneous group of disorders with dementia and parkinsonism, where Alzheimer's disease and PD interact.
Why it matters
In a cell line and an alpha-synuclein transgenic mouse, delivering beclin 1 activated autophagy, reduced alpha-synuclein buildup and improved synaptic and dendritic pathology without significant harmful effects. This is animal and cell work and has not been shown to help patients.
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Several neuropsychiatric disorders involving hippocampal structural changes have been studied extensively using volumetric magnetic resonance imaging (MRI).
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As a more complete picture of the clinical phenotype of Parkinson's disease emerges, non-motor symptoms have become increasingly studied.
Why it matters
This review describes visual symptoms in Parkinson's disease, including visual hallucinations that predict cognitive decline, and evidence of retinal dysfunction. It is a review of visual changes in Parkinson's disease, not a study of treating, curing, or preventing Alzheimer's disease.
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Following neuronal injury, microglia initiate repair by phagocytosing dead neurons without eliciting inflammation.
Why it matters
This study shows that TREM2 interacts with ligands on neurons and promotes microglial phagocytosis of dead neurons without inflammation. It is basic cell and culture work from 2009 and does not test an Alzheimer's therapy.
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Since the identification of tau as the main component of neurofibrillary tangles in Alzheimer's disease and related tauopathies, and the discovery that mutations in the tau gene cause frontotemporal dementia, much effort has been directed towards determining how the aggregation of tau into fibrillar inclusions causes neuronal death.
Why it matters
This review discusses how abnormal tau may cause neuronal death and concludes that tau-mediated neurodegeneration likely results from both toxic gains of function and loss of normal tau function. It is a review, not a treatment, cure or prevention for Alzheimer's disease.
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Alzheimer disease (AD) and related tauopathies are histopathologically characterized by a specific type of slow and progressive neurodegeneration, which involves the abnormal hyperphosphorylation of the microtubule associated protein (MAP) tau.
Why it matters
This review describes how abnormally hyperphosphorylated tau sequesters normal tau and disrupts microtubules, and how its aggregation probably impairs axoplasmic flow and leads to progressive loss of connectivity in affected neurons. It focuses on mechanisms of tau-induced neurodegeneration rather than testing a treatment.
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Deficits in cholinergic function have been postulated to cause delirium and cognitive decline.
Why it matters
This review examines the cholinergic deficiency hypothesis in delirium, proposing that imbalances between cholinergic and other neurotransmitter pathways may result in delirium. It suggests understanding this pathway may yield approaches to diagnosis, prevention, and treatment of delirium, not Alzheimer's disease.
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MicroRNAs (miRNAs) are small regulatory RNAs that participate in posttranscriptional gene regulation in a sequence-specific manner.
Why it matters
Levels of the microRNA miR-107 were found to decrease early in Alzheimer's disease and were predicted to target BACE1 mRNA, which tended to increase as miR-107 decreased. This is a tissue and bioinformatics study and reports no treatment, cure or prevention.
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52/100
The clinical syndrome of pure akinesia has most often been associated with progressive supranuclear palsy (PSP) and is characterized by difficulty initiating gait and "freezing" during walking, writing and speaking.
Why it matters
This study found that the clinical syndrome of pure akinesia with gait freezing had high specificity for progressive supranuclear palsy tau pathology. It is about a clinical phenotype of PSP, not about treating, curing or preventing Alzheimer's disease.
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In multiple sclerosis, inflammation can successfully be prevented, while promoting repair is still a major challenge.
Why it matters
This 2007 mouse study tested whether immune precursor cells genetically modified to carry TREM2, a receptor found on the brain's clean-up cells (microglia), change the course of an animal model of multiple sclerosis. Its title reports that the modified cells "mediate nervous tissue debris clearance and facilitate recovery" in that model; the abstract stored here stops before the results, so no numbers are available. It is an animal study of multiple sclerosis, not Alzheimer's disease, and says nothing about treating people.
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The incidence of Alzheimer disease (AD) and vascular dementia is greatly increased following cerebral ischemia and stroke in which hypoxic conditions occur in affected brain areas. beta-Amyloid peptide (Abeta), which is derived from the beta-amyloid precursor protein (APP) by sequential proteolytic cleavages from beta-secretase (BACE1) and presenilin-1 (PS1)/gamma-secretase, is widely believed to trigger a cascade of pathological events culminating in AD and vascular dementia.
Why it matters
This laboratory study found that hypoxia increases BACE1 expression and beta-amyloid generation through HIF-1alpha, linking hypoxic conditions to amyloid production. It is a mechanistic laboratory study and does not test any treatment, cure, or prevention in people.
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The "Lister family complex," an extensive Swedish family with autosomal dominant Parkinson disease, was first described by Henry Mjönes in 1949.
Why it matters
This study of a large Swedish family with autosomal dominant Parkinson disease found SNCA duplication and triplication as the genetic cause of parkinsonism in the pedigree. It is about Parkinson disease genetics and does not address treating, curing, or preventing Alzheimer's disease.
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Premutation alleles of the fragile X mental retardation 1 (FMR1) gene give rise to a late-onset movement disorder, fragile X-associated tremor/ataxia syndrome (FXTAS), characterized by progressive intention tremor and gait ataxia, with associated dementia and global brain atrophy.
