Brain beta-amyloid measures and magnetic resonance imaging atrophy both predict time-to-progression from mild cognitive impairment to Alzheimer’s disease
Biomarkers of brain Ab amyloid deposition can be measured either by cerebrospinal fluid Ab42 or Pittsburgh compound B positron emission tomography imaging. Our objective was to evaluate the ability of Ab load and neurodegenerative atrophy on magnetic resonance imaging to predict shorter time-to-progression from mild cognitive impairment to Alzheimer’s dementia and
to characterize the effect of these biomarkers on the risk of progression as they become increasingly abnormal.
Potential for primary prevention of Alzheimer’s disease: an analysis of population-based data
Lancet Neurol 2014; 13: 788–94
Background Recent estimates suggesting that over half of Alzheimer’s disease burden worldwide might be attributed to potentially modifi able risk factors do not take into account risk-factor non-independence. We aimed to provide specific estimates of preventive potential by accounting for the association between risk factors.
Biochemistry of Amyloid b-Protein and Amyloid Deposits in Alzheimer Disease
Progressive cerebral deposition of the amyloid b-protein (Ab) in brain regions serving memory and cognition is an invariant and defining feature of Alzheimer disease. A highly similar but less robust process accompanies brain aging in many nondemented humans,
lower primates, and some other mammals.
Tracking pathophysiological processes in Alzheimer’s disease: an updated hypothetical model of dynamic biomarkers
Lancet Neurol 2013; 12: 207–16
We proposed a model of Alzheimer’s disease (AD) biomarkers that was intended to be a framework for invivo staging of the disease. The model focused on the five most well established biomarkers of AD, which we propose can be divided into two major categories: measures of brain amyloid β (Aβ) deposition and measures of neurodegeneration—defi ned as a pro gressive loss of neurons or their processes (axons and dendrites) with a cor responding progressive impairment in neuronal
Alzheimer’s disease and other dementias: advances in 2014
The Lancet : Although a highly eff ective drug has not yet been approved for the treatment of Alzheimer’s disease, pivotal advances were made in 2014, leading to substantial knowledge about therapeutic targets and early stages of disease.
Glutamate system, amyloid β peptides and tau protein: functional interrelationships and relevance to Alzheimer disease pathology
Pubmed PMC3529221 : Alzheimer disease is the most prevalent form of dementia globally and is characterized premortem by a gradual memory loss and deterioration of higher cognitive functions and postmortem by neuritic plaques containing amyloid β peptide and neurofibrillary tangles containing
phospho-tau protein. Glutamate is the most abundant neurotransmitter in the brain and is essential to memory formation through processes such as long-term potentiation and so might be pivotal to Alzheimer disease progression.