Health Information Search Results
Peer Reviewed Scientific Research Reports.
|<< Prev 20 ||Showing 1 to 20 of 59 Matches||Next 20 >>|
1. My own experience in early research on Alzheimer disease.
Match Strength: 7.474
This brief paper reviews the work on dementia by the Neuropathology group at the Einstein College of Medicine and later at the University of California, San Diego, from the time of our first approaches to Alzheimer Disease in 1959. The electron microscope studies concerned the tangle (got it wrong) and then the plaque (got it right). Lysosomes and active mitochondria were noted in the plaques. Axoplasmic transport was suggested to be abnormal. We studied the plaques in old dogs and old monkeys, and then went on to use image analysis to count neurons in the neocortex of Alzheimer cases and in ... Read More »
» Published in J Alzheimers Dis. 2006;9(3 Suppl):117-9.
2. Non-invasive therapy to reduce the body burden of aluminium in Alzheimer's disease.
Match Strength: 7.459
There are unexplained links between human exposure to aluminium and the incidence, progression and aetiology of Alzheimer's disease. The null hypothesis which underlies any link is that there would be no Alzheimer's disease in the effective absence of a body burden of aluminium. To test this the latter would have to be reduced to and retained at a level that was commensurate with an Alzheimer's disease-free population. In the absence of recent human interference in the biogeochemical cycle of aluminium the reaction of silicic acid with aluminium has acted as a geochemical control of the ... Read More »
» Published in J Alzheimers Dis. 2006 Sep;10(1):17-24; discussion 29-31.
3. A metabolic link between S-adenosylhomocysteine and polyunsaturated fatty acid metabolism in Alzheimer's disease.
Match Strength: 7.246
There is evidence that vascular risk factors contribute to the pathology of Alzheimer's disease. Increased concentrations of circulating homocysteine are associated with vascular risk factors and Alzheimer's disease but the mechanisms involved are unclear. Homocysteine inhibits the hydrolysis of S-adenosylhomocysteine (SAH) which is a product inhibitor of S-adenosylmethionine (SAM) dependent methyltransferase reactions. It has been shown previously that SAH inhibits phosphatidylethanolamine N-methyltransferase (PEMT) in the liver. The activity of PEMT in the liver plays an important role in ... Read More »
» Published in Neurobiol Aging. 2006 Sep 21;
4. Brain mechanisms of successful compensation during learning in Alzheimer disease.
Match Strength: 6.678
OBJECTIVE: To determine whether patients with Alzheimer disease (AD) compensate for neuropathologic changes when performing a mnemonic task by recruiting 1) the same brain regions as age-matched, healthy controls, but to a greater extent; 2) additional brain regions not activated by controls; or 3) both. METHODS: Twelve patients with mild probable AD and 12 healthy age- and education-matched controls participated in an fMRI study of successful encoding and retrieval of visuospatial paired associates. To ensure successful performance in both groups, participants were given multiple attempts to ... Read More »
» Published in Neurology. 2006 Sep 26;67(6):1011-7.
5. Lack of association of two chromosome 10q24 SNPs with Alzheimer's disease.
Match Strength: 6.494
Several groups have reported evidence of linkage on chromosome 10 to late-onset Alzheimer's disease (LOAD). In a recent scan of single nucleotide polymorphisms (SNPs) on chromosome 10, significant associations between the rs498055 and rs4417206 SNPs and risk of LOAD were observed. We examined the association of these two SNPs with LOAD risk in a large Caucasian American cohort comprising about 2000 cases and controls. Neither SNP revealed significant association with LOAD risk or age-at-onset. Publication Types: Comparative Study, Research Support, N.I.H., ... Read More »
» Published in Neurosci Lett. 2006 Nov 20;408(3):170-2. Epub 2006 Sep 26.
