Alzheimer Disease

Data used in the preparation of this article were obtained from the Alzheimer's Disease Neuroimaging Initiative ( ADNI) database (). As such, the investigators within the ADNI contributed to the design and ... Published Online First 21 October 2011.

Neuropsychopharmacology, the official publication of the American College of Neuropsychopharmacology, publishing the highest quality original research and advancing our understanding of the brain and behavior.

Inflammation is a prominent feature in Alzheimer's disease (AD). It has been proposed that aging has an effect on the function of inflammation in the brain, thereby contributing to the development of age-related diseases like AD. However, the age-dependent relationship between inflammation and clinical phenotype of AD has never been investigated.|Inflammation is a prominent feature in Alzheimer's disease (AD). It has been proposed that aging has an effect on the function of inflammation in the brain, there

Diagnostic misconceptions. A closer look at clinical research on Alzheimer's disease. ... Published Online First 25 August 2011. The current focus on early intervention trials in Alzheimer's disease research raises particular ethical issues.

Archives of General Psychiatry, a monthly professional medical journal published by the American Medical Association, publishes original, peer-reviewed articles about psychiatry and related fields

Aberrant amyloid- peptide (A) accumulation along with altered expression and function of nicotinic acetylcholine receptors (nAChRs) stand prominently in the etiology of Alzheimer's disease (AD). Since the discovery that A is bound to 7 nAChRs under many experimental settings, including post-mortem AD brain, much effort has been expended to understand the implications of this interaction in the disease milieu. This research update will review the current literature on the 7 nAChR-A interaction in vitro and in vivo, the functional consequences of this interaction from sub-cellular to cognitive levels, and discuss the implications these relationships might have for AD therapies.

Individuals with antemortem preservation of cognition who show autopsy evidence of at least moderate Alzheimer disease (AD) pathology suggest the possibility of brain reserve, that is, functional resistance to structural brain damage. This reserve would, however, only be relevant if the pathologic markers correlate well with dementia. Using data from the Nun Study (n = 498) and the Adult Changes in Thought (ACT) Study (n = 323), we show that Braak staging correlates strongly with dementia status. Moreover, participants with severe(Braak stage V-VI) AD pathology who remained not demented represent only 12% (Nun Study) and 8% (ACT study) of nondemented subjects. Comparison of these subjects to those who were demented revealed that the former group was often significantly memory-impaired despite not being classified as demented. Most of these nondemented participants showed only stage V neurofibrillary pathology and frontal tangle counts that were slightly lower than a comparable (Braak

Guideline for Alzheimer's disease management.

NIH Consensus Development Conference statement on preventing Alzheimer's disease and cognitive decline.

Recommendations for the diagnosis and management of Alzheimer's disease and other disorders associated with dementia: EFNS guideline.

Donepezil, galantamine, rivastigmine and memantine for the treatment of Alzheimer's disease.

Practice guideline for the treatment of patients with Alzheimer's disease and other dementias.