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Nicotinamide adenine dinucleotide (NAD)+-dependent sirtuins have been identified to be key regulators in the lifespan extending effects of calorie restriction (CR) in a number of species.
Why it matters
In mouse neurons grown in the laboratory, manipulating SIRT1 activity reduced beta-amyloid content through a mechanism involving ROCK1. This is in vitro work, so it is early and does not show whether calorie restriction or SIRT1 activation would prevent Alzheimer's disease in people.
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DTI histograms may be used as an adjunct outcome measure in future therapeutic trials.
Why it matters
In CADASIL subjects followed over about two years, T2-lesion volumes and mean diffusivity histogram metrics changed significantly and correlated with clinical measures over time. Diffusion tensor imaging histograms may be used as an adjunct outcome measure in future therapeutic trials and may predict disease progression in CADASIL.
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The presence of either severe WMH or MTA was associated with a modest but non-significant increase in frequency of mild cognitive deficits (severe WMH: odds ratio (OR) = 1.9 (95% confidence interval (CI), 1.0 to 3.7); MTA present: OR = 1.5 (95% CI, 0.8 to 2.8)).
Why it matters
In 581 older people without disability, having either severe white matter hyperintensities or medial temporal lobe atrophy alone was not significantly linked to mild cognitive deficits, but having both together was linked to more than a fourfold increase. This is an observational study and does not test any treatment or prevention.
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Here, we describe the generation of a novel transgenic mouse model of human tauopathy.
Why it matters
This mouse model expresses the P301L tau mutation and develops age-dependent tangles, neuron loss and memory problems, with transgene expression suppressible by doxycycline. It is an animal model of hereditary tauopathy, not a treatment for Alzheimer's disease.
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Future longitudinal studies with trauma control subjects and neuropsychological measures are indicated to further elucidate the relationship between hippocampus and behavioral abnormalities in young PTSD subjects.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder pathologically characterized by deposition of beta-amyloid (Abeta) peptides as senile plaques in the brain.
Why it matters
In mouse neuron-like cells and in a transgenic mouse model, EGCG from green tea reduced amyloid-beta generation and cerebral amyloidosis. This is animal and cell research, so it is too early to know whether EGCG would prevent or treat Alzheimer's disease in people.
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Patients with Alzheimer's disease (AD) have abnormally low positron emission tomography (PET) measurements of the cerebral metabolic rate for glucose (CMRgl) in regions of the precuneus and the posterior cingulate, parietotemporal, and frontal cortex.
Why it matters
In 160 cognitively normal people aged 47 to 68, this PET study examined how APOE ε4 gene dose relates to regional glucose metabolism in the brain. It describes an imaging association in people without dementia and does not test a treatment, cure, or prevention.
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Gene defects play a major role in the pathogenesis of degenerative disorders of the nervous system.
Why it matters
This review discusses the genetic epidemiology of Alzheimer disease and other neurodegenerative diseases and how genetic studies have helped explain their molecular mechanisms. It reports no treatment, cure or prevention.
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Expression of somatostatin in the brain declines during aging in various mammals including apes and humans.
Why it matters
Using in vitro and in vivo methods, this study found that somatostatin regulates the metabolism of amyloid beta peptide by modulating its degradation by neprilysin. It describes a possible mechanism and does not report any treatment, cure, or prevention for Alzheimer's disease in people.
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It is widely accepted that the familial Parkinson's disease (PD)-linked gene product, parkin, functions as a ubiquitin ligase involved in protein turnover via the ubiquitin-proteasome system.
Why it matters
In laboratory work, parkin ubiquitinated synphilin-1 in a nonclassical, proteasome-independent way via K63 linkages, and this enhanced formation of Lewy-body-like inclusions. This is cell-based work on Parkinson's disease inclusion formation, not a treatment or prevention for Alzheimer's.
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.
- Novel Blood-Based Biomarkers of Cognition, Stress, and Physical or Cognitive Training in Older Adults at Risk of Dementia: Preliminary Evidence for a Role of BDNF, Irisin, and the Kynurenine Pathway
- Profound loss of layer II entorhinal cortex neurons occurs in very mild Alzheimer's disease
- The common inhalation anesthetic isoflurane induces apoptosis and increases amyloid beta protein levels
- Trem2 Y38C mutation and loss of Trem2 impairs neuronal synapses in adult mice
- Amygdala, hippocampal and corpus callosum size following severe early institutional deprivation: the English and Romanian Adoptees study pilot
- Activation of beta2-adrenergic receptor stimulates gamma-secretase activity and accelerates amyloid plaque formation
- Amyloid-beta oligomers impair fear conditioned memory in a calcineurin-dependent fashion in mice
- The dietary fatty acids α-linolenic acid (ALA) and linoleic acid (LA) selectively inhibit microglial nitric oxide production
- TREM‐2, triggering receptor expressed on myeloid cell‐2, negatively regulates TLR responses in dendritic cells
- Concussion, microvascular injury, and early tauopathy in young athletes after impact head injury and an impact concussion mouse model