John Growdon (United States of America)
Harvard Medical School
Professor of Neurology
John H. Growdon is Professor of Neurology at the Harvard Medical School and Attending Neurologist at the Massachusetts General Hospital. His clinical care and research studies have focused on Alzheimer disease and Parkinson disease. He is especially interested in the cognitive impairment that accompanies PD, and factors that affect the transition to dementia. In brief, his team has discovered that many of the factors that account for dementia in AD are also operative in PD, including the central effect of Abeta amyloid in raising the risk of cognitive impairment and dementia in non-demented PD patients and stimulating the production of other toxic proteins including tau in neurofibrillary tangles and alpha-synuclein in Lewy bodies.

Presenter of 2 Presentations

 Conference Calendar

Discussants

Session Name
0790 - FORUM ON:TRANSLATIONAL DRUG DISCOVERY IN PD/ LBD PHASE I-III - RECENT UPDATES (ID 42)
Session Type
FORUM
Date
Thu, 17.03.2022
Session Time
03:50 PM - 04:50 PM
Room
ONSITE PLENARY: 115-117
Lecture Time
03:50 PM - 04:50 PM
Presenter

PRE-RECORDED: DEMENTIA COMES TO PARKINSON DISEASE: MOLECULAR BASES AND HOW TO DETECT THEM

Session Name
1730 - DIAGNOSTIC ACCURACY, IMAGING AND FLUID BIOMARKERS IN AD, PD, LBD (ID 89)
Session Type
SYMPOSIUM
Date
Sat, 19.03.2022
Session Time
05:15 PM - 07:15 PM
Room
ONSITE PLENARY: 115-117
Lecture Time
07:00 PM - 07:15 PM
Presenter

Abstract

Abstract Body

Aims: The goal of this study was to identify the molecular bases of dementia in Lewy body diseases, and highlight ways to detect them in life.

Background: Dementia early in the course of disease is one of the defining features of DLB; cognitive impairment and dementia occur later in the course of idiopathic PD but eventually affect >80% by the time of death. As a prelude to developing neuroprotective treatment, it is necessary to identify the putative causes as early as possible.

Methods & Results: We have performed amyloid PET scans in subjects with PD, PDD and DLB, and conducted autopsies on 20 of these. Amyloid Abeta burden is high in most DLB and in many PDD patients; it is associated with faster cognitive decline. Abeta burden is significantly correlated with the extent of tau positive neurofibrillary tangles and alpha-synuclein positive Lewy bodies measured at autopsy.

Conclusions: We conclude that Abeta is a substantial risk factor for developing dementia in Lewy body diseases, that the combination of Abeta, tau and alpha-synuclein is especially neurotoxic, and speculate that efforts to reduce brain Abeta burden may retard cognitive loss in Lewy body diseases.

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