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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Unlabelled beta-amyloid plaques (Abeta plaques) in the brain, containing predominantly fibrillary Abeta peptide aggregates, represent a defining pathologic feature of Alzheimer disease (AD).
Why it matters
This study describes preclinical properties of 18F-AV-45, a PET imaging agent for A beta plaques in the brain, which is in phase III clinical studies. It is a diagnostic tool, not a treatment, cure, or prevention for Alzheimer's disease.
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The primary progressive aphasias (PPA) are paradigmatic disorders of language network breakdown associated with focal degeneration of the left cerebral hemisphere.
Why it matters
Among 32 patients with primary progressive aphasia, the logopenic/phonological group had widespread left hemisphere tissue loss, and five of nine had CSF biomarkers consistent with Alzheimer pathology. This is a descriptive brain-imaging study of a language variant and does not test any treatment.
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We investigated the cognitive and neural bases of impaired speech fluency, a central feature of primary progressive aphasia.
Why it matters
This study found that speech fluency was reduced in different ways across subgroups of frontotemporal lobar degeneration, linked to grammar, semantic content or executive problems. It describes speech symptoms and their brain regions and does not test any treatment, cure or prevention.
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Subjects Naive mice, H4 human neuroglioma cells, and H4 human neuroglioma cells stably transfected to express full-length amyloid precursor protein.
Why it matters
In human neuroglioma cells and mice, the anesthetic sevoflurane caused apoptosis and increased amyloid beta levels. These are laboratory and animal findings and do not show that sevoflurane affects Alzheimer's disease in people.
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Mitochondrial aldehyde dehydrogenase (ALDH2) is one of the most important enzymes in human alcohol metabolism.
Why it matters
This paper describes the geographic distribution of the ALDH2*504Lys variant, which has been associated with late-onset Alzheimer's disease among other conditions. It is a genetic distribution study and does not test any treatment or cure.
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We present a multivariate alternative to the voxel-based morphometry (VBM) approach called source-based morphometry (SBM), to study gray matter differences between patients and healthy controls.
Why it matters
This study presents a brain imaging analysis method and applies it to schizophrenia patients, identifying gray matter differences. It does not study Alzheimer's disease or test any treatment or prevention, so it has no direct implications for treating, curing, or preventing the disease.
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The association of alpha-synuclein (alpha-syn) neuropathology with Parkinson's disease (PD) and several related disorders has led to an intense research effort to develop cerebrospinal fluid (CSF)- or blood-based alpha-syn biomarkers for these types of diseases.
Why it matters
This study describes a new ELISA test for measuring alpha-synuclein in cerebrospinal fluid and compared levels across Alzheimer's disease, Parkinson's disease, dementia with Lewy bodies, and controls. It is a laboratory test study and does not test any treatment, cure, or prevention.
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The presenilin/gamma-secretase complex, an unusual intramembrane aspartyl protease, plays an essential role in cellular signaling and membrane protein turnover.
Why it matters
This laboratory study profiled gamma-secretase substrates and mapped what makes a transmembrane protein a substrate, noting that modulating gamma-secretase is a therapeutic goal for cancer and Alzheimer disease. It is basic research and does not report a treatment, cure or prevention for Alzheimer's disease.
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TAR DNA binding protein-43 (TDP-43) is found in ubiquitinated inclusions (UBIs) in some frontotemporal dementias (FTD-U).
Why it matters
This study found TDP-43 inclusions in muscle tissue of people with a form of frontotemporal dementia linked to inclusion body myopathy, suggesting a shared mechanism between muscle and brain disease. It is a tissue analysis and does not test any treatment, so it does not show how to treat, cure or prevent Alzheimer's disease.
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49/100
Because of their abundance, resistance to proteolysis, rapid aggregation and neurotoxicity, N-terminally truncated and, in particular, pyroglutamate (pE)-modified Abeta peptides have been suggested as being important in the initiation of pathological cascades resulting in the development of Alzheimer's disease.
Why it matters
In mouse and fruit fly models, inhibiting glutaminyl cyclase reduced pyroglutamate-modified Abeta, diminished plaque formation and gliosis, and improved performance on memory and learning tests. This offers a possible new therapeutic option, but the work is in animal models and not yet proven in people.
