March 26-31, 2019 | Lisbon, Portugal
An unparalelled success with 3,886 participants from 75 countries, the 14th International Conference on Alzheimer’s and Parkinson’s Diseases and related neurological disorders AD/PD™ 2019, held in the beautiful city of Lisbon, Portugal was the biggest edition in the series’ 34-year history. The conference offered a high quality scientific program covering the most recent research, clinical trials, developments, and treatments, with emphasis on overlaps and congruent results among AD. This provided participants with unparalleled and powerful insights into distinct neurodegenerative diseases in one setting to examine their similarities and differences.
The continuing success of the AD/PD™ conference is the result of several key ingredients:
- A high-quality scientific program covering most recent research, developments, and treatments, with emphasis on overlaps and congruent results among AD, PD and related neurological disorders.
- A multidisciplinary mix of participants representing both clinical investigators and basic scientists; as well as both established investigators and young upcoming talents.
- An International Scientific Advisory Board covering a broad range of expertise in AD, PD and related neurological disorders.
- A concerted attempt to provide an ambiance at the Conference that encourages interaction, exchange of ideas and networking opportunities among all participants.
- Junior Faculty Awards, intended to encourage attendance by young scientists at the Conference.
Abraham Fisher, Ph.D.
Roger M. Nitsch, M.D.
Manfred Windisch, Ph.D.
Conference Website: https://adpd2019.kenes.com/
“Held in romantically beautiful Lisbon, this AD/PD was the biggest thus far, drawing 3,982 attendees from 73 countries”
“After years of grunt work on next-gen sequencing and expression analysis, geneticists are finally reaping results. The new genes underscore the role of known pathways and cell types in disease.”
“A tool of modern genetics, expression studies link GWAS hits to specific cell types, providing clues to pathogenesis. Microglia come up again and again.”
“Presented at AD/PD, the discovery by scientists in Uppsala is the first APP deletion found to cause Alzheimer’s disease. The same group found the Swedish and Arctic APP mutations.”
“Scientists at AD/PD 2019 see a Goldilocks of microglial activation: Both too little and too much is bad in an injured brain. How could a therapy make it just right?”
“Inhibiting the receptor activates microglia to mop up debris, making CD33 an attractive therapeutic target.”
“Speakers at AD/PD 2019 reported that AD risk factors mess up lipid metabolism in glial cells. In cellular models, speeding the clearance of fats lessened pathology.”
“By slipping human microglia inside the mouse brain, researchers hope to better monitor their response to pathologies, such as Aβ.”
“Scientists are probing saliva and skin secretions for telltale signs of Parkinson’s disease. Their prize? A diagnostic test at the pre-motor stage.”
“Scientists know that the retina changes in people with preclinical AD; alas, there is neither consensus nor convergence in the field of retinal imaging. An upcoming initiative aims to determine which measures are most robust.”
“Microglia cleanup, mitophagy, axonal plasticity, blood-brain barrier. A renewed focus on ApoE4 is revealing new ways in which this isoform renders the brain vulnerable to Alzheimer’s.”
“By aging cultured neurons and manipulating them to stimulate endocytosis or interfere with vesicle release, researchers can bring about characteristics of Alzheimer’s—without adding APP or Aβ.”
“As data increasingly blame the microglia response as a driving force in Alzheimer’s disease, researchers are investigating whether tempering these cells will aid cognition.”
“At AD/PD 2019, scientists implicated both peripheral and central innate immunity in promoting propagation.”
“An electron microscopy study reveals a jumbled mess of membrane chunks and malfunctioning organelles, bound together by phosphorylated or truncated α-synuclein.”
“We are learning” was the tenor of debate about the latest round of setbacks for anti-amyloid trials in symptomatic Alzheimer’s disease at a recent conference in Lisbon.”
“Lanabecestat, elenbecestat, and umibecestat all showed data at the AD/PD conference in Lisbon. Learn what definitely doesn’t work and what might yet.”
“Analysis of a chimeric mouse shows that the cells express the same genes they do in the human brain, survey their environment, and respond to injuries and amyloid.”