6. Progress in the history of Alzheimer's disease: the importance of context.
Match Strength: 6.267
The history of Alzheimer's disease (AD) is typically formulated as the history of great doctors and scientists in the past making great discoveries that are in turn taken up by great doctors and scientists in the present--all sharing the aim of unraveling the mysteries of disease and discovering how it can be prevented or cured. While it can certainly be edifying to study the "great men" and how their contributions laid the foundation for current work, there are problems with this approach to history. First, it oversimplifies the actual historical development of science. Second, using history ... Read More »
» Published in J Alzheimers Dis. 2006;9(3 Suppl):5-13.
7. Differentiation of dementia with Lewy bodies from Alzheimer's disease using Mini-Mental State Examination and brain perfusion SPECT.
Match Strength: 6.266
To determine whether combined studies of Mini-Mental State Examination (MMSE) and brain single photon emission CT (SPECT) would provide more useful means of differentiating between dementia with Lewy bodies (DLB) and Alzheimer's disease (AD), we studied 36 patients with probable DLB and 96 patients with probable AD. DLB patients had significantly better performance on word recall, but more impaired attention and copying than AD patients. We confirmed that a weighted score derived by Ala et al. [Ala, T.A., Hughes, L.F., Kyrouac, G.A., Ghobrial, M.W., Elble, R.J. The Mini-Mental State exam may ... Read More »
» Published in J Neurol Sci. 2006 Dec 1;250(1-2):97-102. Epub 2006 Sep 26.
8. Convergence of genes implicated in Alzheimer's disease on the cerebral cholesterol shuttle: APP, cholesterol, lipoproteins, and atherosclerosis.
Match Strength: 6.039
Polymorphic genes associated with Alzheimer's disease (see ) delineate a clearly defined pathway related to cerebral and peripheral cholesterol and lipoprotein homoeostasis. They include all of the key components of a glia/neurone cholesterol shuttle including cholesterol binding lipoproteins APOA1, APOA4, APOC1, APOC2, APOC3, APOD, APOE and LPA, cholesterol transporters ABCA1, ABCA2, lipoprotein receptors LDLR, LRP1, LRP8 and VLDLR, and the cholesterol metabolising enzymes CYP46A1 and CH25H, whose oxysterol products activate the liver X receptor NR1H2 and are metabolised to esters by SOAT1. ... Read More »
» Published in Neurochem Int. 2007 Jan;50(1):12-38. Epub 2006 Sep 12.
9. Different patterns of Mini Mental Status Examination responses in primary progressive aphasia and Alzheimer's disease.
Match Strength: 5.846
Primary progressive aphasia (PPA) syndrome is frequently misdiagnosed--particularly in favour of Alzheimer's disease (AD). Misdiagnosis is related to the heterogeneity of language disorders at onset, variability in the rate of clinical progression and the low prevalence of PPA syndrome, compared with AD. The aim of this study was to determine whether a patient's first Mini Mental Status Examination (MMSE) might provide insight into differentiating between PPA and AD. We compared item scores for the first, complete MMSE in consecutive patients with PPA versus matched patients with AD. Word ... Read More »
» Published in Eur J Neurol. 2006 Oct;13(10):1124-7.
10. Current strategies for the treatment of Alzheimer's disease and other tauopathies.
Match Strength: 5.740
The pathological hallmarks of Alzheimer's disease (AD) include abnormal intra- and extraneuronal tau and amyloid accumulation, respectively, accompanied by gliosis, oxidative stress and neuron loss. The discovery of mutations within the tau gene itself that cause clinical dementia (i.e., fronto-temporal dementia with Parkinsonism linked to chromosome 17 [FTDP17]) demonstrated that disruption of normal tau function independent of amyloidogenesis was sufficient to cause neuronal loss and clinical dementia. These studies demonstrate the need for therapeutics that either decrease the total pool of ... Read More »
» Published in Expert Opin Ther Targets. 2006 Oct;10(5):665-76.