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Endocytic dysfunction is an early pathological change in Alzheimer's disease (AD) and Down's syndrome (DS).
Why it matters
Using fibroblasts from people with Down syndrome, this laboratory study found increased endocytic uptake and enlarged late endosomes resembling those in Alzheimer disease and Down syndrome neurons, and blocking rab5 reversed these abnormalities. It is cell-based work that suggests a possible disease mechanism but does not test any treatment in patients.
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We previously reported that intraperitoneal (i.p.) injection (20 mg/kg) of (-)-epigallocatechin-3-gallate (EGCG), the main polyphenolic constituent of green tea, decreased beta-amyloid (Abeta) levels and plaques via promotion of the non-amyloidogenic alpha-secretase proteolytic pathway in "Swedish" mutant amyloid precursor protein overexpressing (APPsw, Tg) mice.
Why it matters
In Alzheimer transgenic mice, oral EGCG reduced A beta deposition and plaque burdens in several brain regions. This is an animal study, so it does not show that EGCG treats, cures, or prevents Alzheimer's disease in people.
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49/100
The etiologies of neurodegenerative diseases may be diverse; however, a common pathological denominator is the formation of aberrant protein conformers and the occurrence of pathognomonic proteinaceous deposits.
Why it matters
This review argues that protein misfolding can harm neurons both by gaining a toxic function and by losing a normal function, and that soluble oligomers are linked to early pathological changes. It is a summary of mechanisms and does not test any treatment, cure or prevention.
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49/100
Doublecortin (DCX) is a microtubule-associated protein expressed by migrating neuroblasts and is considered to be a reliable marker of neurogenesis.
Why it matters
This tissue study found that doublecortin is present in differentiated astrocytes in the adult human neocortex and is not a reliable or selective marker of neurogenesis. It is basic tissue work and does not test any treatment, cure, or prevention.
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TAR-DNA-binding protein 43 (TDP-43) has been identified as a major component protein of ubiquitin-positive inclusions in brains from patients with frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U) and amyotrophic lateral sclerosis.
Why it matters
In brains examined after death, this 2007 study found deposits of TDP-43, a protein already known as a major component of inclusions in frontotemporal lobar degeneration (FTLD-U) and ALS, in people who had Alzheimer's disease or dementia with Lewy bodies, but not in Parkinson's disease, Pick's disease, progressive supranuclear palsy, corticobasal degeneration or FTDP-17. In the Alzheimer's and Lewy body cases the deposits were concentrated in the amygdala and hippocampus rather than the frontal cortex and basal ganglia affected in FTLD-U, and they partly overlapped alpha-synuclein but "hardly" overlapped tau. The record gives no case numbers and tests no treatment; the authors say only that TDP-43 "may be related in some way" to Alzheimer's and Lewy body pathology.
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We found that despite a similar severity of dementia, patients with dementia with Lewy bodies (DLB) had more cortical atrophy than patients with Parkinson disease with dementia (PDD), indicating different brain substrates underlying dementia in the two syndromes.
Why it matters
In this imaging study, patients with dementia with Lewy bodies had more pronounced cortical atrophy than patients with Parkinson disease with dementia in the temporal, parietal, and occipital lobes, despite similar dementia severity. Patients with Alzheimer dementia showed reduced gray matter in the temporal lobes bilaterally, including the amygdala, compared with Parkinson disease with dementia.
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Frontotemporal lobar degeneration (FTLD) encompasses a heterogeneous group of clinical syndromes that include frontotemporal dementia (FTD), frontotemporal dementia with motor neurone disease (FTD/MND), progressive non-fluent aphasia (PNFA), semantic dementia (SD) and progressive apraxia (PAX).
Why it matters
This study classified brain tissue from 79 people with frontotemporal lobar degeneration and found significant relationships between clinical syndrome and pathology. It is a pathological study and does not test any treatment or cure.
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Parkinsonian syndrome related to intravenous use of a "designer" psychostimulant, derived from pseudoephedrine using potassium permanganate as the oxidant, has been observed in drug addicts in Estonia.
Why it matters
This report describes four young drug addicts with irreversible parkinsonian syndrome related to intravenous use of a psychostimulant derived from pseudoephedrine using potassium permanganate. None of the four cases scored below the dementia threshold in MMSE, and this is a small descriptive case series, not a study of Alzheimer's treatment, cure, or prevention.
