Sixty-seven older adults who did not have dementia or cognitive impairment completed a laboratory task where they decided whether to give money to an anonymous person or keep it for themselves.
They also completed a series of cognitive tests, such as word and story recall. Those who gave away more money performed worse on the cognitive assessments known to be sensitive to Alzheimer’s disease.
“Our goal is to understand why some older adults might be more susceptible than others to scam, fraud or financial exploitation,” said the study’s senior author, Duke Han, Ph.D., director of neuropsychology in the Department of Family Medicine and a professor of family medicine, neurology, psychology and gerontology at the Keck School of Medicine.
Earlier research that tested the link between altruism and cognition relied on self-report measures, such as asking older adults whether they would be willing to give money in certain scenarios. The present study used real money to examine the link.
“To our knowledge, this is the first study to explore the relationship using a behavioral economics paradigm, meaning a scenario where participants had to make decisions about giving or keeping actual money,” said Gali H. Weissberger, Ph.D., a senior lecturer in the Interdisciplinary Department of Social Sciences at Bar-Ilan University in Israel and first author of the study.
Giving and cognition
In the lab, each participant was told they had been paired with an anonymous person who was completing the study online. They were then given $10 and instructed to allocate it however they wished, in $1 increments, between themselves and the anonymous person.
The older adults in the study also completed a series of neuropsychological tests, including several that are commonly used to help diagnose Alzheimer’s disease in its early stages.
The tests included story and word recall tasks where participants are asked to remember information after a short delay; a category fluency test that involves listing words on a specific topic; and several other cognitive assessments.
Participants who gave more away scored significantly lower on the neuropsychological tests known to be sensitive to early Alzheimer’s disease. There were no significant performance differences on other neuropsychological tests.
Clarifying the link
More research is needed to confirm the nature of the relationship between financial altruism and cognitive health in older adults, including with larger and more representative samples. Future studies could also collect both behavioral and self-report data on financial altruism to better understand participants’ motivations for giving.
Han, Weissberger and their colleagues are now collecting data for a longitudinal study using the same giving task, which could help determine whether some older adults are becoming more altruistic over time.
“If a person is experiencing some kind of change in their altruistic behavior, that might indicate that changes are also happening in the brain,” Weissberger said.
Clarifying these details about the link between altruism and cognition could ultimately improve screening for Alzheimer’s disease and help people protect their loved ones from financial exploitation. It can also help researchers distinguish between what represents healthy giving behavior versus something that could signify underlying problems.
“The last thing we would want is for people to think that financial altruism among older adults is a bad thing,” Han said. “It can certainly be a deliberate and positive use of a person’s money.”
Alzheimer’s Disease (AD) is a worldwide plague affecting millions of people in aging societies. It has huge social and economic costs, also considering the lack of effective therapies; its prevalence is expected to increase, especially in low- and middle-income countries, with an estimated 139 million affected individuals by 2050 (Dementia facts & Figures.
Available online: https://www.alzint.org/about/dementia-facts-figures/ accessed on 21 December 2021).
Deterioration of the cognitive function is thus considered one of the greatest health threats of old age, but what distinguishes cognitive decline linked to “normal” aging from the first signs of dementia is still the subject of debate [1].
Very little is known about the processes that cause conversion from healthy aging to mild cognitive impairment (MCI) and, from this condition, to AD, even if improvements in electroencephalographic (EEG) recordings potentially allow to follow MCI to AD conversion [2,3]. Thus, there is an urgent need for biomarkers that allow identification of AD staging and even more for markers associated with a high probability of disease worsening [4,5].
Cognitive impairments are closely linked to brain circuitry dysfunctions, and the latter are firstly associated with alterations of neuronal connectivity rather than with cell death [6,7,8,9,10]. The aging process itself has been linked to synaptic dysfunctions and the molecular mechanisms involved are starting to be identified [11,12,13].
Besides neuronal deficits, also alterations occurring in astrocytes, glial cells and factors of the innate immunity have been implicated directly in a process known as “inflammaging” [14,15,16,17].
Memory decline, associated with accumulation of amyloid-beta (Aβ), its related peptides and neurofibrillary tangles (NFTs) as well as to neuroinflammation, has thoroughly been investigated in both AD patients and different mouse models of the disease [18,19]. From the functional point of view, there is now a general consensus that AD is characterized by an excitation/inhibition imbalance at different circuitry levels that starts before plaque seeding [20], with neuronal hyperexcitability being consistently found upon single cell and extracellular local field potential (LFP) recordings, as well as with EEG or electrocorticographic (ECG) analyses [21,22,23,24].
Both in vivo studies, with anesthetized or awake subjects [25,26,27,28], and in vitro analyses, with cortical slices or isolated hippocampi, have established defective gamma (30–90 Hz) oscillations [28,29,30] and theta-gamma cross-frequency coupling (CFC) [31], a phenomenon playing a primary role in memory encoding and retrieval, both in humans [32,33,34,35,36] and mice [24,37].
The concept that, in AD, cognitive abnormalities are causally linked to network hyperexcitability and altered oscillatory rhythms, is also supported by the fact that manipulation of network activities, either artificially or following sensory stimulation, can rescue brain functionality and behavior in rodent models [30,38,39] and, possibly, also in humans [4,40,41].
We have recently shown that, in pre-depositing AD mice, brain spontaneous activity is characterized by marked reduction in the relative power of slow oscillations (SO, 0.1–1.7 Hz) [42]. In addition, coupling of SO to higher frequencies as well as SO connectivity are impaired at the hippocampal and cortical levels in plaque-seeding mice [42]. As reported by other groups [38,43,44,45], defective oscillatory activity in the very low frequency range (<3 Hz) is a prominent feature of AD, at its early stages.
We have here expanded the study of spontaneous brain activity to aged AD mice, also taking into account alterations in UP/DOWN-states and spiking activity. By this integrated approach we have analyzed the cross-talk between aging and AD progression in terms of basal network activity, and defined which specific changes are linked to AD progression but are distinct from the aging process. Furthermore, we show evidence that young AD mice have striking similarities to old control mice.
reference link : https://www.mdpi.com/2073-4409/11/2/238/htm
More information: Gali H. Weissberger et al, Increased Financial Altruism is Associated with Alzheimer’s Disease Neurocognitive Profile in Older Adults, Journal of Alzheimer’s Disease (2022). In press. www.j-alz.com/vol88-3