11. Electrophysiological and information processing variability predicts memory decrements associated with normal age-related cognitive decline and Alzheimer's disease (AD).
Match Strength: 5.700
Recent theoretical models of cognitive aging have implicated increased intra-individual variability as a critical marker of decline. The current study examined electrophysiological and information processing variability and memory performance in normal younger and older controls, and older adults with Alzheimer's disease (AD). It was hypothesized that higher levels of variability would be indicative of age-related and disease-related memory deficits. Results indicated both implicit and explicit memory deficits associated with AD. Consistent with previous research, behavioral speed and ... Read More »
» Published in Brain Res. 2006 Nov 13;1119(1):215-26. Epub 2006 Sep 25.
12. Validation study of the three-objects-three-places test: a screening test for Alzheimer's disease.
Match Strength: 5.692
The aim of the present study was to validate a short, ecological test of episodic memory for the screening of Alzheimer's disease (AD). The validation was performed by computing intrarater reliability, homogeneity, internal coherence, convergent, discriminant and known group validities in the performance of normal subjects (N = 65), mild cognitive impairment (MCI) patients (N = 114), and AD (N = 44) and non-AD demented (N = 39) patients. Intrarater reliability was 0.88, homogeneity ranged from 0.81 to 0.97, and internal coherence was 0.87. With respect to convergent and discriminant validities ... Read More »
» Published in Exp Aging Res. 2006 Oct-Dec;32(4):395-410.
13. Senile myoclonic epilepsy in Down syndrome: a video and EEG presentation of two cases.
Match Strength: 5.587
Myoclonic epilepsy is being increasingly recognized as a late-onset complication in middle-aged or elderly patients with Down syndrome, in association with cognitive decline. We show video and EEG recordings of two patients, both aged 56 years, diagnosed with this condition. At onset, myoclonic epilepsy in elderly DS patients may resemble, in its clinical expression, the classical juvenile myoclonic epilepsy with the characteristic occurrence of jerks on awakening. It is clearly associated with an Alzheimer-type dementia, and may also occur in non-DS patients with Alzheimer's disease: hence ... Read More »
» Published in Epileptic Disord. 2006 Sep;8(3):223-7.
14. Exogenous induction of cerebral beta-amyloidogenesis is governed by agent and host.
Match Strength: 5.523
Protein aggregation is an established pathogenic mechanism in Alzheimer's disease, but little is known about the initiation of this process in vivo. Intracerebral injection of dilute, amyloid-beta (Abeta)-containing brain extracts from humans with Alzheimer's disease or beta-amyloid precursor protein (APP) transgenic mice induced cerebral beta-amyloidosis and associated pathology in APP transgenic mice in a time- and concentration-dependent manner. The seeding activity of brain extracts was reduced or abolished by Abeta immunodepletion, protein denaturation, or by Abeta immunization of the ... Read More »
» Published in Science. 2006 Sep 22;313(5794):1781-4.
15. Progression of white matter hyperintensities in Alzheimer disease, dementia with lewy bodies, and Parkinson disease dementia: a comparison with normal aging.
Match Strength: 5.399
OBJECTIVE: The objective of this study was to investigate cross-sectional and longitudinal white matter hyperintensity (WMH) changes in older subjects with clinically diagnosed dementia. METHODS: Fluid-attenuated inversion recovery images were acquired one year apart in subjects with dementia with Lewy bodies (DLB), Parkinson disease dementia (PDD), Alzheimer disease (AD), and also healthy elderly comparison subjects. WMH volume was quantified using an automated technique. RESULTS: Baseline WMH (as a percent of brain volume) was significantly greater compared with healthy subjects (N=33, ... Read More »
» Published in Am J Geriatr Psychiatry. 2006 Oct;14(10):842-9.
