Dementia profoundly affects short-term memory storage by disrupting the brain’s ability to encode, maintain, and retrieve recent information. Short-term memory, also known as working memory, is the cognitive system responsible for temporarily holding and manipulating information over seconds to minutes. It is essential for everyday tasks such as remembering a phone number long enough to dial it or following a conversation. Dementia, a broad category of neurodegenerative disorders including Alzheimer’s disease, impairs this system through multiple pathological mechanisms that alter brain structure and function.
At the core of short-term memory impairment in dementia is damage to brain regions critical for memory processing, particularly the hippocampus and prefrontal cortex. The hippocampus plays a key role in forming new memories and transferring them into long-term storage, while the prefrontal cortex is involved in maintaining and manipulating information in working memory. In dementia, especially Alzheimer’s disease, the accumulation of toxic amyloid plaques and tau protein tangles leads to neuronal death and synaptic dysfunction in these areas. This synaptic loss disrupts the neural circuits that support short-term memory storage, causing the characteristic forgetfulness and difficulty in retaining new information seen in affected individuals [3][6].
Molecular and cellular changes also contribute to short-term memory deficits. Research shows that the brain uses a cascade of molecular “timers” to regulate memory formation and maintenance. These timers involve gene-regulating programs that unfold over time and across brain regions, ensuring that important memories are stabilized while less relevant ones fade. In dementia, these molecular processes are disrupted, impairing the brain’s ability to consolidate short-term memories into more durable forms [2]. Additionally, microglia, the brain’s immune cells, and the extracellular matrix (ECM) that surrounds neurons play roles in synaptic plasticity and memory. Aging and dementia alter microglia-ECM interactions, leading to synapse dysfunction and cognitive decline, further compromising short-term memory storage [3].
Astrocytes, star-shaped glial cells in the brain, are also implicated in dementia-related memory impairment. They normally support neuronal function and help clear toxic amyloid plaques. In Alzheimer’s disease models, enhancing astrocyte activity by increasing the expression of the protein Sox9 improves the clearance of amyloid plaques and preserves cognitive function, including memory. This suggests that astrocyte dysfunction contributes to the accumulation of pathological proteins that damage memory circuits, thereby impairing short-term memory storage [4].
Clinically, one of the earliest signs of dementia-related cognitive decline is a subtle loss of memory precision rather than outright forgetting. This means that memories become less detailed and less accurate, even when they are still accessible. Studies have shown that short-term memory precision is linked to the integrity of the prefrontal cortex, and its decline can be detected in middle-aged adults before traditional memory tests reveal deficits. This loss of precision reflects the brain’s diminishing ability to store and retrieve recent information accurately, a hallmark of early dementia [5].
The physiological stress response also influences memory in dementia. Elevated cortisol levels, often seen in chronic stress, impair hippocampus-dependent declarative memory and striatum-dependent stimulus-response memory. This hormonal disruption can exacerbate short-term memory deficits by further damaging the neural substrates involved in memory encoding and retrieval [1].
In summary, dementia influences short-term memory storage through a combination of neuronal loss, synaptic dysfunction, disrupted molecular memory mechanisms, glial cell alterations, and hormonal imbalances. These changes impair the brain’s ability to encode, maintain, and retrieve recent information, leading to the characteristic short-term memory problems observed in dementia patients.
Sources:
[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC12611907/
[2] https://medicalxpress.com/news/2025-11-brain-reveals-sequentially-molecular-timers.html
[3] https://www.nature.com/articles/s41467-025-66434-z
[4] https://www.news-medical.net/news/20251121/Astrocyte-driven-approach-shows-potential-to-reverse-cognitive-decline-in-Alzheimere28099s.aspx
[5] https://www.medicaldevice-network.com/comment/study-uncovers-the-first-subtle-sign-of-dementia/
[6] https://www.sciencealert.com/we-may-now-know-why-alzheimers-erases-memories-of-our-loved-ones