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Neuroinflammation is a conspicuous feature of Alzheimer disease (AD) pathology and is thought to contribute to the ultimate neurodegeneration that ensues.
Why it matters
In a transgenic mouse model, sustained overexpression of IL-1 beta caused chronic neuroinflammation but surprisingly reduced Alzheimer's plaque pathology. This is animal research only, and the finding that inflammation lessened plaques does not establish any treatment for people.
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Neurofibrillary tangles (NFTs) are a pathological hallmark of Alzheimer's disease and other tauopathies, but recent studies in a conditional mouse model of tauopathy (rTg4510) have suggested that NFT formation can be dissociated from memory loss and neurodegeneration.
Why it matters
In a mouse model of tauopathy, early-stage aggregated tau multimers accumulated before tangles formed and their levels tracked with memory loss, suggesting these early aggregates rather than tangles may be the harmful species. This is animal and tissue research that points to possible targets, but no treatment was tested in patients.
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Frontotemporal dementia with inclusion body myopathy and Paget disease of bone is a rare, autosomal-dominant disorder caused by mutations in the gene valosin-containing protein (VCP).
Why it matters
This study examined whether the ubiquitin pathology seen in frontotemporal dementia caused by VCP gene mutations involves accumulation of TDP-43. It is a pathology study of a rare inherited disorder and does not report any treatment or cure.
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Low levels of BDNF accompany impaired glucose metabolism.
Why it matters
This study found that plasma levels of BDNF were decreased in people with type 2 diabetes and that high blood glucose inhibited BDNF output from the human brain. It concerns glucose metabolism and BDNF, not a treatment, cure, or prevention for Alzheimer's disease.
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We scanned throughout chromosome 21 to assess genetic associations with late-onset Alzheimer disease (AD) using 374 Japanese patients and 375 population-based controls, because trisomy 21 is known to be associated with early deposition of beta-amyloid (Abeta) in the brain.
Why it matters
This genetic study found an association between the DYRK1A gene on chromosome 21 and late-onset Alzheimer disease, and showed that amyloid can increase DYRK1A, which then leads to tau phosphorylation. It suggests a biological pathway linking amyloid and tau but does not test any treatment.
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Classic Parkinson's disease (PD) is characterized by fibrillar alpha-synuclein inclusions known as Lewy bodies in the substantia nigra, which are associated with nigrostriatal degeneration.
Why it matters
This review describes how alpha-synuclein pathology in Parkinson's disease spreads through the brain and suggests that understanding these mechanisms could provide targets for disease-modifying therapies. It is a review, not a treatment, cure or prevention for Alzheimer's disease.
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49/100
The neurotrophins nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) are important mediators of brain and neuronal development, the maintenance of homeostatic conditions in the adult nervous system, and the complex interplay of central and peripheral physiological and pathophysiological factors.
Why it matters
In this large sample of elderly people, neither BDNF nor NGF serum levels proved to be related to the factors examined. It reports no 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.
- Blood biomarkers of vascular dysfunction in small vessel disease progression: Insights from a longitudinal neuroimaging study
- Understanding the role of TDP-43 and FUS/TLS in ALS and beyond
- Mutation in the α-Synuclein Gene Identified in Families with Parkinson's Disease
- Rapidly Progressive Dementia After Platelet-Rich Plasma Therapy: A Case of Sporadic Creutzfeldt-Jakob Disease in the Context of Chronic Ehrlichiosis
- Loss of TREM2 rescues hyperactivation of microglia, but not lysosomal deficits and neurotoxicity in models of progranulin deficiency
- Characterizing spatiotemporal white matter hyperintensity pathophysiology in vivo to disentangle vascular and neurodegenerative contributions
- Making the final cut: pathogenic amyloid-β peptide generation by γ-secretase
- The mitochondrial ATP synthase is a shared drug target for aging and dementia
- Autoidentification of perivascular spaces in white matter using clinical field strength T1 and FLAIR MR imaging
- TREM2 p.H157Y Variant and the Risk of Alzheimer's Disease: A Meta-Analysis Involving 14,510 Subjects