A new study finds that retaining memories is maintained by the quality — not quantity — of dendritic spines, which are part of brain neurons.
Experts used to think that memory loss was due to loss in dendritic spines, which are a key component of synapses. But new research published Aug. 7 in Science Advances shows otherwise.
“This is a paradigm breaker,” Jeremy Herskowitz, PhD, an associate professor in the University of Alabama at Birmingham and study author, said in a statement.
Results show that developing synapses have enough plasticity, even in older individuals in their 80s and 90s, to retain memory. As a result of these findings, the authors said that a therapy to remodel dendritic spines and synapses could improve memory in aging adults or those with dementia.
A dendrite is a part of a neuron that receives impulses from other neurons. Each dendrite can have thousands of protrusions called spines. The head of each spine can form a contact point, called a synapse, to receive an impulse sent from another neuron. Dendritic spines can rapidly change shape or volume as they create new synapses, and as part of the process called brain plasticity.
For the study, the team evaluated 128 participants aged 65 and up who didn’t have dementia. The people had evaluations yearly, and donated their brains for research after they died. The average age at death was 90.5 years.
Researchers evaluated two samples from each brain: one from the temporal cortex, which has structures vital for long-term memory, and one from the frontal premotor cortex, which organizes movements.
After staining the brain samples, photographing thin slices and constructing three-dimensional digital models of dendritic spines on neurons, the team used statistical methods to see if any of 16 different spine morphology measurements correlated with any of 17 different measures of brain function, age and Alzheimer’s disease neuropathology.
For neurons from the temporal cortex, the diameter of the dendritic spine head, but not the quantity of spines, improved prediction of episodic memory in models containing β-amyloid plaque scores, neurofibrillary tangle pathology and sex.
Larger head diameters were linked with better episodic memory. This supported the notion that in the temporal cortex, synaptic strength is more critical than quantity for memory in old age.
“Targeting pathways that maintain spine head diameter or synaptic strength, rather than pathways that maintain or generate new spines or synapses, could potentially yield greater therapeutic benefits for older adults in preclinical phases of Alzheimer’s disease,” Herskowitz said.
