Home Mind & Brain 2021 Alzheimer Award Goes to Giulio Taglialatela and Balaji Krishnan

2021 Alzheimer Award Goes to Giulio Taglialatela and Balaji Krishnan

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The Journal of Alzheimer’s Disease (JAD) is pleased to announce that the joint recipients of the 2021 Alzheimer Award are Giulio Taglialatela, PhD, professor and Vice Chair for Research, and Balaji Krishnan, PhD, Assistant Professor, both of the Department of Neurology and Mitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch.

The 2021 winning paper is entitled: ‘Functional integrity of synapses in the central nervous system of cognitively intact individuals with high Alzheimer’s disease neuropathology is associated with absence of synaptic tau oligomers’. It is openly available to everyone to read, download, and share.

Each year, members of JAD’s extensive editorial board select the article published during the previous year that has had the most significant impact on Alzheimer’s disease (AD) research. The awardees receive the Alzheimer Medal, a bronze medal with the likeness of Alois Alzheimer, and a cash award of $7,500. This year’s award is proudly sponsored by Alzheimer’s Germ Quest.

This year’s award-winning article explores why certain individuals remain cognitively intact despite changes to the brain normally associated with fully symptomatic AD. The study suggests that there is an intrinsic way for the human brain to resist (or significantly delay) the events that lead to cognitive impairment in AD.

‘Understanding the involved cellular mechanism(s) would reveal a very effective target to develop a novel therapeutic concept for AD centred on inducing cognitive resistance in affected patients,’ explains Dr Taglialatela. ‘Such therapy is expected to be effective in humans, as demonstrated by the existence of these resilient individuals.’

Synaptic targeting and disruption by small oligomeric aggregates of amyloid-beta and tau proteins has been widely recognised as a central event underscoring cognitive decline and clinical manifestation of AD. This work shows that contrary to fully demented AD patients, synapses of non-demented individuals with AD neuropathology (NDAN) are devoid of toxic tau oligomers as determined by immunofluorescence histology and western blot studies on synaptosomes isolated from frozen brain specimens. Most notably, using unique approaches of fluorescence assisted single synaptosome-long term potentiation (FASS-LTP) on synaptosomes and microtransplantation of human synaptic membranes in Xenopus oocytes coupled to electrophysiology recording, this work provides a rare insight into human synaptic functionality as determined in frozen autopsy brain specimens.

The results show that absence of tau oligomers is associated with integrity of FASS-LTP as well as preservation of kainite/gamma-aminobutyric acid (GABA) current ratio in synapses from NDAN individuals as compared to demented AD patients.

‘Overall, our research shows, in actual human brains, the causal relationship between synaptic presence of tau oligomers and disruption of synaptic function by illustrating how the absence of both events underscores the retention of cognitive integrity in the face of abundant AD neuropathology, thus providing further support to the credence of tau oligomers and their targeting of synapses as an effective therapeutic target in AD,’ adds Dr Krishnan.

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