Related Experiment Video
Updated: Jun 25, 2026
03:07
Development and Validation of a Methodology for Establishing Obese Rat Models with Typical Fatty Pancreas
Published on: November 11, 2025
Alzheimer-type neuropathological changes in morbidly obese elderly individuals
1Department of Pathology, University of Toledo College of Medicine, 3000 Arlington Avenue, Toledo, OH 43614, USA. Robert.Mrak@UToledo.edu
Clinical Neuropathology
|February 17, 2009
Summary
Morbid obesity in older adults is linked to Alzheimer-like brain changes, even without cognitive issues. These changes were not observed in younger obese individuals, suggesting age and obesity interact to increase Alzheimer disease risk.
Area of Science:
- Neuropathology
- Obesity Research
- Geriatric Medicine
Background:
- Obesity is a growing public health concern, particularly in middle age.
- Middle-aged and older adults with obesity face increased risks for various chronic diseases.
- Alzheimer disease (AD) is a leading cause of cognitive decline in the elderly, with increasing prevalence.
Purpose of the Study:
- To investigate neuropathological changes in morbidly obese individuals.
- To compare brain pathology in morbidly obese patients with non-obese controls and AD patients.
- To determine if age influences the association between obesity and neuropathological markers of AD.
Main Methods:
- Autopsy brain tissue from 12 morbidly obese individuals (ages 21-70) without cognitive impairment was analyzed.
- Tissue was compared to 10 non-obese controls and 3 Alzheimer disease (AD) controls.
- Standard neuropathological stains (Bielschowsky, A beta, tau, A beta PP) were used for semiquantitative evaluation.
Main Results:
- Morbidly obese patients exhibited larger hearts but normal brain size compared to controls.
- Significant neuropathological changes, including elevated tau and A beta PP expression, were found in obese patients over 65.
- These changes in older obese individuals were comparable to those observed in some Alzheimer disease cases.
Conclusions:
- Alzheimer-type neuropathological changes are prevalent in elderly morbidly obese individuals without cognitive impairment.
- Neuropathological changes were absent in younger obese patients, indicating an age-dependent effect.
- Comorbid conditions associated with obesity, like heart failure or sleep apnea, may contribute to these findings.
Related Concept Videos
01:23Alzheimer Disease ll: Pathophysiology
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
01:29Alzheimer Disease l: Introduction
Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
01:26Alzheimer's Disease: Overview
Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
01:24Obesity
The Body Mass Index (BMI) is a numerical value derived from a person's weight and height, used to categorize individuals into weight ranges. It is calculated using the formula: weight in kilograms divided by height in meters squared. Obesity is a health condition characterized by excessive accumulation of adipose tissue that poses health risks, often diagnosed with a BMI ≥ 30. This excess fat storage occurs when surplus dietary calories are converted into triglycerides and stored in adipocytes...
01:22Dementia l: Introduction
Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
01:24Parkinson Disease ll: Pathophysiology
Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...