16. Elucidating amyloid beta-protein folding and assembly: A multidisciplinary approach.
Match Strength: 5.238
Oligomeric, neurotoxic amyloid protein assemblies are thought to be causative agents in Alzheimer's and other neurodegenerative diseases. Development of oligomer-specific therapeutic agents requires a mechanistic understanding of the oligomerization process. This is a daunting task because amyloidogenic protein oligomers often are metastable and comprise structurally heterogeneous populations in equilibrium with monomers and fibrils. A single methodological approach cannot elucidate the entire protein assembly process. An integrated multidisciplinary program is required. We discuss here the ... Read More »
» Published in Acc Chem Res. 2006 Sep;39(9):635-45.
17. Screening for amnestic mild cognitive impairment and early Alzheimer's disease with M@T (Memory Alteration Test) in the primary care population.
Match Strength: 5.038
OBJECTIVES: To design and validate a new screening test for amnestic Mild Cognitive Impairment (A-MCI) and early stage Alzheimer's disease (AD). METHODS: We develop a verbal episodic and semantic memory test: the Memory Alteration Test (M@T). Discriminative validity was assessed in a population sample of 400 aged individuals from primary care population centres in Barcelona, Spain, 50 patients with A-MCI according to Petersen et al. criteria, and 66 with early AD (Global Deterioration Scale-4 stage) according to the NINCDS-ADRDA criteria. RESULTS: The M@T is quick, 5-min, and easy to ... Read More »
» Published in Int J Geriatr Psychiatry. 2006 Sep 22;
18. Impact on health-related quality of life and perceived burden of informal caregivers of individuals with Alzheimer's disease.
Match Strength: 4.982
This study assessed the impact on health-related quality of life (HRQL) and the perceived burden of informal caregivers of individuals with Alzheimer's disease (AD) on the Canary Islands (Spain). We utilized a multicenter, cross-sectional design, based on questionnaire responses of 237 informal caregivers of AD patients. Patients were classified according to the degree of severity utilizing the Clinical Dementia Rating Scale. Sociodemographic, HRQL (EQ-5D) and functional dependency data were gathered together with the degree of caregiver burden. Caregivers had a higher frequency of problems ... Read More »
» Published in Neuroepidemiology. 2006;27(3):136-42. Epub 2006 Sep 13.
19. Neurodegeneration and neuroprotection in multiple sclerosis and other neurodegenerative diseases.
Match Strength: 4.927
Multiple sclerosis is considered a disease of myelin destruction; Parkinson's disease (PD), one of dopaminergic neuron depletion; ALS, a disease of motor neuron death; and Alzheimer's, a disease of plaques and tangles. Although these disorders differ in important ways, they also have common pathogenic features, including inflammation, genetic mutations, inappropriate protein aggregates (e.g., Lewy bodies, amyloid plaques), and biochemical defects leading to apoptosis, such as oxidative stress and mitochondrial dysfunction. In most disorders, it remains uncertain whether inflammation and ... Read More »
» Published in J Neuroimmunol. 2006 Jul;176(1-2):198-215.
20. Small molecule oxidation products trigger disease-associated protein misfolding.
Match Strength: 4.856
Oxidative stress and inflammation are risk factors for both the development of alpha-synucleinopathies, such as Parkinson's disease and dementia with Lewy bodies, and Alzheimer's disease, the two most common neurodegenerative disorders. These diseases are associated with the neurotoxic deposition of misassembled alpha-synuclein and amyloid-beta (Abeta) peptides, respectively. Both occur sporadically, that is, without detectable disease-related mutations, in the vast majority of cases. Small molecule oxidation products, especially secosterols derived from cholesterol and 4-hydroxynonenal ... Read More »
» Published in Acc Chem Res. 2006 Sep;39(9):611-9.
|<< Prev 20 ||Showing results 1 to 20 of 59||Next 20 >>|
* All information on Level1Diet.com is for educational purposes only. These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease. Before changing your diet, or adding supplements to your diet, or beginning an exercise program, everyone should consult a qualified and licensed health practitioner; a physician, dietician or similar professional.